{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:17:30Z","timestamp":1791296250497,"version":"4.1.0"},"reference-count":41,"publisher":"Microbiology Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,10,1]]},"abstract":"<jats:p>The ability of<jats:italic>Listeria monocytogenes<\/jats:italic>to invade non-phagocytic cells is important for development of a systemic listeriosis infection. The authors previously reported that a<jats:italic>L. monocytogenes<\/jats:italic>\u0394<jats:italic>sigB<\/jats:italic>strain is defective in invasion into human intestinal epithelial cells, in part, due to decreased expression of a major invasion gene,<jats:italic>inlA<\/jats:italic>. To characterize additional invasion mechanisms under the control of<jats:italic>\u03c3<\/jats:italic><jats:sup>B<\/jats:sup>, mutants were generated carrying combinations of in-frame deletions in<jats:italic>inlA<\/jats:italic>,<jats:italic>inlB<\/jats:italic>and<jats:italic>sigB<\/jats:italic>. Quantitative assessment of bacterial invasion into the human enterocyte Caco-2 and hepatocyte HepG-2 cell lines demonstrated that<jats:italic>\u03c3<\/jats:italic><jats:sup>B<\/jats:sup>contributes to both InlA and InlB-mediated invasion of<jats:italic>L. monocytogenes<\/jats:italic>. Previous identification of the<jats:italic>\u03c3<\/jats:italic><jats:sup>B<\/jats:sup>-dependent P2<jats:italic><jats:sub>prfA<\/jats:sub><\/jats:italic>promoter upstream of the major virulence gene regulator, positive regulatory factor A (PrfA), suggested that the contributions of<jats:italic>\u03c3<\/jats:italic><jats:sup>B<\/jats:sup>to expression of various virulence genes, including<jats:italic>inlA<\/jats:italic>, could be at least partially mediated through PrfA. To test this hypothesis, relative invasion capabilities of \u0394<jats:italic>sigB<\/jats:italic>and \u0394<jats:italic>prfA<\/jats:italic>strains were compared. Exponential-phase cells of the \u0394<jats:italic>sigB<\/jats:italic>and \u0394<jats:italic>prfA<\/jats:italic>strains were similarly defective at invasion; however, stationary-phase \u0394<jats:italic>sigB<\/jats:italic>cells were significantly less invasive than stationary-phase \u0394<jats:italic>prfA<\/jats:italic>cells, suggesting that the contributions of<jats:italic>\u03c3<\/jats:italic><jats:sup>B<\/jats:sup>to invasion extend beyond those mediated through PrfA in stationary-phase<jats:italic>L. monocytogenes<\/jats:italic>. TaqMan quantitative reverse-transcriptase PCRs further demonstrated that expression of<jats:italic>inlA<\/jats:italic>and<jats:italic>inlB<\/jats:italic>was greatly increased in a<jats:italic>\u03c3<\/jats:italic><jats:sup>B<\/jats:sup>-dependent manner in stationary-phase<jats:italic>L. monocytogenes<\/jats:italic>. Together, results from this study provide strong biological evidence of a critical role for<jats:italic>\u03c3<\/jats:italic><jats:sup>B<\/jats:sup>in<jats:italic>L. monocytogenes<\/jats:italic>invasion into non-phagocytic cells, primarily mediated through control of<jats:italic>inlA<\/jats:italic>and<jats:italic>inlB<\/jats:italic>expression.<\/jats:p>","DOI":"10.1099\/mic.0.28070-0","type":"journal-article","created":{"date-parts":[[2005,10,5]],"date-time":"2005-10-05T22:08:00Z","timestamp":1128550080000},"page":"3215-3222","source":"Crossref","is-referenced-by-count":129,"title":["\u03c3 B contributes to Listeria monocytogenes invasion by controlling expression of inlA and inlB"],"prefix":"10.1099","volume":"151","author":[{"given":"Heesun","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Food Science, Cornell University, Ithaca, NY 14853, 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