{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T15:51:18Z","timestamp":1775231478296,"version":"3.50.1"},"reference-count":31,"publisher":"Microbiology Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,10,1]]},"abstract":"<jats:p>Deletion of the murein (Braun) lipoprotein gene,<jats:italic>lpp<\/jats:italic>, attenuates the<jats:italic>Yersinia pestis<\/jats:italic>CO92 strain in mouse models of bubonic and pneumonic plague. In this report, we characterized the virulence of strains from which the plasminogen activating protease (<jats:italic>pla<\/jats:italic>)-encoding pPCP1 plasmid was cured from either the wild-type (WT) or the \u0394<jats:italic>lpp<\/jats:italic>mutant strain of<jats:italic>Y. pestis<\/jats:italic>CO92 in the mouse model of pneumonic infection. We noted a significantly increased survival rate in mice infected with the<jats:italic>Y. pestis<\/jats:italic>pPCP<jats:sup>\u2212<\/jats:sup>\/\u0394<jats:italic>lpp<\/jats:italic>mutant strain up to a dose of 5000 LD<jats:sub>50<\/jats:sub>. Additionally, mice challenged with the pPCP<jats:bold><jats:sup>\u2212<\/jats:sup><\/jats:bold>\/\u0394<jats:italic>lpp<\/jats:italic>strain had substantially less tissue injury and a strong decrease in the levels of most cytokines and chemokines in tissue homogenates and sera when compared with the WT-infected group. Importantly, the<jats:italic>Y. pestis<\/jats:italic>pPCP<jats:bold><jats:sup>\u2212<\/jats:sup><\/jats:bold>\/\u0394<jats:italic>lpp<\/jats:italic>mutant strain was detectable in high numbers in the livers and spleens of some of the infected mice. In the lungs of pPCP<jats:bold><jats:sup>\u2212<\/jats:sup><\/jats:bold>\/\u0394<jats:italic>lpp<\/jats:italic>mutant-challenged animals, however, bacterial numbers dropped at 48\u2005h after infection when compared with tissue homogenates from 1\u2005h post-infection. Similarly, we noted that this mutant was unable to survive within murine macrophages in an<jats:italic>in vitro<\/jats:italic>assay, whereas survivability of the pPCP<jats:sup>\u2212<\/jats:sup>mutant within the macrophage environment was similar to that of the WT. Taken together, our data indicated that a significant and possibly synergistic attenuation in bacterial virulence occurred in a mouse model of pneumonic plague when both the<jats:italic>lpp<\/jats:italic>gene and the virulence plasmid pPCP1 encoding the<jats:italic>pla<\/jats:italic>gene were deleted from<jats:italic>Y. pestis<\/jats:italic>.<\/jats:p>","DOI":"10.1099\/mic.0.029124-0","type":"journal-article","created":{"date-parts":[[2009,9,29]],"date-time":"2009-09-29T00:25:45Z","timestamp":1254183945000},"page":"3247-3259","source":"Crossref","is-referenced-by-count":26,"title":["Deletion of Braun lipoprotein gene (lpp) and curing of plasmid pPCP1 dramatically alter the virulence of Yersinia pestis CO92 in a mouse model of pneumonic plague"],"prefix":"10.1099","volume":"155","author":[{"given":"Stacy L.","family":"Agar","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas Medical Branch (UTMB), Galveston, TX 77555, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jian","family":"Sha","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas Medical Branch (UTMB), Galveston, TX 77555, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wallace B.","family":"Baze","sequence":"additional","affiliation":[{"name":"Department of Veterinary Sciences, University of Texas M. 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