As part of the gut epithelial barrier, sIgA is important in the development of immune tolerance for normal, beneficial commensal gut organisms, as well as common molecular epitopes found in foods.
Early studies of sIgA focused on immune exclusion (the prevention of pathological material and organisms from gaining entry into the general circulation). Recent studies also show sIgA plays a role in immune inclusion (delivery of commensal bacteria and their products to the gut and systemic immune system) for recognition. This leads to the development of immune tolerance. Immune inclusion spares beneficial organisms from destruction by the immune system which helps to support the immune system in a noninflammatory way to preserve local homeostasis.
Although secretory IgA is the major antibody in the intestinal mucosa, the prevalence of GI disorders in patients with systemic IgA deficiency is not as high as one might expect. It is thought that the transportation of IgM from the mucosa can compensate for a lack of IgA.
In people with genetic immunodeficiency of systemic sIgA, GI symptoms such as diarrhea have been reported. Systemically IgA-deficient patients more often have airway infections since compensatory sIgM is lacking in the airways (in contrast to the gut). Adaptive sIgA responses may allow the host to respond to fluctuations in commensal bacteria to favor mucosal homeostasis.
Considerations for low fecal sIgA:
Because of the lack of clinical evidence, there is no clear cut-off value for low fecal sIgA. People with systemic IgA deficiency can have low levels of fecal secretory IgA. There is a demonstrated link between IgA deficiency and several GI diseases, including:
- celiac disease,
- nodular lymphoid hyperplasia,
- ulcerative colitis,
- Crohn’s disease,
- pernicious anemia,
- and gastric and colonic adenocarcinoma.
Low sIgA may reflect a loss of GI immune response resiliency. Fecal sIgA may be low in severe/prolonged IBD patients due to a switch from intestinal IgA to IgG production as well as a deficiency in producing IgA dimers and polymers.
Secretory IgA demonstrates an array of activities integral to the maintenance of intestinal homeostasis. It influences the composition of intestinal microbiota, down-regulates pro-inflammatory responses normally associated with the uptake of highly pathogenic bacteria and potentially allergenic antigens, and promotes the retro-transport of antigens across the intestinal epithelium to gut-associated lymphoid tissue (GALT). Therefore, a low sIgA is clinically significant.
The test result should be considered together with any other medical condition, other biomarkers, and microbiome profiles when interpreting the data.
Causes of elevated fecal sIgA:
- Any defective epithelial barrier
- A defective epithelial barrier allows bacterial and microbial penetration, which is the strongest stimulator of sIgA production.
- Celiac disease
- Colon cancer
- IBS (especially the diarrhea subtype)
Therapeutic considerations for elevated fecal sIgA:
Assess for and treat root causes of immune upregulation /inflammation:
- Infection (bacterial, parasitic, and/or viral pathogen, potential pathogen)
- Compromised intestinal barrier function (i.e., intestinal permeability)
- Heightened response to noninfectious stimuli (i.e., food sensitivity/allergy, etc.)
Consider Food Antibody testing – If positive, consider elimination diet
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