Listeria monocytogenes Uses Listeria Adhesion Protein (LAP) To Promote Bacterial Transepithelial Translocation and Induces Expression of LAP Receptor Hsp60

Abstract

Listeria monocytogenes interaction with the intestinal epithelium is a key step in the infection process. We demonstrated that

Listeria monocytogenes Triggers the Cell Surface Expression of Gp96 Protein and Interacts with Its N Terminus to Support Cellular Infection

“…Another heat shock protein (Hsp60) was also shown to be expressed at a greater level at the surface of Caco-2 cells infected by Listeria. Hsp60 interacts with Listeria adhesion protein (LAP) (34), promoting transepithelial translocation (35). Recently, it was shown that E. coli K1 infection of neutrophils increases the cell surface expression of Gp96, which acts as a receptor for bacterial entry (23).…”

The arsenal of virulence factors deployed byListeria monocytogenesto promote its cell infection cycle

“…The interaction of this alcohol acetaldehyde dehydrogenase with Hsp60, its host cell receptor, promotes bacterial adhesion to intestinal cells. [29][30][31][32] Anaerobic growth induces significant increases in the level of lap transcript and Lap secretion via the accessory secretion system SecA2 (see regulation section). Oral administration of lap-deficient strains to mice confirmed that Lap is essential for full virulence.…”

Bifidobacterium bifidum PRL2010 Modulates the Host Innate Immune Response

“…These results are in accordance with our in vitro observations using the HT29 model with regard to the upregulation of tight junction-associated proteins. Catenins, cadherins, and claudins, in fact, play a key structural role in the maintenance of the intestinal barrier against infection with enteropathogens like Listeria, which are known to infect the host by penetrating the intestinal epithelium through a paracellular route (71).…”