{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,26]],"date-time":"2025-12-26T14:44:03Z","timestamp":1766760243495},"reference-count":80,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2013,8,1]],"date-time":"2013-08-01T00:00:00Z","timestamp":1375315200000},"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":[[2013,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Recognition of microbial infection by certain intracellular pattern recognition receptors leads to the formation of a multiprotein complex termed the inflammasome. Inflammasome assembly activates caspase-1 and leads to cleavage and secretion of the proinflammatory cytokines interleukin-1 beta (IL-1\u03b2) and IL-18, which help control many bacterial pathogens. However, excessive inflammation mediated by inflammasome activation can also contribute to immunopathology. Here, we investigated whether\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Haemophilus ducreyi<\/jats:named-content>\n            , a Gram-negative bacterium that causes the genital ulcer disease chancroid, activates inflammasomes in experimentally infected human skin and in monocyte-derived macrophages (MDM). Although\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>\n            is predominantly extracellular during human infection, several inflammasome-related components were transcriptionally upregulated in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>\n            -infected skin. Infection of MDM with live, but not heat-killed,\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>\n            induced caspase-1- and caspase-5-dependent processing and secretion of IL-1\u03b2. Blockage of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>\n            uptake by cytochalasin D significantly reduced the amount of secreted IL-1\u03b2. Knocking down the expression of the inflammasome components NLRP3 and ASC abolished IL-1\u03b2 production. Consistent with NLRP3-dependent inflammasome activation, blocking ATP signaling, K\n            <jats:sup>+<\/jats:sup>\n            efflux, cathepsin B activity, and lysosomal acidification all inhibited IL-1\u03b2 secretion. However, inhibition of the production and function of reactive oxygen species did not decrease IL-1\u03b2 production. Polarization of macrophages to classically activated M1 or alternatively activated M2 cells abrogated IL-1\u03b2 secretion elicited by\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>\n            . Our study data indicate that\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>\n            induces NLRP3 inflammasome activation via multiple mechanisms and suggest that the heterogeneity of macrophages within human lesions may modulate inflammasome activation during human infection.\n          <\/jats:p>","DOI":"10.1128\/iai.00354-13","type":"journal-article","created":{"date-parts":[[2013,6,11]],"date-time":"2013-06-11T03:17:08Z","timestamp":1370920628000},"page":"2997-3008","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":7,"title":["Haemophilus ducreyi Infection Induces Activation of the NLRP3 Inflammasome in Nonpolarized but Not in Polarized Human Macrophages"],"prefix":"10.1128","volume":"81","author":[{"given":"Wei","family":"Li","sequence":"first","affiliation":[{"name":"Departments of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barry P.","family":"Katz","sequence":"additional","affiliation":[{"name":"Biostatistics, Indiana University School of Medicine, Indianapolis, Indiana, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Margaret E.","family":"Bauer","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stanley M.","family":"Spinola","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA"},{"name":"Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA"},{"name":"Center for Immunobiology, Indiana University School of Medicine, Indianapolis, Indiana, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"689","volume-title":"Sexually transmitted diseases","author":"Spinola SM","year":"2008","unstructured":"SpinolaSM. 2008. Chancroid and Haemophilus ducreyi, p 689\u2013699. In HolmesKKSparlingPFStammWEPiotPWasserheitJNCoreyLCohenMSWattsDH (ed), Sexually transmitted diseases, 4th ed. 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