Enterocyte apoptosis and barrier function are modulated by SIgA after exposure to bacteria and hypoxia/reoxygenation

Secretory immunoglobulin A (SIgA) is the principal immune defense against luminal pathogens at gut mucosal surfaces. It also has anti-inflammatory activities that may be important for the maintenance of mucosal surface integrity. Enterocyte apoptosis (Apo) is increased after challenge with invasive bacteria and ischemia-reperfusion insults. Increased Apo also has been associated with impaired intestinal barrier function. However, the impact of SIgA on enterocyte apoptosis and mucosal barrier integrity after challenge with commensal bacteria and ischemia-reperfusion is unknown.

Caco2 intestinal epithelial cell monolayers were subjected to 21% O(2) (control) or 95% N(2)/15% CO(2) (hypoxic) conditions for 90 minutes, followed by 21% O(2). Escherichia coli and SIgA were added in subsets. Caco2 cell Apo was identified by flow cytometry and barrier function indexed by permeability to dextran-fluorescein isothiocyanate.

There were no differences in the percentage of Apo Caco2 cells after exposure to either bacteria or hypoxic-reoxygenation versus control. There was a significant increase in Apo after the combined bacteria/hypoxia-reoxygenation challenge. SIgA abrogated the Apo response and preserved barrier function after this combined challenge.

Modulation of enterocyte Apo by SIgA may serve to maintain intestinal barrier function and thereby decrease the systemic inflammatory response after clinical conditions associated with gut ischemia-reperfusion insults.