Paneth cells and innate mucosal immunity

Abstract

Purpose of review: Recent evidence shows that disruption of Paneth cell homeostasis by induction of endoplasmic reticulum stress or autophagy, with consequent apoptosis, contributes to inflammation and morbidity in a variety of experimental mouse models.

Recent findings: Recent advances show that proinflammatory mediators in Paneth cell dense core secretory granules mediate tumor necrosis factor-α-induced shock, that Paneth cell α-defensins modulate the composition of the small intestinal microflora, that development of crypt organoid culture systems provides a novel means for investigating the crypt microenvironment, and that varied genetic defects that disrupt Paneth cell homeostasis are emergent as risk factors in inflammatory bowel disease.

Summary: This recent literature identifies Paneth cells as particularly sensitive targets of endoplasmic reticulum stress responses and implicates this unique small intestinal lineage in inflammatory bowel disease pathogenesis resulting from diverse heritable and environmental causes.