{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T06:23:42Z","timestamp":1792477422693,"version":"4.5.0"},"reference-count":30,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2012,3,1]],"date-time":"2012-03-01T00:00:00Z","timestamp":1330560000000},"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":[[2012,3]]},"abstract":"<jats:p>\n            <jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>\n            O157:H7 causes food and waterborne enteric infections that can result in hemorrhagic colitis and life-threatening hemolytic uremic syndrome. Intimate adherence of the bacteria to intestinal epithelial cells is mediated by intimin, but\n            <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n            O157:H7 also possess several other putative adhesins, including curli and two operons that encode long polar fimbriae (Lpf). To assess the importance of Lpf for intestinal colonization, we performed competition experiments between\n            <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n            O157:H7 and an isogenic \u0394\n            <jats:italic>lpfA1<\/jats:italic>\n            \u0394\n            <jats:italic>lpfA2<\/jats:italic>\n            double mutant in the infant rabbit model. The mutant was outcompeted in the ileum, cecum, and midcolon, suggesting that Lpf contributes to intestinal colonization. In contrast, the \u0394\n            <jats:italic>lpfA1<\/jats:italic>\n            \u0394\n            <jats:italic>lpfA2<\/jats:italic>\n            mutant showed increased adherence to colonic epithelial cells\n            <jats:italic>in vitro<\/jats:italic>\n            . Transmission electron microscopy revealed curli-like structures on the surface of the \u0394\n            <jats:italic>lpfA1<\/jats:italic>\n            \u0394\n            <jats:italic>lpfA2<\/jats:italic>\n            mutant, and the presence of curli was confirmed by Congo red binding, immunogold-labeling electron microscopy, immunoblotting, and quantitative real-time reverse transcription-PCR (qRT-PCR) measuring\n            <jats:italic>csgA<\/jats:italic>\n            expression. However, deletion of\n            <jats:italic>csgA<\/jats:italic>\n            , which encodes the major curli subunit, does not appear to affect intestinal colonization. In addition to suggesting that Lpf can contribute to EHEC intestinal colonization, our observations indicate that the regulatory pathways governing the expression of Lpf and curli are interdependent.\n          <\/jats:p>","DOI":"10.1128\/iai.05945-11","type":"journal-article","created":{"date-parts":[[2012,1,10]],"date-time":"2012-01-10T01:32:22Z","timestamp":1326159142000},"page":"914-920","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":50,"title":["A Double, Long Polar Fimbria Mutant of Escherichia coli O157:H7 Expresses Curli and Exhibits Reduced\n            <i>In Vivo<\/i>\n            Colonization"],"prefix":"10.1128","volume":"80","author":[{"given":"Sonja J.","family":"Lloyd","sequence":"first","affiliation":[{"name":"Departments of Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer M.","family":"Ritchie","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maricarmen","family":"Rojas-Lopez","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carla A.","family":"Blumentritt","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vsevolod L.","family":"Popov","sequence":"additional","affiliation":[{"name":"Pathology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer L.","family":"Greenwich","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew K.","family":"Waldor","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alfredo G.","family":"Torres","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology"},{"name":"Pathology"},{"name":"Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.micro.60.080805.142106"},{"issue":"53","key":"e_1_3_3_3_2","first-page":"1","article-title":"Summary of notifiable diseases\u2014United States, 2007","volume":"56","author":"CDC","year":"2009","unstructured":"CDC. 2009. 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