{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,29]],"date-time":"2025-12-29T11:06:27Z","timestamp":1767006387236},"reference-count":33,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2009,12,1]],"date-time":"2009-12-01T00:00:00Z","timestamp":1259625600000},"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":[[2009,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Melioidosis is a tropical disease endemic in southeast Asia and northern Australia caused by the gram-negative soil saprophyte\n            <jats:italic>Burkholderia pseudomallei<\/jats:italic>\n            . Although infection is often systemic, the lung is frequently involved.\n            <jats:italic>B. thailandensis<\/jats:italic>\n            is a closely related organism that at high doses causes lethal pneumonia in mice. We examined the role of Toll-like receptors (TLRs), essential components of innate immunity, in vitro and in vivo during murine\n            <jats:italic>B. thailandensis<\/jats:italic>\n            pneumonia. TLR2, TLR4, and TLR5 mediate NF-\u03baB activation by\n            <jats:italic>B. thailandensis<\/jats:italic>\n            in transfected HEK293 or CHO cells. In macrophages, TLR4 and the adaptor molecule MyD88, but not TLR2 or TLR5, are required for tumor necrosis factor alpha production induced by\n            <jats:italic>B. thailandensis<\/jats:italic>\n            . In low-dose airborne infection, TLR4 is needed for early, but not late, bacterial containment, and MyD88 is essential for control of infection and host survival. TLR2 and TLR5 are not necessary to contain low-dose infection. In high-dose airborne infection, TLR2 deficiency confers a slight survival advantage. Lung and systemic inflammatory responses are induced by low-dose inhaled\n            <jats:italic>B. thailandensis<\/jats:italic>\n            independently of individual TLRs or MyD88. These findings suggest that redundancy in TLR signaling or other MyD88-dependent pathways may be important in pneumonic\n            <jats:italic>B. thailandensis<\/jats:italic>\n            infection but that MyD88-independent mechanisms of inflammation are also activated. TLR signaling in\n            <jats:italic>B. thailandensis<\/jats:italic>\n            infection is substantially comparable to signaling induced by virulent\n            <jats:italic>B. pseudomallei<\/jats:italic>\n            . These studies provide additional insights into the host-pathogen interaction in pneumonic\n            <jats:italic>Burkholderia<\/jats:italic>\n            infection.\n          <\/jats:p>","DOI":"10.1128\/iai.00618-09","type":"journal-article","created":{"date-parts":[[2009,9,22]],"date-time":"2009-09-22T01:48:31Z","timestamp":1253584111000},"page":"5612-5622","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":19,"title":["Toll-Like Receptor Signaling in Airborne\n            <i>Burkholderia thailandensis<\/i>\n            Infection"],"prefix":"10.1128","volume":"77","author":[{"given":"T. Eoin","family":"West","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas R.","family":"Hawn","sequence":"additional","affiliation":[{"name":"Division of Allergy and Infectious Diseases, Department of Medicine, University of Washington School of Medicine, Seattle, Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shawn J.","family":"Skerrett","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.1.352-361.2005"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.02049-05"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.179.6.3937"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.01489-07"},{"key":"e_1_3_2_6_2","first-page":"E17","volume":"9","year":"2004","unstructured":"Bossi, P., A. 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