{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T10:02:58Z","timestamp":1789725778012,"version":"4.0.1"},"reference-count":67,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2009,4,28]],"date-time":"2009-04-28T00:00:00Z","timestamp":1240876800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["1P01A10157986"],"award-info":[{"award-number":["1P01A10157986"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["NS35974"],"award-info":[{"award-number":["NS35974"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AI 59703"],"award-info":[{"award-number":["AI 59703"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,4,28]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Excessive host inflammatory responses negatively impact the disease outcome in pneumonic tularemia.<\/jats:p>\n               <jats:p>The bacterial or host determinants of lethality associated with respiratory Francisella infections are currently unknown. No exo\u2013 or endotoxins that contribute to the severity of this disease have been identified. However, a deregulated host immune response upon infection is characterized by an initial 36\u2013 to 48\u2013h delay followed by a rapid and excessive inflammatory response prior to death at 72\u2013120 h. Here, we extend these findings by comparing host immune responses between sublethal and lethal respiratory infections of mice with an attenuated transposon mutant (Mut) of F. novicida (F.n.) strain U112 (sublethal) versus the wild\u2013type (WT) strain (lethal). Infection with WT bacteria, but not the Mut, was characterized by sustained bacteremia and systemic dissemination of the pathogen with temporal increases in bacterial burdens in liver and spleen. Severe pathology with large foci of infiltrates associated with extensive tissue damage was evident in WT\u2013infected lungs, and Mut\u2013infected mice displayed much reduced pathology with intact lung architecture. Similar to other experimental models of severe sepsis, WT\u2013 but not the Mut\u2013infected mice exhibited a robust increase in numbers of Gr1+ and CD11b+ cells, while displaying a significant depletion of \u03b1\u03b2 T cells. Further, a dramatic up\u2013regulation of multiple cytokines and chemokines was observed only in lethal WT infection. In addition, an earlier and larger increased expression of S100A9, a known mediator of sepsis, was observed in WT\u2013infected mice. Taken together, these results show that a hyperinflammatory host immune response, culminating in severe sepsis, is responsible for the lethal outcome of respiratory tularemia.<\/jats:p>","DOI":"10.1189\/jlb.1208728","type":"journal-article","created":{"date-parts":[[2009,4,29]],"date-time":"2009-04-29T01:14:21Z","timestamp":1240967661000},"page":"491-504","source":"Crossref","is-referenced-by-count":43,"title":["Lethal pulmonary infection with <i>Francisella novicida<\/i> is associated with severe sepsis"],"prefix":"10.1093","volume":"86","author":[{"given":"Jyotika","family":"Sharma","sequence":"first","affiliation":[{"name":"South Texas Center for Emerging Diseases and Department of Biology, University of Texas at San Antonio , San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qun","family":"Li","sequence":"additional","affiliation":[{"name":"South Texas Center for Emerging Diseases and Department of Biology, University of Texas at San Antonio , San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bibhuti B","family":"Mishra","sequence":"additional","affiliation":[{"name":"South Texas Center for Emerging Diseases and Department of Biology, University of Texas at San Antonio , San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher","family":"Pena","sequence":"additional","affiliation":[{"name":"South Texas Center for Emerging Diseases and Department of Biology, University of Texas at San Antonio , San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judy M","family":"Teale","sequence":"additional","affiliation":[{"name":"South Texas Center for Emerging Diseases and Department of Biology, University of Texas at San Antonio , San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,4,28]]},"reference":[{"key":"2023032913015649500_jlb0491-cit-B1","doi-asserted-by":"crossref","first-page":"2763","DOI":"10.1001\/jama.285.21.2763","article-title":"Tularemia as a biological weapon: medical and public health management","volume":"285","author":"Dennis","year":"2001","journal-title":"JAMA"},{"key":"2023032913015649500_jlb0491-cit-B2","doi-asserted-by":"crossref","first-page":"167","DOI":"10.1146\/annurev.micro.60.080805.142126","article-title":"Francisella tularensis. taxonomy, genetics, and immunopathogenesis of a potential agent of biowarfare","volume":"60","author":"McLendon","year":"2006","journal-title":"Annu. Rev. Microbiol."},{"key":"2023032913015649500_jlb0491-cit-B3","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1196\/annals.1409.009","article-title":"Tularemia: history, epidemiology, pathogen physiology, and clinical manifestations","volume":"1105","author":"Sjostedt","year":"2007","journal-title":"Ann. N. Y. Acad. Sci."},{"key":"2023032913015649500_jlb0491-cit-B4","doi-asserted-by":"crossref","first-page":"3001","DOI":"10.1128\/IAI.00215-08","article-title":"Initial delay in the immune response to Francisella tularensis is followed by hypercytokinemia characteristic of severe sepsis and correlating with upregulation and release of damage-associated molecular patterns","volume":"76","author":"Mares","year":"2008","journal-title":"Infect. Immun."},{"key":"2023032913015649500_jlb0491-cit-B5","doi-asserted-by":"crossref","first-page":"3690","DOI":"10.1128\/IAI.00262-08","article-title":"Combined deletion of four Francisella novicida acid phosphatases attenuates virulence and macrophage vacuolar escape","volume":"76","author":"Mohapatra","year":"2008","journal-title":"Infect. Immun."},{"key":"2023032913015649500_jlb0491-cit-B6","doi-asserted-by":"crossref","first-page":"5376","DOI":"10.1128\/IAI.00238-07","article-title":"Identification of Francisella tularensis Himar1-based transposon mutants defective for replication in macrophages","volume":"75","author":"Maier","year":"2007","journal-title":"Infect. Immun."},{"key":"2023032913015649500_jlb0491-cit-B7","doi-asserted-by":"crossref","first-page":"247","DOI":"10.1046\/j.1365-2958.1998.00926.x","article-title":"MglA and MglB are required for the intramacrophage growth of","volume":"29","author":"Baron","year":"1998","journal-title":"Francisella novicida. Mol. 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