{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T06:39:36Z","timestamp":1791095976371,"version":"4.1.0"},"reference-count":37,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2011,6,1]],"date-time":"2011-06-01T00:00:00Z","timestamp":1306886400000},"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":[[2011,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>The ability of pathogens to evade host antimicrobial mechanisms is crucial to their virulence. The dimorphic fungal pathogen<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Blastomyces dermatitidis<\/jats:named-content>can infect immunocompetent patients, producing a primary pulmonary infection that can later disseminate to other organs.<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. dermatitidis<\/jats:named-content>possesses a remarkable ability to resist killing by alveolar macrophages. To date, no mechanism to explain this resistance has been described. Here, we focus on macrophage production of the toxic molecule nitric oxide as a potential target of subversion by<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. dermatitidis<\/jats:named-content>yeast cells. We report that<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. dermatitidis<\/jats:named-content>yeast cells reduce nitric oxide levels in the supernatants of activated alveolar macrophages. This reduction is not due to detoxification of nitric oxide, but rather to suppression of macrophage nitric oxide production. We show that<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. dermatitidis<\/jats:named-content>yeast cells do not block upregulation of macrophage inducible nitric oxide synthase (iNOS) expression or limit iNOS access to its arginine substrate. Instead,<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. dermatitidis<\/jats:named-content>yeast cells appear to inhibit iNOS enzymatic activity. Further investigation into the genetic basis of this potential virulence mechanism could lead to the identification of novel antifungal drug targets.<\/jats:p>","DOI":"10.1128\/iai.01249-10","type":"journal-article","created":{"date-parts":[[2011,3,29]],"date-time":"2011-03-29T02:06:34Z","timestamp":1301364394000},"page":"2385-2395","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":46,"title":["Blastomyces dermatitidis Yeast Cells Inhibit Nitric Oxide Production by Alveolar Macrophage Inducible Nitric Oxide Synthase"],"prefix":"10.1128","volume":"79","author":[{"given":"Nicole M.","family":"Rocco","sequence":"first","affiliation":[{"name":"Microbiology Doctoral Training Program, Madison, Wisconsin 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John C.","family":"Carmen","sequence":"additional","affiliation":[{"name":"Internal Medicine, Madison, Wisconsin 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce S.","family":"Klein","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics, Madison, Wisconsin 53792"},{"name":"Internal Medicine, Madison, Wisconsin 53792"},{"name":"Medical Microbiology and Immunology, Madison, Wisconsin 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1042\/bj3570593"},{"key":"e_1_3_2_3_2","doi-asserted-by":"crossref","first-page":"6072","DOI":"10.4049\/jimmunol.160.12.6072","article-title":"Blockade of endogenous TNF-alpha exacerbates primary and secondary pulmonary histoplasmosis by differential mechanisms","volume":"160","author":"Allendoerfer R.","year":"1998","unstructured":"AllendoerferR.DeepeG. 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