{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T10:15:34Z","timestamp":1790244934327,"version":"4.1.0"},"reference-count":60,"publisher":"National Academy of Sciences","issue":"16","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2000,8]]},"abstract":"<jats:p>\n                    Microbial pathogens have evolved many ingenious ways to infect\n their hosts and cause disease, including the subversion and\n exploitation of target host cells. One such subversive microbe is\n enteropathogenic\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    (EPEC). A major cause\n of infantile diarrhea in developing countries, EPEC poses a significant\n health threat to children worldwide. Central to EPEC-mediated disease\n is its colonization of the intestinal epithelium. After initial\n adherence, EPEC causes the localized effacement of microvilli and\n intimately attaches to the host cell surface, forming characteristic\n attaching and effacing (A\/E) lesions. Considered the prototype for a\n family of A\/E lesion-causing bacteria, recent\n                    <jats:italic>in vitro<\/jats:italic>\n                    studies of EPEC have revolutionized our understanding of how these\n pathogens infect their hosts and cause disease. Intimate attachment\n requires the type III-mediated secretion of bacterial proteins, several\n of which are translocated directly into the infected cell, including\n the bacteria's own receptor (Tir). Binding to this membrane-bound,\n pathogen-derived protein permits EPEC to intimately attach to mammalian\n cells. The translocated EPEC proteins also activate signaling pathways\n within the underlying cell, causing the reorganization of the host\n actin cytoskeleton and the formation of pedestal-like structures\n beneath the adherent bacteria. This review explores what is known about\n EPEC's subversion of mammalian cell functions and how this knowledge\n has provided novel insights into bacterial pathogenesis and\n microbe-host interactions. Future studies of A\/E pathogens in animal\n models should provide further insights into how EPEC exploits not only\n epithelial cells but other host cells, including those of the immune\n system, to cause diarrheal disease.\n                  <\/jats:p>","DOI":"10.1073\/pnas.97.16.8799","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:41:48Z","timestamp":1027680108000},"page":"8799-8806","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":196,"title":["Exploitation of host cells by enteropathogenic\n                    <i>Escherichia<\/i>\n                    <i>coli<\/i>"],"prefix":"10.1073","volume":"97","author":[{"given":"B. A.","family":"Vallance","sequence":"first","affiliation":[{"name":"Biotechnology Laboratory, University of British Columbia,\r Vancouver, BC, Canada V6T 1Z3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. 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