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B contributes to Listeria monocytogenes invasion by controlling expression of inlA and inlB
1 Department of Food Science, Cornell University, Ithaca, NY 14853, USA
2 Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853, USA
Correspondence
Kathryn J. Boor
kjb4{at}cornell.edu
The ability of Listeria monocytogenes to invade non-phagocytic cells is important for development of a systemic listeriosis infection. The authors previously reported that a L. monocytogenes 
sigB strain is defective in invasion into human intestinal epithelial cells, in part, due to decreased expression of a major invasion gene, inlA. To characterize additional invasion mechanisms under the control of 
B, mutants were generated carrying combinations of in-frame deletions in inlA, inlB and sigB. Quantitative assessment of bacterial invasion into the human enterocyte Caco-2 and hepatocyte HepG-2 cell lines demonstrated that B contributes to both InlA and InlB-mediated invasion of L. monocytogenes. Previous identification of the B-dependent P2prfA promoter upstream of the major virulence gene regulator, positive regulatory factor A (PrfA), suggested that the contributions of B to expression of various virulence genes, including inlA, could be at least partially mediated through PrfA. To test this hypothesis, relative invasion capabilities of sigB and prfA strains were compared. Exponential-phase cells of the sigB and prfA strains were similarly defective at invasion; however, stationary-phase sigB cells were significantly less invasive than stationary-phase prfA cells, suggesting that the contributions of B to invasion extend beyond those mediated through PrfA in stationary-phase L. monocytogenes. TaqMan quantitative reverse-transcriptase PCRs further demonstrated that expression of inlA and inlB was greatly increased in a B-dependent manner in stationary-phase L. monocytogenes. Together, results from this study provide strong biological evidence of a critical role for B in L. monocytogenes invasion into non-phagocytic cells, primarily mediated through control of inlA and inlB expression.
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