{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T20:43:30Z","timestamp":1792183410266,"version":"4.4.0"},"reference-count":36,"publisher":"Microbiology Society","issue":"10","funder":[{"name":"Canada Research Chair in Gastrointestinal Disease"},{"DOI":"10.13039\/501100000024","name":"CIHR","doi-asserted-by":"crossref","award":["MOP-89894"],"award-info":[{"award-number":["MOP-89894"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100005156","name":"Alexander von Humboldt Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100005156","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Feodor Lynen"},{"name":"CAG"},{"DOI":"10.13039\/501100000019","name":"CCFC","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100000019","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100000024","name":"CIHR","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,10,1]]},"abstract":"<jats:p>Enterohaemorrhagic <jats:italic>Escherichia coli<\/jats:italic> (EHEC), serotype O157\u200a:\u200aH7 is a non-invasive, pathogenic bacterium that employs a type III secretion system (T3SS) to inject effector proteins into infected cells. In this study, we demonstrate that EHEC blocks tumour necrosis factor-alpha (TNF\u03b1)-induced NF-\u03baB signalling in infected epithelial cells. HEK293T and INT407 epithelial cells were challenged with EHEC prior to stimulation with TNF\u03b1. Using complementary techniques, stimulation with TNF\u03b1 caused activation of NF-\u03baB, as determined by luciferase reporter assay (increase in gene expression), Western blotting (phosphorylation of I\u03baB\u03b1), immunofluorescence (p65 nuclear translocation) and immunoassay (CXCL-8 secretion), and each was blocked by EHEC O157\u200a:\u200aH7 infection. In contrast, subversion of host cell signalling was not observed following exposure to either enteropathogenic <jats:italic>E. coli<\/jats:italic>, strain E2348\/69 (O127\u200a:\u200aH6) or the laboratory <jats:italic>E. coli<\/jats:italic> strain HB101. Heat-killed EHEC had no effect on NF-\u03baB activation by TNF\u03b1. Inhibition was mediated, at least in part, by Shiga toxins and by the O157 plasmid, but not by the T3SS or flagellin, as demonstrated by using isogenic mutant strains. These findings indicate the potential for developing novel therapeutic targets to interrupt the infectious process.<\/jats:p>","DOI":"10.1099\/mic.0.051094-0","type":"journal-article","created":{"date-parts":[[2011,7,29]],"date-time":"2011-07-29T02:18:41Z","timestamp":1311905921000},"page":"2963-2973","source":"Crossref","is-referenced-by-count":7,"title":["Enterohaemorrhagic, but not enteropathogenic, Escherichia coli infection of epithelial cells disrupts signalling responses to tumour necrosis factor-alpha"],"prefix":"10.1099","volume":"157","author":[{"given":"M\u00e9lanie G.","family":"Gareau","sequence":"first","affiliation":[{"name":"Research Institute, Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathan K.","family":"Ho","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathobiology University of Toronto, Medical Sciences Building, 1 King\u2019s 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