IBD Causes High Secretory IgA (SIgA) in Stool
Inflammatory Bowel Disease causes elevated levels of secretory IgA in stool, particularly during active disease, with both IgA and IgG antibodies coating intestinal bacteria at significantly higher rates than in healthy individuals.
Elevated Fecal IgA Levels in Active IBD
Soluble fecal IgA concentrations are significantly elevated in patients with active IBD compared to healthy controls, with levels positively correlating with disease activity markers including CRP, ESR, Mayo score, UCEIS, SES-CD, and CDAI 1
The increase in fecal IgA represents an exaggerated mucosal immune response directed against commensal intestinal bacteria, particularly their cytoplasmic proteins 2
While total mucosal IgA concentrations may not differ dramatically between IBD and controls, the percentage of IgA-coated bacteria in feces markedly increases in IBD patients, especially in Crohn's disease patients aged 17-40 years, those with terminal ileal lesions, perianal lesions, and in E2 ulcerative colitis patients 1
IgG Also Significantly Elevated
In contrast to healthy individuals where IgA predominates, active IBD patients produce high concentrations of IgG from intestinal lymphocytes, with median mucosal IgG levels of 512 μg/mL in active UC and 256 μg/mL in active CD versus only 1.43 μg/mL in irritable bowel syndrome controls 2
Both soluble IgG levels and the percentage of IgG-coated bacteria are significantly elevated in fecal samples from IBD patients and correlate closely with disease activity 1
The mucosal IgG binding to commensal bacteria is higher in active Crohn's disease than in ulcerative colitis, and both are significantly greater than controls 2
Pathophysiologic Significance
IgA-coated bacteria from IBD patients can drive intestinal inflammation when transplanted into mice, demonstrating that highly IgA-coated bacterial strains are potentially responsible for perpetuating gut inflammation 3
The altered IgA-microbiota interactions in IBD contribute to dysbiosis, with distinct IgA1- and IgA2-associated microbiota patterns in Crohn's disease versus ulcerative colitis 4
This represents a breakdown of tolerance to normal commensal flora, with reverse-transcytosis mechanisms being abrogated in UC while extended to IgA1 in CD 4
Clinical Implications
Fecal calprotectin levels <50 μg/g may be reassuring for ruling out active inflammation, while values between 50-250 μg/g require further evaluation as they can indicate low-grade inflammation 5, 6
The elevation of fecal immunoglobulins reflects active mucosal immune responses even when endoscopic healing appears complete, as up to 27% of patients with healed mucosa still experience persistent symptoms 7
Serial monitoring of inflammatory biomarkers at 3-6 month intervals may facilitate early recognition of impending disease flares in patients with mild symptoms 5