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Type 2 diabetes (T2D) is the most common comorbidity associated with melioidosis.<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>isolates from melioidosis patients with T2D are less virulent in animal models than those from patients with melioidosis and no identifiable risk factors. We developed an<jats:italic>ex vivo<\/jats:italic>whole-blood assay as a tool for comparison of early inflammatory profiles generated by T2D and nondiabetic (ND) individuals in response to a<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>strain of low virulence. Peripheral blood from individuals with T2D, with either poorly controlled glycemia (PC-T2D [<jats:italic>n<\/jats:italic>= 6]) or well-controlled glycemia (WC-T2D [<jats:italic>n<\/jats:italic>= 8]), and healthy ND (<jats:italic>n<\/jats:italic>= 13) individuals was stimulated with<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>. Oxidative burst, myeloperoxidase (MPO) release, expression of pathogen recognition receptors (TLR2, TLR4, and CD14), and activation markers (CD11b and HLA-DR) were measured on polymorphonuclear (PMN) leukocytes and monocytes. Concentrations of plasma inflammatory cytokine (interleukin-6 [IL-6], IL-12p70, tumor necrosis factor alpha [TNF-\u03b1], monocyte chemoattractant protein 1 [MCP-1], IL-8, IL-1\u03b2, and IL-10) were also determined. Following stimulation, oxidative burst and MPO levels were significantly elevated in blood from PC-T2D subjects compared to controls. Differences were also observed in expression of Toll-like receptor 2 (TLR2), CD14, and CD11b on phagocytes from T2D and ND individuals. Levels of IL-12p70, MCP-1, and IL-8 were significantly elevated in blood from PC-T2D subjects compared to ND individuals. Notably, differential inflammatory responses of PC-T2D, WC-T2D, and ND individuals to<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>occur independently of bacterial load and confirm the efficacy of this model of T2D-melioidosis comorbidity as a tool for investigation of dysregulated PMN and monocyte responses to<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>underlying susceptibility of T2D individuals to melioidosis.<\/jats:p>","DOI":"10.1128\/iai.00212-12","type":"journal-article","created":{"date-parts":[[2012,4,3]],"date-time":"2012-04-03T04:59:56Z","timestamp":1333429196000},"page":"2089-2099","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":28,"title":["Burkholderia pseudomallei Triggers Altered Inflammatory Profiles in a Whole-Blood Model of Type 2 Diabetes-Melioidosis Comorbidity"],"prefix":"10.1128","volume":"80","author":[{"given":"Jodie","family":"Morris","sequence":"first","affiliation":[{"name":"Infectious Diseases and Immunopathogenesis Research Group, Discipline of Microbiology and Immunology, James Cook University, Townsville, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natasha","family":"Williams","sequence":"additional","affiliation":[{"name":"Infectious Diseases and Immunopathogenesis Research Group, Discipline of Microbiology and Immunology, James Cook University, Townsville, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine","family":"Rush","sequence":"additional","affiliation":[{"name":"Infectious Diseases and Immunopathogenesis Research Group, Discipline of Microbiology and Immunology, James Cook University, Townsville, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brenda","family":"Govan","sequence":"additional","affiliation":[{"name":"Infectious Diseases and Immunopathogenesis Research Group, Discipline of Microbiology and Immunology, James Cook University, Townsville, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kunwarjit","family":"Sangla","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Townsville Hospital, Townsville, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Norton","sequence":"additional","affiliation":[{"name":"Pathology Queensland, Townsville Hospital, Townsville, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natkunam","family":"Ketheesan","sequence":"additional","affiliation":[{"name":"Infectious Diseases and Immunopathogenesis Research Group, Discipline of Microbiology and Immunology, James Cook University, Townsville, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0900196106"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00134-010-1845-1"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.5694\/j.1326-5377.1987.tb133542.x"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0901219"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.3201\/eid1104.041051"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1711.2001.01038.x"},{"key":"e_1_3_3_8_2","doi-asserted-by":"crossref","first-page":"1567","DOI":"10.4049\/jimmunol.147.5.1567","article-title":"Shedding as a mechanism of down-modulation of CD14 on stimulated human monocytes","volume":"147","author":"Bazil V","year":"1991","unstructured":"BazilVStromingerJL. 1991. 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