Crossing the Intestinal Barrier via Listeria Adhesion Protein and Internalin A.

Abstract

The intestinal epithelial cell lining provides the first line of defense, yet foodborne pathogens such as Listeria monocytogenes can overcome this barrier; however, the underlying mechanism is not well understood. Though the host M cells in Peyer's patch and the bacterial invasion protein internalin A (InlA) are involved, L. monocytogenes can cross the gut barrier in their absence. The interaction of Listeria adhesion protein (LAP) with the host cell receptor (heat shock protein 60) disrupts the epithelial barrier, promoting bacterial translocation. InlA aids L. monocytogenes transcytosis via interaction with the E-cadherin receptor, which is facilitated by epithelial cell extrusion and goblet cell exocytosis; however, LAP-induced cell junction opening may be an alternative bacterial strategy for InlA access to E-cadherin and its translocation. Here, we summarize the strategies that L. monocytogenes employs to circumvent the intestinal epithelial barrier and compare and contrast these strategies with other enteric bacterial pathogens. Additionally, we provide implications of recent findings for food safety regulations.