Listeria monocytogenes and Host Hsp60 – An Invasive Pairing
Microbial infection has a dramatic impact on host cell function and can induce host stress-response programs, including the heat shock response. Listeria monocytogenes is a human foodborne bacterial pathogen which interacts with the host gastrointestinal epithelium during the initial phase of the systemic disease, listeriosis. The early interaction of L. monocytogenes with the intestinal epithelium is a critical determinant of the outcome of infection, and is mediated by multiple bacterial factors, including Listeria adhesion protein (LAP). The epithelial receptor for LAP is human heat shock protein 60 (Hsp60), and the LAP-Hsp60 interaction facilitates bacterial adhesion to and translocation through intestinal epithelial monolayers. Interestingly, L. monocytogenes infection induces the expression of Hsp60 in epithelial cells, a phenomenon which renders host cells more susceptible to subsequent LAP-mediated L. monocytogenes infection. This chapter describes the importance of the host heat shock response during microbial infection, and highlights the role for LAP and host Hsp60 in mediating infection by L. monocytogenes.
KeywordsVirulence Factor Listeria Monocytogenes Hsp60 Expression Bacterial Translocation Heat Shock Response
Research in Bhunia laboratory is supported by grants from the United States Department of Agriculture (1935-42,000-072-02G; 201,995) and the Center for Food Safety Engineering at Purdue University.
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