{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:01:04Z","timestamp":1791295264769,"version":"4.1.0"},"reference-count":55,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2008,1,1]],"date-time":"2008-01-01T00:00:00Z","timestamp":1199145600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Enteropathogenic<jats:italic>Escherichia coli<\/jats:italic>(EPEC) and<jats:italic>Shigella flexneri<\/jats:italic>are human host-specific pathogens that infect intestinal epithelial cells. However, each bacterial species employs a different infection strategy within this environmental niche. EPEC attaches to the apical surface of small intestine enterocytes, causing microvillus effacement and rearrangement of the host cell cytoskeleton beneath adherent bacteria. In contrast,<jats:italic>S. flexneri<\/jats:italic>invades the large intestine epithelium at the basolateral membrane, replicates, and spreads cell to cell. Both EPEC and<jats:italic>S. flexneri<\/jats:italic>rely on type three secretion systems (T3SS) to secrete effectors into host cells, and both pathogens recruit polymorphonuclear leukocytes (PMNs) from the submucosa to the lumen of the intestine. In this report, we compared the virulence functions of the EPEC T3SS effector NleE and the homologous<jats:italic>Shigella<\/jats:italic>protein Orf212. We discovered that Orf212 was secreted by the<jats:italic>S. flexneri<\/jats:italic>T3SS and renamed this protein OspZ. Infection of polarized T84 intestinal epithelial cells with an<jats:italic>ospZ<\/jats:italic>deletion mutant of<jats:italic>S. flexneri<\/jats:italic>resulted in reduced PMN transepithelial migration compared to infection by the wild type. An<jats:italic>nleE<\/jats:italic>deletion mutant of EPEC showed a similar reduction of PMN migration. The ability to induce PMN migration was restored in both mutants when either<jats:italic>ospZ<\/jats:italic>or<jats:italic>nleE<\/jats:italic>was expressed from a plasmid. An infection of T84 cells with the \u0394<jats:italic>ospZ<\/jats:italic>mutant resulted in reduced extracellular signal-related kinase phosphorylation and NF-\u03baB activation compared to infection with the wild type. Therefore, we conclude that OspZ and NleE have similar roles in the upstream induction of host signaling pathways required for PMN transepithelial migration in<jats:italic>Shigella<\/jats:italic>and EPEC infections.<\/jats:p>","DOI":"10.1128\/iai.00684-07","type":"journal-article","created":{"date-parts":[[2007,11,6]],"date-time":"2007-11-06T01:44:07Z","timestamp":1194313447000},"page":"369-379","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":44,"title":["The NleE\/OspZ Family of Effector Proteins Is Required for Polymorphonuclear Transepithelial Migration, a Characteristic Shared by Enteropathogenic<i>Escherichia coli<\/i>and<i>Shigella flexneri<\/i>Infections"],"prefix":"10.1128","volume":"76","author":[{"given":"Daniel V.","family":"Zurawski","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen L.","family":"Mumy","sequence":"additional","affiliation":[{"name":"Mucosal Immunology Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts"},{"name":"Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luminita","family":"Badea","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Monash University, Clayton, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia A.","family":"Prentice","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Monash University, Clayton, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth L.","family":"Hartland","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Monash University, Clayton, Victoria, Australia"},{"name":"Department of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beth A.","family":"McCormick","sequence":"additional","affiliation":[{"name":"Mucosal Immunology Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts"},{"name":"Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony T.","family":"Maurelli","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"87","volume":"57","year":"2003","unstructured":"Ahmetagic, S., E. 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