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We identified a homolog of the<jats:italic>Salmonella enterica<\/jats:italic>serovar Typhimurium lipoprotein (<jats:italic>lpp<\/jats:italic>) gene in<jats:italic>Yersinia<\/jats:italic>species and prepared<jats:italic>lpp<\/jats:italic>gene deletion mutants of<jats:italic>Y. pseudotuberculosis<\/jats:italic>YPIII,<jats:italic>Y. pestis<\/jats:italic>KIM\/D27 (pigmentation locus minus), and<jats:italic>Y. pestis<\/jats:italic>CO92 with reduced virulence. Mice injected via the intraperitoneal route with 5 \u00d7 10<jats:sup>7<\/jats:sup>CFU of the \u0394<jats:italic>lpp<\/jats:italic>KIM\/D27 mutant survived a month, even though this would have constituted a lethal dose for the parental KIM\/D27 strain. Subsequently, these \u0394<jats:italic>lpp<\/jats:italic>KIM\/D27-injected mice were solidly protected against an intranasally administered, highly virulent<jats:italic>Y. pestis<\/jats:italic>CO92 strain when it was given as five 50% lethal doses (LD<jats:sub>50<\/jats:sub>). In a parallel study with the pneumonic plague mouse model, after 72 h postinfection, the lungs of animals infected with wild-type (WT)<jats:italic>Y. pestis<\/jats:italic>CO92 and given a subinhibitory dose of levofloxacin had acute inflammation, edema, and masses of bacteria, while the lung tissue appeared essentially normal in mice inoculated with the \u0394<jats:italic>lpp<\/jats:italic>mutant of CO92 and given the same dose of levofloxacin. Importantly, while WT<jats:italic>Y. pestis<\/jats:italic>CO92 could be detected in the bloodstreams and spleens of infected mice at 72 h postinfection, the \u0394<jats:italic>lpp<\/jats:italic>mutant of CO92 could not be detected in those organs. Furthermore, the levels of cytokines\/chemokines detected in the sera were significantly lower in animals infected with the \u0394<jats:italic>lpp<\/jats:italic>mutant than in those infected with WT CO92. Additionally, the \u0394<jats:italic>lpp<\/jats:italic>mutant was more rapidly killed by macrophages than was the WT CO92 strain. These data provided evidence that the \u0394<jats:italic>lpp<\/jats:italic>mutants of yersiniae were significantly attenuated and could be useful tools in the development of new vaccines.<\/jats:p>","DOI":"10.1128\/iai.01529-07","type":"journal-article","created":{"date-parts":[[2008,1,29]],"date-time":"2008-01-29T01:46:26Z","timestamp":1201571186000},"page":"1390-1409","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":73,"title":["Braun Lipoprotein (Lpp) Contributes to Virulence of Yersiniae: Potential Role of Lpp in Inducing Bubonic and Pneumonic Plague"],"prefix":"10.1128","volume":"76","author":[{"given":"Jian","family":"Sha","sequence":"first","affiliation":[{"name":"Departments of Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stacy L.","family":"Agar","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wallace B.","family":"Baze","sequence":"additional","affiliation":[{"name":"Department of Veterinary Sciences, University of Texas, M. 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