{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T13:15:45Z","timestamp":1740143745888,"version":"3.37.3"},"reference-count":57,"publisher":"Public Library of Science (PLoS)","issue":"11","license":[{"start":{"date-parts":[[2023,11,1]],"date-time":"2023-11-01T00:00:00Z","timestamp":1698796800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100009619","name":"Japan Agency for Medical Research and Development","doi-asserted-by":"publisher","award":["22wm0125007, 22wm0225004, 22wm0225022"],"award-info":[{"award-number":["22wm0125007, 22wm0225004, 22wm0225022"]}],"id":[{"id":"10.13039\/100009619","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100009619","name":"Japan Agency for Medical Research and Development","doi-asserted-by":"publisher","award":["22wm0125007, 22wm0225004, 22wm0225022"],"award-info":[{"award-number":["22wm0125007, 22wm0225004, 22wm0225022"]}],"id":[{"id":"10.13039\/100009619","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100009619","name":"Japan Agency for Medical Research and Development","doi-asserted-by":"publisher","award":["22wm0225022"],"award-info":[{"award-number":["22wm0225022"]}],"id":[{"id":"10.13039\/100009619","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["19KK0217, 19H03467, 22H02865"],"award-info":[{"award-number":["19KK0217, 19H03467, 22H02865"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["19KK0217"],"award-info":[{"award-number":["19KK0217"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["19KK0217"],"award-info":[{"award-number":["19KK0217"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]},{"name":"T.E.N. Ghana MV25 B.V."}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>Buruli ulcer is an emerging chronic infectious skin disease caused by <jats:italic>Mycobacterium ulcerans<\/jats:italic>. Mycolactone, an exotoxin produced by the bacterium, is the only identified virulence factor so far, but the functions of this toxin and the mechanisms of disease progression remain unclear. By interfering Sec61 translocon, mycolactone inhibits the Sec61-dependent co-translational translocation of newly synthesized proteins, such as induced cytokines and immune cell receptors, into the endoplasmic reticulum. However, in regard to IL-1\u03b2, which is secreted by a Sec61-independent mechanism, mycolactone has been shown to induce IL-1\u03b2 secretion via activation of inflammasomes. In this study, we clarified that cytokine induction, including that of IL-1\u03b2, in infected macrophages was suppressed by mycolactone produced by <jats:italic>M<\/jats:italic>. <jats:italic>ulcerans<\/jats:italic> subsp. <jats:italic>shinshuense<\/jats:italic>, despite the activation of caspase-1 through the inflammasome activation triggered in a manner independent of mycolactone. Intriguingly, mycolactone suppressed the expression of proIL-1\u03b2 as well as TNF-\u03b1 at the transcriptional level, suggesting that mycolactone of <jats:italic>M<\/jats:italic>. <jats:italic>ulcerans<\/jats:italic> subsp. <jats:italic>shinshuense<\/jats:italic> may exert additional inhibitory effect on proIL-1\u03b2 expression. Remarkably, constitutively produced IL-18 was cleaved and mature IL-18 was actually released from macrophages infected with the causative mycobacterium. IL-18-deficient mice infected subcutaneously with <jats:italic>M<\/jats:italic>. <jats:italic>ulcerans<\/jats:italic> exhibited exacerbated skin inflammation during the course of disease progression. On the other hand, IL-1\u03b2 controls bacterial multiplication in skin tissues. These results provide information regarding the mechanisms and functions of the induced cytokines in the pathology of Buruli ulcer.<\/jats:p>","DOI":"10.1371\/journal.ppat.1011747","type":"journal-article","created":{"date-parts":[[2023,11,1]],"date-time":"2023-11-01T17:37:56Z","timestamp":1698860276000},"page":"e1011747","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":1,"title":["Inflammasome-triggered IL-18 controls skin inflammation in the progression of Buruli ulcer"],"prefix":"10.1371","volume":"19","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3853-0106","authenticated-orcid":true,"given":"Toshihiko","family":"Suzuki","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kotchakorn","family":"Boonyaleka","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tokuju","family":"Okano","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tamako","family":"Iida","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mitsunori","family":"Yoshida","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hanako","family":"Fukano","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshihiko","family":"Hoshino","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoichiro","family":"Iwakura","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anthony 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