{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T06:00:47Z","timestamp":1760853647153},"reference-count":79,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2012,10,1]],"date-time":"2012-10-01T00:00:00Z","timestamp":1349049600000},"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":[[2012,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Yersinia pestis<\/jats:named-content>\n            and many other Gram-negative pathogenic bacteria use the chaperone\/usher (CU) pathway to assemble virulence-associated surface fibers termed pili or fimbriae.\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            has two well-characterized CU pathways: the\n            <jats:italic>caf<\/jats:italic>\n            genes coding for the F1 capsule and the\n            <jats:italic>psa<\/jats:italic>\n            genes coding for the pH 6 antigen. The\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            genome contains additional CU pathways that are capable of assembling pilus fibers, but the roles of these pathways in the pathogenesis of plague are not understood. We constructed deletion mutations in the usher genes for six of the additional\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            CU pathways. The wild-type (WT) and usher deletion strains were compared in the murine bubonic (subcutaneous) and pneumonic (intranasal) plague infection models.\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            strains containing deletions in CU pathways\n            <jats:italic>y0348-0352<\/jats:italic>\n            ,\n            <jats:italic>y1858-1862<\/jats:italic>\n            , and\n            <jats:italic>y1869-1873<\/jats:italic>\n            were attenuated for virulence compared to the WT strain by the intranasal, but not subcutaneous, routes of infection, suggesting specific roles for these pathways during pneumonic plague. We examined binding of the\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            WT and usher deletion strains to A549 human lung epithelial cells, HEp-2 human cervical epithelial cells, and primary human and murine macrophages.\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            CU pathways\n            <jats:italic>y0348-0352<\/jats:italic>\n            and\n            <jats:italic>y1858-1862<\/jats:italic>\n            were found to contribute to adhesion to all host cells tested, whereas pathway\n            <jats:italic>y1869-1873<\/jats:italic>\n            was specific for binding to macrophages. The correlation between the virulence attenuation and host cell binding phenotypes of the usher deletion mutants identifies three of the additional CU pathways of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            as mediating interactions with host cells that are important for the pathogenesis of plague.\n          <\/jats:p>","DOI":"10.1128\/iai.00434-12","type":"journal-article","created":{"date-parts":[[2012,7,31]],"date-time":"2012-07-31T07:45:32Z","timestamp":1343720732000},"page":"3490-3500","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":11,"title":["Roles of Chaperone\/Usher Pathways of Yersinia pestis in a Murine Model of Plague and Adhesion to Host Cells"],"prefix":"10.1128","volume":"80","author":[{"given":"Matthew","family":"Hatkoff","sequence":"first","affiliation":[{"name":"Center for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA"},{"name":"Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lisa M.","family":"Runco","sequence":"additional","affiliation":[{"name":"Department of Life Sciences, New York Institute of Technology, Old Westbury, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Celine","family":"Pujol","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA"},{"name":"Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Indralatha","family":"Jayatilaka","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA"},{"name":"Department of Pathology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martha B.","family":"Furie","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA"},{"name":"Department of Pathology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James B.","family":"Bliska","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA"},{"name":"Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David G.","family":"Thanassi","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA"},{"name":"Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0408026101"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.24.14043"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1099\/mic.0.2008\/017335-0"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.micpath.2004.04.001"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0309146"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.2000.02021.x"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0966-842X(00)01738-8"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-2920.2007.01554.x"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.4.3.309"},{"key":"e_1_3_2_11_2","first-page":"111","article-title":"The genus Yersinia: biochemistry and genetics of virulence","volume":"57","author":"Brubaker RR","year":"1972","unstructured":"BrubakerRR. 1972. 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