Intestinal adherence of commensal bacteria in IGA- and J chain-deficient mice following surgical stress

Despite being heavily colonized with bacteria, under normal conditions the intestinal epithelium is relatively free of adherent bacteria(AB). Secretory IgA may inhibit the epithelial adherence of commensal gram-negative bacteria in part by binding to bacterial type 1 fimbriae via mannose residues. We previously have shown that hepatectomy and starvation(Hep/Starv) in the mouse was associated with increased intestinal adherence of Escherichia coli(E. coli) and electrophysiologic perturbations of the cecal mucosa. In the current study, we report that AB isolated from Hep/Starv(HSAB) mice exhibited a greater density of surface fimbriae and mannose-inhibitable binding to mouse colon cells and guinea pig red blood cells, suggesting type 1 fimbrial expression. To investigate whether intestinal IgA deficiency is associated with increased E. coli adherence, we determined the numbers of AB in Starv±Hep IgA-deficient(IgA^-), J chain-deficient(Jch^-) and control(CT) ceca. Hep/Starv IgA^- and Jch^- mice did not exhibit higher mortality rates though a trend toward greater weight loss was noted in the IgA^- mice 48 hrs post-surgery (Mean wt loss in grams±SD: CT 4.49±0.74 vs. IgA^- 5.46±1.30, p=0.08). Cecal E. coli adherence was not significantly different in Jch^- and IgA^- compared to CT experimental mice (Mean Log¹⁰ CFU/gram tissue±SD: Hep/Starv CT 4.93±0.99 vs. IgA^- 5.44±0.88, p=0.31). We conclude that intestinal IgA deficiency was not associated with greater numbers of adherent gram-negative bacteria in the cecum after physiologic stress.