@article{mbs:/content/journal/micro/10.1099/mic.0.28070-0, author = "Kim, Heesun and Marquis, Hélène and Boor, Kathryn J.", title = "σB contributes to Listeria monocytogenes invasion by controlling expression of inlA and inlB", journal= "Microbiology", year = "2005", volume = "151", number = "10", pages = "3215-3222", doi = "https://doi.org/10.1099/mic.0.28070-0", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.28070-0", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", keywords = "qRT-PCR, quantitative reverse-transcriptase polymerase chain reaction", abstract = "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 ΔsigB 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 σ 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 σ B contributes to both InlA and InlB-mediated invasion of L. monocytogenes. Previous identification of the σ B-dependent P2 prfA promoter upstream of the major virulence gene regulator, positive regulatory factor A (PrfA), suggested that the contributions of σ 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 ΔsigB and ΔprfA strains were compared. Exponential-phase cells of the ΔsigB and ΔprfA strains were similarly defective at invasion; however, stationary-phase ΔsigB cells were significantly less invasive than stationary-phase ΔprfA cells, suggesting that the contributions of σ 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 σ B-dependent manner in stationary-phase L. monocytogenes. Together, results from this study provide strong biological evidence of a critical role for σ B in L. monocytogenes invasion into non-phagocytic cells, primarily mediated through control of inlA and inlB expression.", }