Role of intestinal epithelial apoptosis in survival

Abstract

Purpose of review: To outline evidence that suggests increased intestinal epithelial apoptosis (programmed cell death) plays an important role in critical illness of infectious and noninfectious origin.

Recent findings: Both human and animal studies demonstrate that the gut epithelium has increased levels of cellular death in sepsis and noninfectious inflammation. Importantly, gut apoptosis appears to be detrimental to survival in sepsis. Transgenic mice that overexpress the antiapoptotic protein Bcl-2 in their gut epithelia have increased survival compared with wild-type littermates in murine models of ruptured appendicitis and Pseudomonas aeruginosa pneumonia.

Summary: These animal studies offer a possible new mechanism underlying the gut's role as the "motor" of the systemic inflammatory response syndrome and suggest that intestinal epithelial apoptosis may be a novel therapeutic target in future critical care research.