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.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology