{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T18:44:26Z","timestamp":1775673866427,"version":"3.50.1"},"reference-count":73,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2021,8,1]],"date-time":"2021-08-01T00:00:00Z","timestamp":1627776000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000009","name":"Foundation for the National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HL140837"],"award-info":[{"award-number":["R01 HL140837"]}],"id":[{"id":"10.13039\/100000009","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000009","name":"Foundation for the National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AR072212"],"award-info":[{"award-number":["R01 AR072212"]}],"id":[{"id":"10.13039\/100000009","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["T32 HL 125241-3"],"award-info":[{"award-number":["T32 HL 125241-3"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by genetic defects in leukocyte NADPH oxidase, which has both microbicidal and immunomodulatory roles. Hence, CGD is characterized by recurrent bacterial and fungal infections as well as aberrant inflammation. Fungal cell walls induce neutrophilic inflammation in CGD; yet, underlying mechanisms are incompletely understood. This study investigated the receptors and signaling pathways driving aberrant proinflammatory cytokine production in CGD neutrophils activated by fungal cell walls. Although cytokine responses to \u03b2-glucan particles were similar in NADPH oxidase\u2013competent and NADPH oxidase\u2013deficient mouse and human neutrophils, stimulation with zymosan, a more complex fungal particle, induced elevated cytokine production in NADPH oxidase\u2013deficient neutrophils. The dectin-1 C-type lectin receptor, which recognizes \u03b2-glucans (1\u20133), and TLRs mediated cytokine responses by wild-type murine neutrophils. In the absence of NADPH oxidase, fungal pathogen-associated molecular patterns engaged additional collaborative signaling with Mac-1 and TLRs to markedly increase cytokine production. Mechanistically, this cytokine overproduction is mediated by enhanced proximal activation of tyrosine phosphatase SHP2\u2013Syk and downstream Card9-dependent NF-\u03baB and Card9-independent JNK\u2013c-Jun. This activation and amplified cytokine production were significantly decreased by exogenous H2O2 treatment, enzymatic generation of exogenous H2O2, or Mac-1 blockade. Similar to zymosan, Aspergillus fumigatus conidia induced increased signaling in CGD mouse neutrophils for activation of proinflammatory cytokine production, which also used Mac-1 and was Card9 dependent. This study, to our knowledge, provides new insights into how NADPH oxidase deficiency deregulates neutrophil cytokine production in response to fungal cell walls.<\/jats:p>","DOI":"10.4049\/jimmunol.2001298","type":"journal-article","created":{"date-parts":[[2021,7,23]],"date-time":"2021-07-23T19:10:14Z","timestamp":1627067414000},"page":"923-937","source":"Crossref","is-referenced-by-count":17,"title":["NADPH Oxidase Limits Collaborative Pattern-Recognition Receptor Signaling to Regulate Neutrophil Cytokine Production in Response to Fungal Pathogen-Associated Molecular Patterns"],"prefix":"10.1093","volume":"207","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6330-9975","authenticated-orcid":false,"given":"Dae-goon","family":"Yoo","sequence":"first","affiliation":[{"name":"Department of Pediatrics, School of Medicine, Washington University in St. Louis , St. Louis, MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5928-3215","authenticated-orcid":false,"given":"Luana C","family":"Paracatu","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, Washington University in St. Louis , St. Louis, MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6132-8374","authenticated-orcid":false,"given":"Evan","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, Washington University in St. Louis , St. Louis, MO"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xin","family":"Lin","sequence":"additional","affiliation":[{"name":"Institute for Immunology, Tsinghua University School of Medicine, Tsinghua University-Peking University Joint Center for Life Sciences , Beijing ,","place":["China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7796-2908","authenticated-orcid":false,"given":"Mary C","family":"Dinauer","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, Washington University in St. Louis , St. Louis, MO"},{"name":"Department of Pathology and Immunology, School of Medicine, Washington University in St. Louis , St. Louis, MO"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2021,8,1]]},"reference":[{"key":"2025022610275276200_r1","doi-asserted-by":"crossref","first-page":"2130","DOI":"10.1182\/blood-2018-11-844563","article-title":"Inflammatory consequences of inherited disorders affecting neutrophil function","volume":"133","author":"Dinauer","year":"2019","journal-title":"Blood"},{"key":"2025022610275276200_r2","doi-asserted-by":"crossref","first-page":"1176","DOI":"10.1093\/cid\/ciu1154","article-title":"Common severe infections in chronic granulomatous disease","volume":"60","author":"Marciano","year":"2015","journal-title":"Clin. 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