{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T06:34:22Z","timestamp":1776321262398,"version":"3.50.1"},"reference-count":37,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"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":[[2012,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The Gram-negative bacterium\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Burkholderia mallei<\/jats:named-content>\n            causes rapidly fatal illness in equines and humans when contracted by inhalation and also has the potential to be used as a bioweapon. However, little is known regarding the early innate immune responses and signaling mechanisms required to generate protection from pneumonic\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. mallei<\/jats:named-content>\n            infection. We showed previously that monocyte chemoattractant protein 1 (MCP-1) was a critical chemokine required for protection from pneumonic\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. mallei<\/jats:named-content>\n            infection. We have now extended those studies to identify key Toll-like receptor (TLR) signaling pathways, effector cells, and cytokines required for protection from respiratory\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. mallei<\/jats:named-content>\n            infection. We found that MyD88\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice were highly susceptible to pulmonary challenge with\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. mallei<\/jats:named-content>\n            and had significantly short survival times, increased bacterial burdens, and severe organ pathology compared to wild-type mice. Notably, MyD88\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice had significantly fewer monocytes and dendritic cells (DCs) in lung tissues and airways than infected wild-type mice despite markedly higher bacterial burdens. The MyD88\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice were also completely unable to produce gamma interferon (IFN-\u03b3) at any time points following infection. In wild-type mice, NK cells were the primary cells producing IFN-\u03b3 in the lungs following\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. mallei<\/jats:named-content>\n            infection, while DCs and monocytes were the primary cellular sources of interleukin-12 (IL-12) production. Treatment with recombinant IFN-\u03b3 (rIFN-\u03b3) was able to significantly restore protective immunity in MyD88\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. Thus, we conclude that the MyD88-dependent recruitment of inflammatory monocytes and DCs to the lungs and the local production of IL-12, followed by NK cell production of IFN-\u03b3, are the key initial cellular responses required for early protection from\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. mallei<\/jats:named-content>\n            infection.\n          <\/jats:p>","DOI":"10.1128\/iai.05819-11","type":"journal-article","created":{"date-parts":[[2011,10,25]],"date-time":"2011-10-25T02:21:28Z","timestamp":1319509288000},"page":"110-120","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":16,"title":["MyD88-Dependent Recruitment of Monocytes and Dendritic Cells Required for Protection from Pulmonary Burkholderia mallei Infection"],"prefix":"10.1128","volume":"80","author":[{"given":"Andrew","family":"Goodyear","sequence":"first","affiliation":[{"name":"Rocky Mountain RCE and Department of Microbiology, Immunology, and Pathology, Ft. 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Collins, Colorado, USA, and School of Veterinary Science, University of Queensland, Gatton, Queensland, Australia"},{"name":"Department of Clinical Sciences, Ft. Collins, Colorado, USA, and School of Veterinary Science, University of Queensland, Gatton, Queensland, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"379","article-title":"Susceptibility to Burkholderia pseudomallei is associated with host immune responses involving tumor necrosis factor receptor-1 (TNFR1) and TNF receptor-2 (TNFR2). FEMS Immunol","volume":"52","author":"Barnes JL","year":"2008","unstructured":"BarnesJLWilliamsNLKetheesanN. 2008. Susceptibility to Burkholderia pseudomallei is associated with host immune responses involving tumor necrosis factor receptor-1 (TNFR1) and TNF receptor-2 (TNFR2). FEMS Immunol. Med. Microbiol. 52: 379\u2013388.","journal-title":"Med. 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