{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T15:33:39Z","timestamp":1791214419279,"version":"4.1.0"},"reference-count":39,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2006,9,1]],"date-time":"2006-09-01T00:00:00Z","timestamp":1157068800000},"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":[[2006,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Burkholderia mallei<\/jats:italic>is a gram-negative bacterium which causes the potentially fatal disease glanders in humans; however, there is little information concerning cell-mediated immunity to this pathogen. The role of gamma interferon (IFN-\u03b3) during<jats:italic>B. mallei<\/jats:italic>infection was investigated using a disease model in which infected BALB\/c mice normally die between 40 and 60 days postinfection. IFN-\u03b3 knockout mice infected with<jats:italic>B. mallei<\/jats:italic>died within 2 to 3 days after infection, and there was uncontrolled bacterial replication in several organs, demonstrating the essential role of IFN-\u03b3 in the innate immune response to this pathogen. Increased levels of IFN-\u03b3, interleukin-6 (IL-6), and monocyte chemoattractant protein 1 were detected in the sera of immunocompetent mice in response to infection, and splenic mRNA expression of IFN-\u03b3, IL-6, IL-12p35, and IL-27 was elevated 24 h postinfection. The effects of IL-18, IL-27, and IL-12 on stimulation of the rapid IFN-\u03b3 production were investigated in vitro by analyzing IFN-\u03b3 production in the presence of heat-killed<jats:italic>B. mallei<\/jats:italic>. IL-12 was essential for IFN-\u03b3 production in vitro; IL-18 was also involved in induction of IFN-\u03b3, but IL-27 was not required for IFN-\u03b3 production in response to heat-killed<jats:italic>B. mallei<\/jats:italic>. The main cellular sources of IFN-\u03b3 were identified in vitro as NK cells, CD8<jats:sup>+<\/jats:sup>T cells, and TCR\u03b3\u03b4 T cells. Our data show that<jats:italic>B. mallei<\/jats:italic>is susceptible to cell-mediated immune responses which promote expression of type 1 cytokines. This suggests that development of effective vaccines against glanders should target the production of IFN-\u03b3.<\/jats:p>","DOI":"10.1128\/iai.02046-05","type":"journal-article","created":{"date-parts":[[2006,8,22]],"date-time":"2006-08-22T22:13:07Z","timestamp":1156284787000},"page":"5333-5340","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":35,"title":["Critical Role of Type 1 Cytokines in Controlling Initial Infection with<i>Burkholderia mallei<\/i>"],"prefix":"10.1128","volume":"74","author":[{"given":"Caroline A.","family":"Rowland","sequence":"first","affiliation":[{"name":"Dstl, Porton Down, Salisbury, SP4 0JQ, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ganjana","family":"Lertmemongkolchai","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology, Faculty of Associated Medical Sciences, Khon Kaen University, Khon Kaen, 40002 Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alison","family":"Bancroft","sequence":"additional","affiliation":[{"name":"University of Manchester, Manchester, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashraful","family":"Haque","sequence":"additional","affiliation":[{"name":"London School of Hygiene and Tropical Medicine, Keppel St., London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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