{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T05:43:16Z","timestamp":1792734196692,"version":"4.5.0"},"reference-count":31,"publisher":"National Academy of Sciences","issue":"49","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2005,12,6]]},"abstract":"<jats:p>\n                    Although pneumonic plague is the deadliest manifestation of disease caused by the bacterium\n                    <jats:italic>Yersinia pestis<\/jats:italic>\n                    , there is surprisingly little information on the cellular and molecular mechanisms responsible for\n                    <jats:italic>Y. pestis<\/jats:italic>\n                    -triggered pathology in the lung. Therefore, to understand the progression of this unique disease, we characterized an intranasal mouse model of primary pneumonic plague. Mice succumbed to a purulent multifocal severe exudative bronchopneumonia that closely resembles the disease observed in humans. Analyses revealed a strikingly biphasic syndrome, in which the infection begins with an antiinflammatory state in the first 24-36 h that rapidly progresses to a highly proinflammatory state by 48 h and death by 3 days. To assess the adaptation of\n                    <jats:italic>Y. pestis<\/jats:italic>\n                    to a mammalian environment, we used DNA microarray technology to analyze the transcriptional responses of the bacteria during interaction with the mouse lung. Included among the genes up-regulated\n                    <jats:italic>in vivo<\/jats:italic>\n                    are those comprising the\n                    <jats:italic>yop-ysc<\/jats:italic>\n                    type III secretion system and genes contained within the chromosomal pigmentation locus, validating the use of this technology to identify loci essential to the virulence of\n                    <jats:italic>Y. pestis<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1073\/pnas.0506840102","type":"journal-article","created":{"date-parts":[[2005,11,23]],"date-time":"2005-11-23T20:44:55Z","timestamp":1132778695000},"page":"17786-17791","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":257,"title":["Progression of primary pneumonic plague: A mouse model of infection, pathology, and bacterial transcriptional activity"],"prefix":"10.1073","volume":"102","author":[{"given":"Wyndham W.","family":"Lathem","sequence":"first","affiliation":[{"name":"Departments of Molecular Microbiology and Pediatrics and Genome Sequencing Center, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seth D.","family":"Crosby","sequence":"additional","affiliation":[{"name":"Departments of Molecular Microbiology and Pediatrics and Genome Sequencing Center, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Virginia L.","family":"Miller","sequence":"additional","affiliation":[{"name":"Departments of Molecular Microbiology and Pediatrics and Genome Sequencing Center, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William E.","family":"Goldman","sequence":"additional","affiliation":[{"name":"Departments of Molecular Microbiology and Pediatrics and Genome Sequencing Center, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2005,11,23]]},"reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"crossref","unstructured":"Inglesby T. 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