{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T05:29:36Z","timestamp":1782365376357,"version":"3.54.5"},"update-to":[{"DOI":"10.1371\/journal.ppat.1009782","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2021,8,9]],"date-time":"2021-08-09T00:00:00Z","timestamp":1628467200000}}],"reference-count":54,"publisher":"Public Library of Science (PLoS)","issue":"7","license":[{"start":{"date-parts":[[2021,7,28]],"date-time":"2021-07-28T00:00:00Z","timestamp":1627430400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"national institute of allergy and infectious diseases","doi-asserted-by":"publisher","award":["R01AI132674"],"award-info":[{"award-number":["R01AI132674"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"national institute of allergy and infectious diseases","doi-asserted-by":"publisher","award":["T32AI007526-20"],"award-info":[{"award-number":["T32AI007526-20"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"national institute of allergy and infectious diseases","doi-asserted-by":"publisher","award":["R21AI156536-01"],"award-info":[{"award-number":["R21AI156536-01"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"national institute of allergy and infectious diseases","doi-asserted-by":"publisher","award":["R21AI153586"],"award-info":[{"award-number":["R21AI153586"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"name":"utmb institute for human infections and immunity pilot grant"},{"name":"niaid emerging and tropical infectious diseases t32 fellowship"},{"name":"utmb john w. mclaughlin fund"}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p><jats:italic>Orientia tsutsugamushi<\/jats:italic> is an obligately intracellular bacterium and the etiological agent of scrub typhus. The lung is a major target organ of infection, displaying type 1-skewed proinflammatory responses. Lung injury and acute respiratory distress syndrome are common complications of severe scrub typhus; yet, their underlying mechanisms remain unclear. In this study, we investigated whether the C-type lectin receptor (CLR) Mincle contributes to immune recognition and dysregulation. Following lethal infection in mice, we performed pulmonary differential expression analysis with NanoString. Of 671 genes examined, we found 312 significantly expressed genes at the terminal phase of disease. Mincle (<jats:italic>Clec4e<\/jats:italic>) was among the top 5 greatest up-regulated genes, accompanied with its signaling partners, type 1-skewing chemokines (<jats:italic>Cxcr3<\/jats:italic>, <jats:italic>Ccr5<\/jats:italic>, and their ligands), as well as <jats:italic>Il27<\/jats:italic>. To validate the role of Mincle in scrub typhus, we exposed murine bone marrow-derived macrophages (M\u03a6) to live or inactivated <jats:italic>O<\/jats:italic>. <jats:italic>tsutsugamushi<\/jats:italic> and analyzed a panel of CLRs and proinflammatory markers via qRT-PCR. We found that while heat-killed bacteria stimulated transitory Mincle expression, live bacteria generated a robust response in M\u03a6, which was validated by indirect immunofluorescence and western blot. Notably, infection had limited impact on other tested CLRs or TLRs. Sustained proinflammatory gene expression in M\u03a6 (<jats:italic>Cxcl9<\/jats:italic>, <jats:italic>Ccl2<\/jats:italic>, <jats:italic>Ccl5<\/jats:italic>, <jats:italic>Nos2<\/jats:italic>, <jats:italic>Il27<\/jats:italic>) was induced by live, but not inactivated, bacteria; infected Mincle<jats:sup>-\/-<\/jats:sup> M\u03a6 significantly reduced proinflammatory responses compared with WT cells. Together, this study provides the first evidence for a selective expression of Mincle in sensing <jats:italic>O<\/jats:italic>. <jats:italic>tsutsugamushi<\/jats:italic> and suggests a potential role of Mincle- and IL-27-related pathways in host responses to severe infection. Additionally, it provides novel insight into innate immune recognition of this poorly studied bacterium.<\/jats:p>","DOI":"10.1371\/journal.ppat.1009782","type":"journal-article","created":{"date-parts":[[2021,7,28]],"date-time":"2021-07-28T17:41:00Z","timestamp":1627494060000},"page":"e1009782","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":30,"title":["Orientia tsutsugamushi selectively stimulates the C-type lectin receptor Mincle and type 1-skewed proinflammatory immune 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