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Longevity Library · Lab reference

Written by Daniel Tagge, MD
Updated October 23, 2026
Reviewed October 24, 2026
48 sources · Measured in mg/L

System: Gut-Immune Health

Secretory IgA (stool)sIgA · Fecal secretory IgA · Stool IgA · Secretory immunoglobulin A

Secretory IgA is the antibody the gut makes more of than any other, several grams a day, exported across the lining to coat bacteria and hold them in the lumen without inflammation; the biology is rich and well studied. The stool measurement is a different thing: no study ties a stool sIgA level in an adult to any outcome, no validated cutoff exists, the one published healthy-adult series found values up to 300 mg/L in 122 controls and far higher values in Crohn's disease, and the bacteria in the sample degrade the antibody itself. The outcome literature that gets quoted for it was done on saliva, in athletes and students, not on stool.

Secretory IgA is the main antibody of the gut lining, built as a dimer with a J chain, carried across the epithelium by the polymeric immunoglobulin receptor, and left wearing a piece of that receptor, the secretory component, which protects it in the lumen. It coats bacteria rather than killing them. On a stool panel it is sold as a gauge of gut immune strength, read low as weakness and high as activation. The measurement has no validated reference range, no outcome study behind any value, and in the one adult series the highest values belonged to people with inflammatory bowel disease. A truly absent IgA is a blood diagnosis, selective IgA deficiency, and that is where a very low value should send the conversation.

01 · The scale

Where the laboratory range and the evidence sit.

No outcome evidence exists for the stool value. No cohort, trial or guideline ties a stool secretory IgA level in an adult to infection, disease, symptoms or longevity, and no validated cutoff exists in either direction. What is established is at the edges and in other fluids: a true absence of IgA, diagnosed in blood, carried 2.4 times the prevalence of any hospital-recorded infection in 2,100 Swedish patients, while 177 IgA-deficient blood donors had no excess of hospital infections at all; the highest stool values in the one adult series belonged to Crohn's disease; and the salivary IgA literature in athletes and students, where a falling level preceded colds, is about saliva, with within-person variation of 48 percent and no link between the absolute level and illness.

010030050010001500

  1. Range of 122 healthy adults in the one published series (total fecal IgA, mg/L of stool extract, 1997 assay); other laboratories' ranges are in other units on other methods

    0 to 300 mg/L · Schoof 1997

  2. No evidence band exists anywhere on this scale: no study ties any value in a healthy adult to any outcome

    0 and above mg/L · This entry, 2026

  3. Above the healthy upper limit in the same series: means of 1,073 and 1,253 mg/L in inactive and active Crohn's disease, 486 in active ulcerative colitis

    300 and above mg/L · Schoof 1997

  • Laboratory range
  • Guideline goal or unstudied
  • Higher risk in studies
Scale in mg/L. Laboratories report stool sIgA in mg/dL, mg/L, µg/mL or µg/g of stool, each on its own extraction method and its own range, and results from different methods are not interchangeable. The scale on this page uses the one published healthy-adult series, which reported mg/L of stool extract on a 1997 research assay. Bands show where studies found something, not a recommendation for any one person.

02 · What it is

What Secretory IgA (stool) measures.

Immunoglobulin A is the antibody the body makes most of. By estimating output at every site, Conley and Delacroix calculated that humans synthesize and secrete more IgA each day than IgG and IgM combined, with about a third of it going straight into the blood and never reaching a mucosal surface; later reviews put the amount released into the intestine at several grams a day, from the largest population of antibody-secreting plasma cells in the body, which sits in the gut wall. In the blood IgA is mostly monomeric IgA1; in secretions it is mostly dimeric IgA2, and the two pools are, as the 1987 paper put it, separate but related systems.1,2,3,4Grade C

The 'secretory' in the name is a structure, not a location. Plasma cells in the gut lining make IgA as polymers, mainly dimers, joined by a small polypeptide called the J chain; only J-chain polymers bind with high affinity to the polymeric immunoglobulin receptor on the basolateral side of the epithelial cell, which carries them across and is cleaved at the apical surface, so that the antibody arrives in the lumen still wearing a piece of its receptor, the secretory component. The secretory component protects secretory IgA from proteolysis and has antimicrobial properties of its own. Mice lacking the receptor export no IgA or IgM across their epithelia at all, grow and breed normally, but leak albumin into saliva and feces and carry raised serum IgG against gut bacteria, which is the experimental definition of what the system does: it keeps the lumen and the body politely apart.5,6,7,8Grade C

What secretory IgA does to bacteria is called immune exclusion, a term coined for non-inflammatory antibody shielding of internal surfaces: it blocks access to epithelial receptors, entraps microbes in mucus, and lets peristalsis carry them away; it can quench bacterial virulence factors, shape the composition of the microbiota, carry antigens back across the epithelium to dendritic cells, and dampen the inflammatory response that pathogenic bacteria would otherwise provoke. The J chain gives the polymer many binding sites for agglutination and little or no complement-activating potential, which is how the antibody works without starting a fire. That is why a stool sIgA cannot be read the way a white cell count is read; it is the quietest arm of the immune system, and its job is to prevent inflammation rather than to signal it.7,9,5Grade C

03 · Origins

Where it came from, and where it sits in the network.

A mucosal antibody is older than IgA. Teleost fish, the most primitive bony vertebrates with immunoglobulins, have no IgA or any equivalent, which had suggested that the split between mucosal and systemic antibodies arose with the land vertebrates; in 2010 rainbow trout were shown to use a different isotype, IgT, as a mucosal antibody, responding to a gut parasite only in the gut while IgM responded only in serum, and coating most intestinal bacteria. IgT and IgA are phylogenetically distant, so the two lineages arrived at the same job separately, by convergent evolution. In mice, a significant share of the IgA made against commensal bacteria is induced without T cell help and without organized follicles, which the authors read as an evolutionarily primitive form of specific defense that persists alongside the newer, high-affinity machinery.10,11Grade C

The antibody and the microbiota built each other. Intestinal dendritic cells carry small numbers of live commensal bacteria for several days and use them to induce IgA locally, while the mesenteric lymph nodes keep those cells from reaching the rest of the body, so the response to the resident bacteria stays in the gut. The receptor that exports the antibody is itself switched on by microbial products through Toll-like receptor signaling. In a mouse carrying a single gut species and a single IgA against it, the antibody reduced the bacterium's inflammatory signaling and the host's oxidative response while the bacterium adjusted which surface molecules it expressed, a negotiation the authors called a mediator of gut homeostasis. Much of the IgA that coats the microbiota is polyreactive, with innate specificity for a defined subset of bacteria, selected in Peyer's patches whether or not the microbiota or dietary antigens are present; in humans the two subclasses divide the work, with Bacteroidetes in the colon preferentially targeted by IgA2 and gut-derived monoclonal antibodies binding many bacterial targets at once.12,6,13,14,3Grade C

The coat is readable, and that is where the modern work went. Sorting stool bacteria by how heavily IgA coats them and sequencing each fraction, Palm and colleagues found that high IgA coating picked out the bacteria that drove colitis in mice, and that IgA-coated bacteria cultured from people with inflammatory bowel disease conferred dramatic susceptibility to colitis when given to germ-free mice. In two cohorts of Malawian infants and children, IgA responses to several bacterial taxa, including Enterobacteriaceae, tracked nutritional status, and an IgA-targeted consortium of 11 strains from an undernourished child produced a diet-dependent enteropathy with barrier breakdown, weight loss and sepsis in gnotobiotic mice, preventable by two IgA-targeted species from a healthy microbiota. In 40 healthy US twin pairs the pattern of IgA responses to gut bacteria was distinctive for each family in the first months and converged across families in the second year, and most of the responses were robust to diet. Which bacteria the antibody coats carries information; how much antibody is in the stool is a different and cruder quantity.15,16,17Grade C

The first secretory IgA a person meets is someone else's. In a breeding scheme that gave or withheld maternal secretory IgA in milk, pups that received it were protected from translocation of aerobic bacteria to their lymph nodes, had a different gut microbiota by weaning, with the difference magnified in adulthood, a different pattern of epithelial gene expression as adults, and less colonic damage from a chemical injury. Where secretory IgA sits in the network is as the exclusion arm of the gut barrier: in people who lack IgA, the gut ecology is not massively perturbed in quantity, but pathobionts expand, some typically beneficial symbionts are depleted, mouth species colonize the gut, and IgM only partly fills the gap because not all of IgA's usual targets are bound by it; the authors place IgA at the forefront of the immune and microbial interface, away from the barrier itself, ranging from pathobiont control to regulation of systemic inflammation. Calprotectin, which this shelf covers separately, reports the inflammatory arm, neutrophils arriving in the lumen; secretory IgA reports the tolerant arm, and in infants the two rise together rather than in opposition.18,19,20Grade C

04 · The laboratory range

What a laboratory calls normal.

Laboratory-specific and not derived from outcomes; the one published healthy-adult series put the upper limit at 300 mg/L of stool extract (mean 73) on a 1997 research assay, and commercial panels print their own ranges in their own units.

There is one published healthy-adult reference series. In 1997 a German group validated a luminescence immunoassay for IgA in feces, measuring monomeric and polymeric IgA together, with assay coefficients of variation of 4.5 to 12.9 percent; in 122 healthy controls the mean was 73 mg/L and the upper limit of normal 300 mg/L. In the same series 14 patients with inactive Crohn's disease had a mean of 1,073 mg/L with values up to 3,317, 26 with active Crohn's disease ranged from 49 to 4,094 (mean 1,253), 18 with active ulcerative colitis averaged 486 and 16 in remission 176. The authors offered the assay for the detection of elevated fecal IgA in gut disease, especially Crohn's disease. Nothing in the paper defines a low value, and nothing in the later literature does either.21Grade C

The range a commercial panel prints is a distribution of that laboratory's samples on that laboratory's method, and the methods differ in what they extract, what they count and the unit they count it in. The question of whether a reference range for stool IgA can be built at all has been studied most carefully in dogs: across 356 healthy dogs of four breeds, the differences between a single defecation and the next, between individuals of the same breed, and the lack of any internal control molecule led the authors to conclude that a normal reference range for all dogs was impossible and the usefulness of fecal immunoglobulin quantification limited; a second group found the within-dog variability high enough that a reliable value needed four samples, two on consecutive days and two more 28 days later. No comparable study of day-to-day variation in healthy adult humans was found.22,23Grade C

The microbiome testing field has said the same thing about its own reference ranges. A 2025 international consensus of 70 experts on microbiome testing in clinical practice, written because commercial providers offer direct-to-consumer tests without any proven value in clinical practice, agreed that there is not enough information to report strict healthy reference ranges of species abundance (90 percent agreement), that there is insufficient evidence to include any dysbiosis index in a report (90 percent), that there is insufficient evidence to widely recommend routine microbiome testing (90 percent), that any change in management should be made only by the referring physician (100 percent), and that post-testing therapeutic advice from the testing provider is discouraged (98 percent). The statement addresses sequencing-based tests, not the sIgA line on the same panels, and this entry does not stretch it further than that; the stool sIgA literature is thinner still.24Grade A

05 · The evidence

What the studies support.

The claim that a low stool sIgA means a weak gut immune system has not been tested in adults, and the available human data run the other way as often as not. In the 1997 series the patients stood out by having more fecal IgA than the healthy controls, not less, with Crohn's disease means 15 to 17 times the healthy mean. In 44 people with diarrhea-predominant irritable bowel syndrome compared with 32 healthy volunteers, fecal IgA, particularly IgA1, was raised, IgA class switching was increased in the terminal ileum, and the share of IgA-coated bacteria was higher, with the coating of Escherichia-Shigella correlating with anxiety and depression scores. In 1975, children just recovered from infectious enteritis had higher fecal IgA than healthy children. A high value reads at least as naturally as a mucosa under provocation as a mucosa in good health.21,25,26Grade C

In infants, where stool IgA has been studied prospectively, higher values went with less allergy and with more inflammation at the same time. Among 237 allergy-prone infants in a Finnish prevention trial, those with high fecal IgA at 6 months had half the odds of an IgE-associated allergic disease by age 2 (odds ratio 0.49), and every fecal inflammation marker measured, alpha-1-antitrypsin, tumor necrosis factor alpha and calprotectin, correlated positively with fecal IgA; a high calprotectin at 6 months carried the same lower odds (0.49). In Mali, 6-month-old infants had stool sIgA 4.0 times higher than age-matched Nicaraguan infants alongside 31.6 times the fecal myeloperoxidase, and sIgA correlated with the enteropathy marker alpha-1-antitrypsin (0.52). The number rises when the gut is being challenged; whether that is the immune system doing well or the gut doing badly depends on everything else in the picture.20,27Grade C

The edge that is established is absence, and it is diagnosed in blood, not stool. Selective IgA deficiency, a serum IgA below the detection threshold with normal IgG and IgM, is the most common primary antibody deficiency; most people who have it are asymptomatic and found by accident, and some have recurrent respiratory and gastrointestinal infections, allergy or autoimmunity. In a Swedish nationwide cohort of 2,100 people with IgA below 0.07 g/L and 18,653 matched controls, 36.1 percent against 18.8 percent had a hospital-recorded infection (prevalence ratio 2.4), with respiratory infections 17.8 against 6.3 percent, gastrointestinal infections 6.0 against 1.8 and sepsis 1.5 against 0.45. Across the pooled literature, 64.8 percent of IgA-deficient patients had infections, 26.2 percent allergic disease and 22.0 percent autoimmunity, with celiac disease in 6.6 percent and inflammatory bowel disease in 4.0 percent of those with the selective form. Those are people with no IgA, found through the clinic; the cohorts say nothing about a low-normal stool value in a well adult.4,28,29Grade B

Even true absence is often silent. Among 177 IgA-deficient Danish blood donors compared with 1,770 control donors, the hazard ratio for a filled antimicrobial prescription was 1.19 (P = 0.05), for a hospital-recorded infection 1.02, self-reported physical health did not differ, and the authors concluded that the findings did not warrant specific health precautions for donors with IgA deficiency. Stool measurements in people with no IgA have shown no detectable fecal IgA and a raised fecal IgM instead, and in a 2018 study of human IgA deficiency the gut microbiota was not massively perturbed in quantity, with pathobiont expansion, loss of some beneficial symbionts and partial rescue by IgM. If the complete loss of the antibody is compatible with an ordinary life in most people who have it, a modestly low stool reading in a person with a normal serum IgA cannot carry the meaning the panels give it.30,26,19Grade C

The outcome literature that gets borrowed for the stool test is the salivary IgA literature, and it is instructive in a different way. In 26 elite swimmers followed 7 months, pretraining salivary IgA was 4.1 percent lower for each additional month of training and 5.8 percent lower for each infection, and the season's trend predicted infections; in 38 professional sailors sampled weekly for 50 weeks, salivary IgA varied by 48 percent within a person and 71 percent between people, the absolute concentration did not correlate with upper respiratory infections at all (r = 0.11), and what predicted illness was a 28 percent fall over the three weeks before it, with a value below 40 percent of a person's own healthy mean carrying a one in two chance of infection within three weeks. In 98 marathon runners the secretion rate fell 25 percent by 90 minutes after the race, 16 of 93 (17 percent) reported an infection in the next 15 days, and their post-race IgA-to-protein ratio was lower (254 against 388 µg/g) and correlated inversely with cortisol. Saliva can be sampled daily at rest, which is why its trajectory means something; a single stool value has no trajectory and no personal baseline.31,32,33Grade C

Stress lowers salivary IgA, which is the origin of the idea that stress lowers gut IgA. In 64 first-year dental students sampled five times across a year, the salivary IgA secretion rate was lower during the three examination periods than in the low-stress periods, and in 27 medical students giving daily morning saliva from six days before a major examination to 14 days after, the concentration remained below that of 27 controls at day 14 with no recovery, even though self-reported stress had returned to normal. For stool, the human evidence is one infant study: among 403 Canadian infants, those whose mothers had clinically significant depressive symptoms both before and after birth had a median stool sIgA of 4.4 against 6.3 mg/g, with threefold odds of being in the lowest quarter after adjustment for breastfeeding, age and antibiotics. In 23 semi-free-ranging Barbary macaques, 340 fecal samples showed high variability within and between animals, no change when their worm burden was treated away, and a correlation with fecal glucocorticoid metabolites, which led the authors to conclude that the responsiveness of fecal IgA to the stress axis limits its use as a measure of mucosal immunity. A number that moves with a person's week is not a number that measures a person's gut.34,35,36,37Grade C

The sample itself sets the number. In wild-type mice of the same strain in the same facility, fecal IgA levels fell into two groups, high and low, because of transmissible bacteria in the low group that degrade both the secretory component and the antibody; cohousing or fecal transfer from a low mouse lowered a high mouse, and the low mice were more vulnerable to intestinal injury, a difference that traveled with the stool. In 1975, immunoglobulins in freeze-dried stool extracts seemed to mirror the total amount of IgA secreted into the gut at the time of sampling, which is the hopeful reading; the 2015 mouse work is the caution: what reaches the cup is what the resident bacteria have left intact. A low stool sIgA can mean less antibody made, more antibody eaten, or a different extraction on a different day, and the test cannot tell those apart.38,26Grade C

06 · What moves it

The levers with evidence behind them.

What is listed here has been tested. The size of each effect, and the size of the study, are in the sentence, so a small effect reads as a small effect.

  • Probiotic supplements

    move the stool number in trials, in both directions, with no outcome attached

    Probiotics are the lever the panels point to, and the trials show a number that moves without showing what the movement means. In 100 healthy Spanish volunteers given one of three strains, a mixture or placebo for 30 days, one strain significantly increased fecal sIgA while gastrointestinal symptoms, stool frequency and consistency did not change in anyone. In two Chinese sub-trials of 70 adults each with functional constipation or functional diarrhea, four weeks of a multi-strain product raised fecal sIgA alongside better symptom scores. In 33 children with newly diagnosed celiac disease starting a gluten-free diet, three months of a single strain lowered stool sIgA compared with placebo (P = 0.011) while reducing activated T cells in blood, and the authors read that as improvement. The most cited immune trial, 211 healthy adults given one of two strains for six weeks around an influenza vaccine, measured vaccine-specific antibodies in saliva and plasma, found greater rises in both probiotic groups, and did not measure infections or any other outcome. Up has been called good and down has been called good; the number is not the outcome.39,40,41,42Grade C

  • Fermentable fiber and prebiotics

    raised it in one adult trial and did nothing in another

    In 45 overweight adults with features of the metabolic syndrome, a 12-week crossover trial of a galacto-oligosaccharide mixture against maltodextrin increased fecal bifidobacteria and fecal secretory IgA and decreased fecal calprotectin, plasma C-reactive protein, insulin, total cholesterol and triglycerides; the abstract reports directions, not sizes. In 52 healthy young adults and 48 healthy older adults given 15 g a day of pectin or placebo for four weeks, salivary and fecal sIgA and serum IgA did not differ (P at or above 0.128), nor did any measure of gut permeability. A fermentable fiber that feeds the bacteria the antibody is directed at can be expected to change the antibody; the fiber entry on this shelf makes the case for fiber on outcomes that have been measured, and that case does not depend on this number.43,44Grade C

  • Psychological stress

    lowers salivary IgA for weeks; for stool, one infant study and one primate study

    The dental students' secretion rate fell during examinations and the medical students' concentration had not recovered two weeks after theirs; in the infants of mothers with depressive symptoms through pregnancy and after birth, stool sIgA ran a third lower; and in the macaques, fecal IgA tracked fecal glucocorticoids rather than parasite load. Stress is a real input to this number. That is an argument for asking about the month a sample was collected in, not for treating the sample as a verdict on the gut.34,35,36,37Grade C

  • Heavy training load

    lowers salivary IgA after hard sessions and across a heavy season; no stool study in humans

    After a marathon the salivary IgA secretion rate fell 25 percent within 90 minutes and the runners who then caught a cold had the lower post-race IgA-to-protein ratio; across a swimming season, each added month of training took 4.1 percent off the pretraining level and each additional kilometer in a session took 8.5 percent off the posttraining level; across 50 weeks of professional sailing, the fall before an infection was 28 percent. Every one of those is saliva, sampled repeatedly against a personal baseline. No study of training load and stool sIgA in people was found, and a result on a stool panel collected during a heavy block should be read with that in mind.33,31,32Grade C

  • Sleep

    lowered salivary IgA in one small study when restricted during hard training; untested for stool

    In 16 youth soccer players followed for seven weeks, two weeks of a 75 percent increase in training load both lowered salivary IgA, but only the week in which total sleep also fell by about 10 percent (44 minutes) brought more severe upper respiratory symptoms, more fatigue and less vigor; the week with unrestricted sleep did not. It is a small study in saliva and the only one found that separates sleep from load. Nothing connects sleep to a stool sIgA value in any published human study.45Grade C

  • Infancy, breast milk and the first bacteria

    set the system up; the first stool IgA a baby passes is mostly the mother's

    Maternal secretory IgA in milk shaped the pups' microbiota and epithelial gene expression into adulthood in the breeding experiments, and in healthy human twins the IgA response to the microbiota was a family signature in the first months before it generalized in the second year. Nothing on this page about adult stool values applies to infants, in whom the number reflects feeding, maternal antibody, colonization and the timing of the switch to the child's own production.18,17Grade C

07 · Reading it well

Caveats, and what belongs with a physician.

The number has no validated range and no outcome behind any value. The one healthy-adult series is from 1997, on a research assay, in mg/L of extract, measuring total rather than specifically secretory IgA; the commercial panels report other units on other methods; the reference-range problem has been studied carefully only in dogs, where it was judged unsolvable from single samples; and no human study of day-to-day variation in adults was found. A single stool value cannot be placed on any scale that has been shown to matter.21,22,23Grade C

High is not reassuring and low is not alarming on the evidence available. The highest values in the adult series were Crohn's disease; diarrhea-predominant irritable bowel syndrome, recovery from infectious enteritis and infant enteropathy all raised the number; the complete absence of IgA was compatible with ordinary health in most blood donors who had it. The marketing reading, low means weak and high means strong, is not what the human studies show.21,25,27,30Grade C

The stool value is not a test for selective IgA deficiency, and the deficiency is the one thing a very low value should raise. The diagnosis is a serum IgA below the laboratory's detection limit with normal IgG and IgM; in people who have it the stool has shown no IgA and a compensating IgM. A stool result cannot make that diagnosis and a serum IgA can, in one tube.4,28,26Grade B

IgA deficiency changes how celiac disease is tested for, and stool antibody tests do not rescue it. The standard screening antibody, tissue transglutaminase IgA, is uninterpretable in a person who makes no IgA, which is why the European pediatric guideline asks for total serum IgA alongside it and an IgG-based test only when total IgA is low or undetectable; among 325 IgA-deficient subjects, an IgG anti-transglutaminase test had a sensitivity of 98.7 percent and a specificity of 98.6 percent, and 9.8 percent of symptom-free IgA-deficient blood donors tested positive, which led the authors to recommend that all IgA-deficient people be evaluated for celiac disease. Stool tests for secretory IgA antibodies against transglutaminase and gliadin, when validated in 20 children with celiac disease and 64 controls, had sensitivities of 10 and 6 percent and were judged unsuitable for screening.46,47,48Grade A

The saliva literature does not transfer. Salivary IgA was informative in athletes because it was sampled weekly or daily against each person's own mean, and even then the absolute level did not correlate with illness; its within-person variation was 48 percent. A stool panel gives one value, in another fluid, with no baseline, and the inference from athletes' saliva to a patient's stool is not one any of those studies made.32,31Grade C

What the panel sells as a lever has not been tied to anything. Probiotic trials moved the number up in healthy adults whose symptoms did not change and down in celiac children whose immune markers improved; the vaccine trial measured antibodies, not infections; one fiber trial raised it and another did not. No trial has changed a stool sIgA and shown fewer infections, fewer symptoms or a better anything as a result of the change.39,41,42,44Grade C

See a physician

  • Recurrent sinus, ear or chest infections, repeated courses of antibiotics in a year, or repeated gut infections, whatever the stool sIgA shows; the question is a serum IgA, IgG and IgM, and in the Swedish cohort people with no IgA had about three times the prevalence of hospital-recorded respiratory and gastrointestinal infections.
  • A serum IgA reported as undetectable or below the laboratory's limit, which is selective IgA deficiency if IgG and IgM are normal; most people with it are well, and the ones who are not need an immunologist rather than a supplement.
  • A diagnosis of IgA deficiency in anyone being tested for celiac disease, because the standard tissue transglutaminase IgA test cannot work without IgA, an IgG-based test is needed instead, and about one in ten symptom-free IgA-deficient blood donors carried celiac antibodies.
  • Any stool panel ordered for persistent diarrhea, blood in the stool, weight loss, nighttime symptoms, anemia or a family history of inflammatory bowel disease, because in the only adult series a very high fecal IgA kept company with Crohn's disease and active ulcerative colitis, and those are diagnosed by calprotectin, blood tests and endoscopy, not by sIgA.
  • Anyone about to start a supplement regimen or an elimination diet on the strength of a stool sIgA result, who should hear first that no value on that line has been tied to an outcome and that the trials which moved it did not show benefit from moving it.
  • Any stool result in an infant or young child, where the number reflects feeding and maternal antibody and belongs with a pediatrician.

This page is education, not individual medical advice, and reading it creates no physician-patient relationship.

08 · Open questions

What the literature does not settle.

  • Whether a stool secretory IgA level in a healthy adult predicts anything at all has not been studied prospectively: no cohort has measured it at baseline and followed infections, symptoms, inflammatory bowel disease or mortality.
  • What the normal day-to-day and week-to-week variation of stool sIgA is in adults, and how much of it comes from stool water content, transit time, extraction method and bacterial degradation of the antibody, is unknown in humans; the dog studies suggest it is large.
  • Whether a low stool value ever reflects low mucosal production in a person with a normal serum IgA, rather than degradation in the lumen or sampling, has not been tested; it would need paired tissue, luminal and stool measurements in the same people.
  • Whether the direction that matters is up or down, and in which context, is unresolved: trials have called a rise improvement in healthy and constipated adults and a fall improvement in celiac children, and in infants the number rose with both protection from allergy and with inflammation.
  • Whether the salivary IgA findings in athletes, which depend on repeated sampling against a personal baseline, have any stool equivalent, and whether a personal stool baseline could be established affordably enough to make a trend readable, has not been studied.
  • Whether IgA coating of specific bacteria, which has mechanistic and diagnostic promise in inflammatory bowel disease and childhood undernutrition, will ever be a clinical test, and whether it has any relationship to the total sIgA concentration the panels report, is open.
  • How the two human subclasses, IgA1 and IgA2, divide the work in adults, and whether an assay that counts them together is counting the right thing, is a laboratory question that the current panels do not address.

09 · In practice

How Dr. Tagge reads it in his own practice.

Secretory IgA comes back on the stool panels I order, and I want to be plain about how I read it: as a question, not a result. I know the biology is beautiful and I know the stool number has no validated cutoff, so I do not let the first lend weight to the second. One marker is a clue and three are a story, and this one is never the story on its own. I read it beside calprotectin, elastase, the microbiome report, the person's symptoms, their sleep, the month they were having when they collected the sample, and their training load, because the saliva work says all of those move the antibody and nothing says the stool value sits still while they do. A high value makes me look harder at inflammation and symptoms rather than congratulate anyone. A very low value does one specific thing for me: it makes me ask about sinus and chest infections, antibiotic courses and gut infections, and if there is any such history I check a serum IgA, because selective IgA deficiency is a blood diagnosis with real consequences, including how celiac disease has to be tested for, and a stool panel can neither make it nor rule it out. I do not sell a supplement to move this number, and I tell people that the trials which moved it did not show anyone better for it. Where I am ahead of the evidence is in ordering the panel at all; the elastase and calprotectin lines earn their place, and the sIgA line rides along. I keep looking at it because a pattern across people and across time may teach me something a single value cannot, and I say so rather than pretend it has already taught me.

A practice judgment, labeled as one (Grade D): it is how one physician reads the number for the people he cares for, not a recommendation for you.

10

Questions

11 · Sources

48 sources, read in full.

Numbered in the order they appear. Each line says what this page relies on from the paper; the link opens the record at PubMed or the publisher.

  1. 1.

    Conley ME, Delacroix DL. Intravascular and mucosal immunoglobulin A: two separate but related systems of immune defense?. Annals of Internal Medicine. 1987. PMID 3579073. DOI 10.7326/0003-4819-106-6-892.

    Review · By estimating production at every site, humans synthesize and secrete more IgA each day than IgG and IgM combined; about one third is secreted directly into the vascular compartment and never reaches a mucosal surface; mucosal surfaces are neither the source nor the destination of serum IgA.

  2. 2.

    Pabst O. New concepts in the generation and functions of IgA. Nature Reviews Immunology. 2012. PMID 23103985. DOI 10.1038/nri3322.

    Review · The intestinal mucosa holds the largest population of antibody-secreting plasma cells in the body and in humans several grams of secretory IgA are released into the intestine each day; SIgA serves as a first-line barrier and regulates host-commensal relations.

  3. 3.

    Sterlin D, Fadlallah J, Adams O, Fieschi C, Parizot C, Dorgham K, et al.. Human IgA binds a diverse array of commensal bacteria. Journal of Experimental Medicine. 2020. PMID 31891367. DOI 10.1084/jem.20181635.

    Laboratory method study · Several grams of IgA are secreted daily into the human intestinal lumen; humans make IgA1 and IgA2, most small-intestinal commensals are targeted by both, Bacteroidetes in the colon is preferentially targeted by IgA2, and gut-derived monoclonal IgAs are cross-reactive, binding multiple bacterial targets.

  4. 4.

    Yel L. Selective IgA deficiency. Journal of Clinical Immunology. 2010. PMID 20101521. DOI 10.1007/s10875-009-9357-x.

    Review · IgA deficiency is the most common primary immunodeficiency, defined as a decreased serum IgA with normal levels of the other isotypes; most individuals are asymptomatic and found coincidentally, some have recurrent respiratory and gastrointestinal infections, allergy or autoimmunity; monomeric IgA1 dominates blood and dimeric IgA2 dominates secretions.

  5. 5.

    Johansen FE, Braathen R, Brandtzaeg P. Role of J chain in secretory immunoglobulin formation. Scandinavian Journal of Immunology. 2000. PMID 10972899. DOI 10.1046/j.1365-3083.2000.00790.x.

    Review · The J chain regulates polymer formation of IgA (mainly dimers) and IgM, giving high valency for agglutination, little or no complement-activating potential, and, decisively, high affinity for the polymeric Ig receptor; secretory IgA, secretory IgM and free secretory component are generated by cleavage of the receptor's extracellular domain.

  6. 6.

    Kaetzel CS. The polymeric immunoglobulin receptor: bridging innate and adaptive immune responses at mucosal surfaces. Immunological Reviews. 2005. PMID 16048543. DOI 10.1111/j.0105-2896.2005.00278.x.

    Review · Epithelial transcytosis of polymeric IgA is mediated by the polymeric immunoglobulin receptor; its cleaved extracellular region, secretory component, has innate antimicrobial properties and protects SIgA from proteolysis; pIgR expression is regulated by microbial products through Toll-like receptor signaling and by cytokines and hormones.

  7. 7.

    Brandtzaeg P. Secretory IgA: Designed for Anti-Microbial Defense. Frontiers in Immunology. 2013. PMID 23964273. DOI 10.3389/fimmu.2013.00222.

    Review · Immune exclusion is non-inflammatory antibody shielding of internal surfaces mediated principally by SIgA; the exported antibodies are polymeric, mainly dimers, complexed with secretory component; pIgR is the only receptor exporting IgA and IgM, and pIgR-deficient mice show mucosal defense defects and changes in their intestinal microbiota; the mucosal system must discriminate symbionts, pathobionts and pathogens.

  8. 8.

    Johansen FE, Pekna M, Norderhaug IN, Haneberg B, Hietala MA, Krajci P, Betsholtz C, Brandtzaeg P. Absence of epithelial immunoglobulin A transport, with increased mucosal leakiness, in polymeric immunoglobulin receptor/secretory component-deficient mice. Journal of Experimental Medicine. 1999. PMID 10510081. DOI 10.1084/jem.190.7.915.

    Laboratory method study · pIgR knockout mice completely lack active external IgA and IgM transport, are of normal size and fertility, have increased serum IgG including antibodies to Escherichia coli, and leak albumin into saliva and feces; SIgA was not essential for health under experimental conditions but contributes to mucosal homeostasis.

  9. 9.

    Mantis NJ, Rol N, Corthésy B. Secretory IgA's complex roles in immunity and mucosal homeostasis in the gut. Mucosal Immunology. 2011. PMID 21975936. DOI 10.1038/mi.2011.41.

    Review · Through immune exclusion SIgA blocks access to epithelial receptors, entraps microbes in mucus and facilitates their removal by peristalsis; it can quench bacterial virulence factors, influence microbiota composition, retro-transport antigens to dendritic cells and downregulate proinflammatory responses to pathogenic bacteria and allergens.

  10. 10.

    Zhang YA, Salinas I, Li J, Parra D, Bjork S, Xu Z, LaPatra SE, Bartholomew J, Sunyer JO. IgT, a primitive immunoglobulin class specialized in mucosal immunity. Nature Immunology. 2010. PMID 20676094. DOI 10.1038/ni.1913.

    Laboratory method study · Teleost fish lack IgA or a functional equivalent, yet rainbow trout IgT acts as a mucosal antibody, responding to an intestinal parasite only in the gut while IgM responded only in serum, and coating most intestinal bacteria; IgT and IgA are phylogenetically distant, so mucosal specialization arose independently by convergent evolution.

  11. 11.

    Macpherson AJ, Gatto D, Sainsbury E, Harriman GR, Hengartner H, Zinkernagel RM. A primitive T cell-independent mechanism of intestinal mucosal IgA responses to commensal bacteria. Science. 2000. PMID 10864873. DOI 10.1126/science.288.5474.2222.

    Laboratory method study · IgA against intestinal commensal antigens was specifically induced and responded to changes in an established flora; a significant proportion of this anti-commensal IgA was induced independently of T cell help and of follicular lymphoid organization, which may reflect an evolutionarily primitive form of specific defense.

  12. 12.

    Macpherson AJ, Uhr T. Induction of protective IgA by intestinal dendritic cells carrying commensal bacteria. Science. 2004. PMID 15016999. DOI 10.1126/science.1091334.

    Laboratory method study · Intestinal dendritic cells retain small numbers of live commensal bacteria for several days and selectively induce IgA that protects against mucosal penetration; the commensal-loaded cells are confined to the mucosal immune compartment by the mesenteric lymph nodes, so responses are induced locally without systemic immunity.

  13. 13.

    Peterson DA, McNulty NP, Guruge JL, Gordon JI. IgA response to symbiotic bacteria as a mediator of gut homeostasis. Cell Host and Microbe. 2007. PMID 18005754. DOI 10.1016/j.chom.2007.09.013.

    Laboratory method study · In gnotobiotic mice with one bacterial species and one monoclonal IgA against its capsule, the absence of IgA produced a more robust innate immune response; IgA reduced intestinal proinflammatory signaling and bacterial epitope expression, balancing suppression of the oxidative burst against the antibody's cost to bacterial fitness.

  14. 14.

    Bunker JJ, Erickson SA, Flynn TM, Henry C, Koval JC, Meisel M, Jabri B, Antonopoulos DA, Wilson PC, Bendelac A. Natural polyreactive IgA antibodies coat the intestinal microbiota. Science. 2017. PMID 28971969. DOI 10.1126/science.aan6619.

    Laboratory method study · Murine intestinal IgAs were not specific to individual taxa but polyreactive, with broad reactivity to a defined subset of the microbiota, selected into the IgA repertoire in Peyer's patches independently of microbiota or dietary antigens; somatic mutations did not substantially change their reactivity.

  15. 15.

    Palm NW, de Zoete MR, Cullen TW, Barry NA, Stefanowski J, Hao L, et al.. Immunoglobulin A coating identifies colitogenic bacteria in inflammatory bowel disease. Cell. 2014. PMID 25171403. DOI 10.1016/j.cell.2014.08.006.

    Laboratory method study · Sorting intestinal bacteria by IgA coating (IgA-SEQ) showed that high coating uniquely identifies colitogenic bacteria in a mouse model, and bacteria from IBD patients selected for high IgA coating conferred dramatic susceptibility to colitis in germ-free mice.

  16. 16.

    Kau AL, Planer JD, Liu J, Rao S, Yatsunenko T, Trehan I, et al.. Functional characterization of IgA-targeted bacterial taxa from undernourished Malawian children that produce diet-dependent enteropathy. Science Translational Medicine. 2015. PMID 25717097. DOI 10.1126/scitranslmed.aaa4877.

    Laboratory method study · In two cohorts of Malawian infants and children, IgA responses to several taxa including Enterobacteriaceae correlated with nutritional status; an IgA-targeted consortium of 11 strains from an undernourished child produced diet-dependent enteropathy, weight loss and sepsis in gnotobiotic mice, prevented by two IgA-targeted species from a healthy microbiota.

  17. 17.

    Planer JD, Peng Y, Kau AL, Blanton LV, Ndao IM, Tarr PI, Warner BB, Gordon JI. Development of the gut microbiota and mucosal IgA responses in twins and gnotobiotic mice. Nature. 2016. PMID 27279225. DOI 10.1038/nature17940.

    Prospective cohort · In 40 healthy US twin pairs followed over the first two years, gut mucosal IgA responses to members of the microbiota were highly distinctive for each family in the first months and generalized across pairs in the second year; most responses were robust to diet when recapitulated in gnotobiotic mice.

  18. 18.

    Rogier EW, Frantz AL, Bruno ME, Wedlund L, Cohen DA, Stromberg AJ, Kaetzel CS. Secretory antibodies in breast milk promote long-term intestinal homeostasis by regulating the gut microbiota and host gene expression. Proceedings of the National Academy of Sciences of the United States of America. 2014. PMID 24569806. DOI 10.1073/pnas.1315792111.

    Laboratory method study · Using pIgR-sufficient and -deficient dams, early exposure to maternal SIgA in milk prevented translocation of aerobic bacteria to draining lymph nodes, produced a different gut microbiota by weaning that diverged further in adulthood, altered adult epithelial gene expression, and ameliorated dextran sulfate sodium colitis.

  19. 19.

    Fadlallah J, El Kafsi H, Sterlin D, Juste C, Parizot C, Dorgham K, et al.. Microbial ecology perturbation in human IgA deficiency. Science Translational Medicine. 2018. PMID 29720448. DOI 10.1126/scitranslmed.aan1217.

    Cross-sectional study · Human IgA deficiency is not associated with massive quantitative perturbation of gut microbial ecology; metagenomics showed pathobiont expansion, depletion of some typically beneficial symbionts and colonization by oropharyngeal species; IgM only partially rescues the deficiency because not all IgA targets are bound by IgM.

  20. 20.

    Kukkonen K, Kuitunen M, Haahtela T, Korpela R, Poussa T, Savilahti E. High intestinal IgA associates with reduced risk of IgE-associated allergic diseases. Pediatric Allergy and Immunology. 2010. PMID 19566584. DOI 10.1111/j.1399-3038.2009.00907.x.

    Prospective cohort · In a nested case-control study of 237 allergy-prone infants, high fecal IgA at 6 months reduced the odds of IgE-associated disease by age 2 (OR 0.49), high fecal calprotectin carried the same lower odds (0.49), all fecal inflammation markers correlated positively with fecal IgA (p < 0.001), and probiotics tended to augment fecal IgA (p = 0.085).

  21. 21.

    Schoof E, John MR, Arndt B, Gao P, Theuer D, Sieg A, Schmidt-Gayk H. Solid phase competitive luminescence immunoassay for immunoglobulin A in faeces: development and clinical validation. Clinica Chimica Acta. 1997. PMID 9187500. DOI 10.1016/s0009-8981(96)06510-2.

    Laboratory method study · A luminescence immunoassay measuring monomeric and polymeric fecal IgA (coefficients of variation 4.5 to 12.9 percent) gave an upper limit of normal of 300 mg/L in 122 healthy controls (mean 73); inactive Crohn's disease (n = 14) averaged 1,073 mg/L (up to 3,317), active Crohn's (n = 26) 1,253 (range 49 to 4,094), active ulcerative colitis (n = 18) 486 and remission (n = 16) 176.

  22. 22.

    Peters IR, Calvert EL, Hall EJ, Day MJ. Measurement of immunoglobulin concentrations in the feces of healthy dogs. Clinical and Diagnostic Laboratory Immunology. 2004. PMID 15358641. DOI 10.1128/CDLI.11.5.841-848.2004.

    Laboratory method study · In 356 healthy dogs of four breeds, differences in fecal immunoglobulin concentrations from a single defecation, between individuals of the same breed and between breeds, together with the lack of an internal control molecule, made a normal reference range impossible and the usefulness of fecal immunoglobulin quantification limited.

  23. 23.

    Tress U, Suchodolski JS, Williams DA, Steiner JM. Development of a fecal sample collection strategy for extraction and quantification of fecal immunoglobulin A in dogs. American Journal of Veterinary Research. 2006. PMID 17014328. DOI 10.2460/ajvr.67.10.1756.

    Laboratory method study · In 23 healthy dogs, intraindividual variability of fecal IgA required a collection strategy of four samples, on two consecutive days and again 28 days later, to characterize an animal; the derived reference range was 0.22 to 3.24 mg/g of feces.

  24. 24.

    Porcari S, Mullish BH, Asnicar F, Ng SC, Zhao L, Hansen R, et al.. International consensus statement on microbiome testing in clinical practice. Lancet Gastroenterology and Hepatology. 2025. PMID 39647502. DOI 10.1016/S2468-1253(24)00311-X.

    Consensus statement · Convened because commercial providers offer direct-to-consumer microbiome tests without proven clinical value, the panel agreed there is not enough information to report strict healthy reference ranges of species abundance (90 percent), insufficient evidence for any dysbiosis index (90 percent) or for routine clinical use (90 percent), that management changes belong only to the referring physician (100 percent) and that post-testing therapeutic advice from the provider is discouraged (98 percent).

  25. 25.

    Liu Y, Yuan X, Li L, Lin L, Zuo X, Cong Y, Li Y. Increased Ileal Immunoglobulin A Production and Immunoglobulin A-Coated Bacteria in Diarrhea-Predominant Irritable Bowel Syndrome. Clinical and Translational Gastroenterology. 2020. PMID 32352710. DOI 10.14309/ctg.0000000000000146.

    Cross-sectional study · In 44 patients with diarrhea-predominant IBS and 32 healthy volunteers, fecal IgA, particularly IgA1, was raised, IgA class switching was increased in the terminal ileum, the proportion of IgA-coated fecal bacteria was higher, and the Escherichia-Shigella IgA coating index correlated with anxiety and depression.

  26. 26.

    Haneberg B, Aarskog D. Human faecal immunoglobulins in healthy infants and children, and in some with diseases affecting the intestinal tract or the immune system. Clinical and Experimental Immunology. 1975. PMID 813931.

    Laboratory method study · Immunoglobulins quantified in freeze-dried faecal extracts seemed to mirror total IgA secreted into the gut at the time of sampling; children just recovered from infectious enteritis had higher faecal IgA; two IgA-deficient patients had no detectable faecal IgA and increased faecal IgM; three agammaglobulinaemic patients had none.

  27. 27.

    Vilander AC, Hess A, Abdo Z, Ibrahim H, Doumbia L, Douyon S, et al.. A Randomized Controlled Trial of Dietary Rice Bran Intake on Microbiota Diversity, Enteric Dysfunction, and Fecal Secretory IgA in Malian and Nicaraguan Infants. Journal of Nutrition. 2022. PMID 35441218. DOI 10.1093/jn/nxac087.

    Randomized trial · Six-month-old Malian infants had stool sIgA 4.0 times higher than age-matched Nicaraguan infants with 31.6 times the fecal myeloperoxidase and 1.8 times the alpha-1-antitrypsin; sIgA correlated with alpha-1-antitrypsin (0.523) in the Nicaraguan cohort and with neopterin (0.544) in the Malian rice bran group at 12 months.

  28. 28.

    Ludvigsson JF, Neovius M, Hammarström L. Risk of Infections Among 2100 Individuals with IgA Deficiency: a Nationwide Cohort Study. Journal of Clinical Immunology. 2016. PMID 26739713. DOI 10.1007/s10875-015-0230-9.

    Prospective cohort · Among 2,100 Swedish individuals with IgA below 0.07 g/L and 18,653 matched controls, 36.1 versus 18.8 percent had a hospital-recorded infection (prevalence ratio 2.4, 2.2 to 2.6), with respiratory infections 17.8 versus 6.3 percent (PR 3.2), gastrointestinal 6.0 versus 1.8 (3.5) and sepsis 1.5 versus 0.45 (3.4).

  29. 29.

    Vosughimotlagh A, Rasouli SE, Rafiemanesh H, Safarirad M, Sharifinejad N, Madanipour A, et al.. Clinical manifestation for immunoglobulin A deficiency: a systematic review and meta-analysis. Allergy, Asthma and Clinical Immunology. 2023. PMID 37641141. DOI 10.1186/s13223-023-00826-y.

    Systematic review and meta-analysis · Pooled across studies to January 2022, infection affected 64.8 percent of IgA-deficient patients, allergic disease 26.16 percent and autoimmunity 22.0 percent; in selective IgA deficiency celiac disease (6.57 percent), inflammatory bowel disease (4.01) and rheumatoid arthritis (3.80) led the autoimmune conditions and respiratory infection (50.74 percent) led the infections.

  30. 30.

    Hauge SC, Jensen CK, Nielsen LK, Pedersen OB, Sørensen E, Thørner LW, et al.. The association of IgA deficiency on infection rate, self-perceived health, and levels of C-reactive protein in healthy blood donors. APMIS. 2018. PMID 29484746. DOI 10.1111/apm.12807.

    Prospective cohort · Among 177 IgA-deficient blood donors and 1,770 controls, the hazard ratio for a filled antimicrobial prescription was 1.19 (p = 0.05) and for hospital infections 1.02; self-reported physical health did not differ, mental health was lower and CRP higher in small subsets, and the authors judged the evidence insufficient to warrant specific precautions.

  31. 31.

    Gleeson M, McDonald WA, Pyne DB, Cripps AW, Francis JL, Fricker PA, Clancy RL. Salivary IgA levels and infection risk in elite swimmers. Medicine and Science in Sports and Exercise. 1999. PMID 9927012. DOI 10.1097/00005768-199901000-00012.

    Prospective cohort · In 26 elite swimmers over a 7-month season and 12 moderately exercising controls, salivary IgA correlated inversely with physician-verified infections; pretraining levels were 4.1 percent lower per additional month of training and 5.8 percent lower per additional infection, posttraining levels 8.5 percent lower per additional kilometer swum, and the season's trend predicted infections (P = 0.03).

  32. 32.

    Neville V, Gleeson M, Folland JP. Salivary IgA as a risk factor for upper respiratory infections in elite professional athletes. Medicine and Science in Sports and Exercise. 2008. PMID 18580401. DOI 10.1249/MSS.0b013e31816be9c3.

    Prospective cohort · In 38 professional sailors sampled weekly for 50 weeks, salivary IgA varied 48 percent within and 71 percent between subjects; absolute concentration did not correlate with upper respiratory infection (r = 0.11), a 28 percent fall occurred over the 3 weeks before episodes, and a value below 40 percent of a person's healthy mean gave a one in two chance of infection within 3 weeks.

  33. 33.

    Nieman DC, Henson DA, Fagoaga OR, Utter AC, Vinci DM, Davis JM, Nehlsen-Cannarella SL. Change in salivary IgA following a competitive marathon race. International Journal of Sports Medicine. 2002. PMID 11774070. DOI 10.1055/s-2002-19375.

    Prospective cohort · In 98 marathon runners, salivary IgA concentration, IgA-to-protein ratio and secretion rate fell 21, 31 and 25 percent by 1.5 hours after the race; 16 of 93 (17 percent) reported upper respiratory infection within 15 days, and their post-race IgA-to-protein ratio was lower (254 versus 388 µg/g) and correlated negatively with plasma cortisol (r = -0.36); carbohydrate, age and sex made no difference.

  34. 34.

    Jemmott JB 3rd, Borysenko JZ, Borysenko M, McClelland DC, Chapman R, Meyer D, Benson H. Academic stress, power motivation, and decrease in secretion rate of salivary secretory immunoglobulin A. Lancet. 1983. PMID 6134179. DOI 10.1016/s0140-6736(83)92354-1.

    Prospective cohort · In 64 first-year dental students sampled five times, during an initial low-stress period, three examination periods and a final low-stress period, the salivary secretory IgA secretion rate was significantly lower in high-stress than low-stress periods; personality characteristics differentiated the patterns.

  35. 35.

    Deinzer R, Kleineidam C, Stiller-Winkler R, Idel H, Bachg D. Prolonged reduction of salivary immunoglobulin A (sIgA) after a major academic exam. International Journal of Psychophysiology. 2000. PMID 10858568. DOI 10.1016/s0167-8760(99)00112-9.

    Prospective cohort · Twenty-seven medical students taking a major examination and 27 controls gave daily waking saliva from 6 days before the last exam to 14 days after; salivary IgA concentration in the exam students remained significantly below controls at day 14 (P = 0.004) with no recovery, although self-reported stress no longer differed.

  36. 36.

    Kang LJ, Koleva PT, Field CJ, Giesbrecht GF, Wine E, Becker AB, et al.; CHILD Study Investigators. Maternal depressive symptoms linked to reduced fecal Immunoglobulin A concentrations in infants. Brain, Behavior, and Immunity. 2018. PMID 29032226. DOI 10.1016/j.bbi.2017.10.007.

    Prospective cohort · Among 403 term infants in the Canadian CHILD cohort, infants of mothers with clinically significant depressive symptoms both prenatally and postnatally had a lower median stool sIgA (4.4 versus 6.3 mg/g feces, p = 0.033) and threefold odds of the lowest quartile (1.25 to 7.55) after adjustment for breastfeeding, infant age and antibiotics.

  37. 37.

    Behringer V, Müller-Klein N, Strube C, Schülke O, Heistermann M, Ostner J. Responsiveness of fecal immunoglobulin A to HPA-axis activation limits its use for mucosal immunity assessment. American Journal of Primatology. 2021. PMID 34554596. DOI 10.1002/ajp.23329.

    Laboratory method study · In 340 fecal samples from 14 female and 9 male semi-free-ranging Barbary macaques, fecal IgA was highly variable within and between individuals, higher in males, unchanged by anthelmintic treatment and the fall in worm burden, and correlated with fecal glucocorticoid metabolites; its responsiveness to the stress axis limits its use as a measure of mucosal immunity.

  38. 38.

    Moon C, Baldridge MT, Wallace MA, Burnham CA, Virgin HW, Stappenbeck TS. Vertically transmitted faecal IgA levels determine extra-chromosomal phenotypic variation. Nature. 2015. PMID 25686606. DOI 10.1038/nature14139.

    Laboratory method study · Wild-type mice within one facility showed dichotomous faecal IgA levels driven by vertically transmitted bacteria; bacteria from IgA-low mice dominantly lowered faecal IgA in IgA-high mice after cohousing or faecal transplantation, IgA-low mice showed more injury that transferred with faeces, and the bacteria degraded both the secretory component and IgA itself.

  39. 39.

    Plaza-Diaz J, Gomez-Llorente C, Campaña-Martin L, Matencio E, Ortuño I, Martínez-Silla R, et al.. Safety and immunomodulatory effects of three probiotic strains isolated from the feces of breast-fed infants in healthy adults: SETOPROB study. PLoS One. 2013. PMID 24205115. DOI 10.1371/journal.pone.0078111.

    Randomized trial · In 100 healthy volunteers randomized to placebo, one of three strains or a two-strain mixture for 30 days, gastrointestinal symptoms, defecation frequency and stool consistency were unchanged, bacterial populations shifted slightly, and one strain significantly increased fecal secretory IgA; serum IL-4 and IL-10 rose and IL-12 fell with any strain.

  40. 40.

    Zheng Y, Xu L, Zhang S, Liu Y, Ni J, Xiao G. Effect of a probiotic formula on gastrointestinal health, immune responses and metabolic health in adults with functional constipation or functional diarrhea. Frontiers in Nutrition. 2023. PMID 37497057. DOI 10.3389/fnut.2023.1196625.

    Randomized trial · In two randomized sub-trials of 70 Chinese adults each with functional constipation or functional diarrhea, four weeks of a multi-strain probiotic reduced symptom scores (p < 0.0001), raised weekly stool frequency from 3.3 to 6.2 in constipation, and increased serum IgA and fecal sIgA while lowering hs-CRP in both groups.

  41. 41.

    Olivares M, Castillejo G, Varea V, Sanz Y. Double-blind, randomised, placebo-controlled intervention trial to evaluate the effects of Bifidobacterium longum CECT 7347 in children with newly diagnosed coeliac disease. British Journal of Nutrition. 2014. PMID 24774670. DOI 10.1017/S0007114514000609.

    Randomized trial · In 33 children with newly diagnosed celiac disease on a gluten-free diet for 3 months, the probiotic strain reduced stool secretory IgA content compared with placebo (P = 0.011), reduced the Bacteroides fragilis group (P = 0.020) and peripheral CD3+ T lymphocytes (P = 0.004), with greater height percentile gains (P = 0.048).

  42. 42.

    Rizzardini G, Eskesen D, Calder PC, Capetti A, Jespersen L, Clerici M. Evaluation of the immune benefits of two probiotic strains Bifidobacterium animalis ssp. lactis, BB-12 and Lactobacillus paracasei ssp. paracasei, L. casei 431 in an influenza vaccination model: a randomised, double-blind, placebo-controlled study. British Journal of Nutrition. 2012. PMID 21899798. DOI 10.1017/S000711451100420X.

    Randomized trial · In 211 healthy adults (mean age 33.2) taking one of two probiotic strains or placebo for 6 weeks around a seasonal influenza vaccine, vaccine-specific plasma IgG and salivary secretory IgA rose more in both probiotic groups than placebo (saliva P = 0.017 and 0.035); no infections or clinical outcomes were measured and plasma cytokines and innate parameters did not differ.

  43. 43.

    Vulevic J, Juric A, Tzortzis G, Gibson GR. A mixture of trans-galactooligosaccharides reduces markers of metabolic syndrome and modulates the fecal microbiota and immune function of overweight adults. Journal of Nutrition. 2013. PMID 23303873. DOI 10.3945/jn.112.166132.

    Randomized trial · In a 12-week double-blind crossover trial in 45 overweight adults with three or more metabolic syndrome risk factors, a galacto-oligosaccharide mixture against maltodextrin increased fecal bifidobacteria and fecal secretory IgA and decreased fecal calprotectin, plasma C-reactive protein, insulin, total cholesterol, triglycerides and the total-to-HDL cholesterol ratio.

  44. 44.

    Wilms E, Jonkers DMAE, Savelkoul HFJ, Elizalde M, Tischmann L, de Vos P, Masclee AAM, Troost FJ. The Impact of Pectin Supplementation on Intestinal Barrier Function in Healthy Young Adults and Healthy Elderly. Nutrients. 2019. PMID 31324040. DOI 10.3390/nu11071554.

    Randomized trial · In 52 healthy young adults and 48 healthy elderly randomized to 15 g a day of pectin or placebo for four weeks, salivary and fecal sIgA and serum IgA did not differ between groups (p at or above 0.128), nor did in vivo gut permeability, transepithelial resistance or barrier gene expression.

  45. 45.

    Ferreira ABM, Halson S, Galvão-Coelho NL, Almeida RN, Nakamura FY, Mortatti AL. Impact of Sleep Restriction and Intensified Training on Mucosal Immunity and Psychological Responses in Young Soccer Players. Journal of Strength and Conditioning Research. 2026. PMID 42139594. DOI 10.1519/JSC.0000000000005416.

    Prospective cohort · In 16 male youth soccer players over 7 weeks, two weeks with a 75 percent rise in internal training load both lowered salivary IgA; only the week with about 10 percent less total sleep (minus 44 minutes) brought increased upper respiratory symptom severity, fatigue, lower vigor and worse recovery, while the week with more sleep did not.

  46. 46.

    Husby S, Koletzko S, Korponay-Szabó I, Kurppa K, Mearin ML, Ribes-Koninckx C, et al.. European Society Paediatric Gastroenterology, Hepatology and Nutrition Guidelines for Diagnosing Coeliac Disease 2020. Journal of Pediatric Gastroenterology and Nutrition. 2020. PMID 31568151. DOI 10.1097/MPG.0000000000002497.

    Guideline · If celiac disease is suspected, measurement of total serum IgA together with IgA antibodies against transglutaminase 2 is superior to other combinations; only if total IgA is low or undetectable is an IgG-based test indicated.

  47. 47.

    Korponay-Szabó IR, Dahlbom I, Laurila K, Koskinen S, Woolley N, Partanen J, Kovács JB, Mäki M, Hansson T. Elevation of IgG antibodies against tissue transglutaminase as a diagnostic tool for coeliac disease in selective IgA deficiency. Gut. 2003. PMID 14570724. DOI 10.1136/gut.52.11.1567.

    Cross-sectional study · In 325 IgA-deficient subjects (78 with celiac disease, 73 disease controls, 174 blood donors), IgG anti-transglutaminase had a sensitivity of 98.7 percent and specificity of 98.6 percent; 9.8 percent of IgA-deficient blood donors were positive and 11 of 12 typed carried DQ2 or DQ8, so all IgA-deficient persons should be evaluated for celiac disease.

  48. 48.

    Kappler M, Krauss-Etschmann S, Diehl V, Zeilhofer H, Koletzko S. Detection of secretory IgA antibodies against gliadin and human tissue transglutaminase in stool to screen for coeliac disease in children: validation study. BMJ. 2006. PMID 16377644. DOI 10.1136/bmj.38688.654028.AE.

    Cross-sectional study · In stool from 20 children with newly diagnosed celiac disease and 64 controls, secretory IgA antibodies against tissue transglutaminase had 10 percent sensitivity and 98 percent specificity and anti-gliadin 6 and 97 percent; neither stool test was suitable for screening.

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