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Immediately downstream of\n            <jats:italic>flaA<\/jats:italic>\n            , two genes,\n            <jats:italic>cheY<\/jats:italic>\n            and\n            <jats:italic>cheA<\/jats:italic>\n            , encoding products with homology to chemotaxis proteins of other bacteria, are located. In this study we constructed deletion mutants with mutations in\n            <jats:italic>flaA. cheY<\/jats:italic>\n            , and\n            <jats:italic>cheA<\/jats:italic>\n            to elucidate their role in the biology of infection with\n            <jats:italic>L. monocytogenes<\/jats:italic>\n            . The \u0394\n            <jats:italic>cheY<\/jats:italic>\n            , \u0394\n            <jats:italic>cheA<\/jats:italic>\n            , and double-mutant \u0394\n            <jats:italic>cheYA<\/jats:italic>\n            mutants, but not \u0394\n            <jats:italic>flaA<\/jats:italic>\n            mutant, were motile in liquid media. However, the \u0394\n            <jats:italic>cheA<\/jats:italic>\n            mutant had impaired swarming and the \u0394\n            <jats:italic>cheY<\/jats:italic>\n            and \u0394\n            <jats:italic>cheYA<\/jats:italic>\n            mutants were unable to swarm on soft agar plates, suggesting that\n            <jats:italic>cheY<\/jats:italic>\n            and\n            <jats:italic>cheA<\/jats:italic>\n            genes encode proteins involved in chemotaxis. The \u0394\n            <jats:italic>flaA<\/jats:italic>\n            , \u0394\n            <jats:italic>cheY<\/jats:italic>\n            , \u0394\n            <jats:italic>cheA<\/jats:italic>\n            , and \u0394\n            <jats:italic>cheYA<\/jats:italic>\n            mutants (grown at 24\u00b0C) showed reduced association with and invasion of Caco-2 cells compared to the wild-type strain. However, spleens from intragastrically infected BALB\/c and C57BL\/6 mice showed larger and similar numbers of the \u0394\n            <jats:italic>flaA<\/jats:italic>\n            and \u0394\n            <jats:italic>cheYA<\/jats:italic>\n            mutants, respectively, compared to the wild-type controls. Such a discrepancy could be explained by the fact that tumor necrosis factor receptor p55 deficient mice showed dramatically exacerbated susceptibility to the wild-type but unchanged or only slightly increased levels of the \u0394\n            <jats:italic>flaA<\/jats:italic>\n            or \u0394\n            <jats:italic>cheYA<\/jats:italic>\n            mutant. In summary, we show that listerial\n            <jats:italic>flaA. cheY<\/jats:italic>\n            , and\n            <jats:italic>cheA<\/jats:italic>\n            gene products facilitate the initial contact with epithelial cells and contribute to effective invasion but that\n            <jats:italic>flaA<\/jats:italic>\n            could also be involved in the triggering of immune responses.\n          <\/jats:p>","DOI":"10.1128\/iai.72.6.3237-3244.2004","type":"journal-article","created":{"date-parts":[[2004,5,20]],"date-time":"2004-05-20T20:43:12Z","timestamp":1085085792000},"page":"3237-3244","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":134,"title":["Role of Flagellin and the Two-Component CheA\/CheY System of\n            <i>Listeria monocytogenes<\/i>\n            in Host Cell Invasion and 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