{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T16:41:47Z","timestamp":1791996107186,"version":"4.4.0"},"reference-count":89,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2024,8,23]],"date-time":"2024-08-23T00:00:00Z","timestamp":1724371200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000057","name":"HHS | NIH | National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["R35GM147464"],"award-info":[{"award-number":["R35GM147464"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["K22AI134677"],"award-info":[{"award-number":["K22AI134677"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Glucocorticoids are a major class of therapeutic anti-inflammatory and immunosuppressive drugs prescribed to patients with inflammatory diseases, to avoid transplant rejection, and as part of cancer chemotherapy. However, exposure to these drugs increases the risk of opportunistic infections such as with the fungus Aspergillus fumigatus, which causes mortality in &amp;gt;50% of infected patients. The mechanisms by which glucocorticoids increase susceptibility to A. fumigatus are poorly understood. In this article, we used a zebrafish larva Aspergillus infection model to identify innate immune mechanisms altered by glucocorticoid treatment. Infected larvae exposed to dexamethasone succumb to infection at a significantly higher rate than control larvae. However, both macrophages and neutrophils are still recruited to the site of infection, and dexamethasone treatment does not significantly affect fungal spore killing. Instead, the primary effect of dexamethasone manifests later in infection with treated larvae exhibiting increased invasive hyphal growth. In line with this, dexamethasone predominantly inhibits neutrophil function rather than macrophage function. Dexamethasone-induced mortality also depends on the glucocorticoid receptor. Dexamethasone partially suppresses NF-\u03baB activation at the infection site by inducing the transcription of I\u03baB via the glucocorticoid receptor. Independent CRISPR\/Cas9 targeting of IKK\u03b3 to prevent NF-\u03baB activation also increases invasive A. fumigatus growth and larval mortality. However, dexamethasone treatment of IKK\u03b3 crispant larvae further increases invasive hyphal growth and host mortality, suggesting that dexamethasone may suppress other pathways in addition to NF-\u03baB to promote host susceptibility. Collectively, we find that dexamethasone acts through the glucocorticoid receptor to suppress NF-\u03baB\u2013mediated neutrophil control of A. fumigatus hyphae in zebrafish larvae.<\/jats:p>","DOI":"10.4049\/jimmunol.2400021","type":"journal-article","created":{"date-parts":[[2024,8,23]],"date-time":"2024-08-23T12:36:21Z","timestamp":1724416581000},"page":"971-987","source":"Crossref","is-referenced-by-count":22,"title":["Glucocorticoids Suppress NF-\u03baB\u2013Mediated Neutrophil Control of\n                    <i>Aspergillus fumigatus<\/i>\n                    Hyphal Growth"],"prefix":"10.1093","volume":"213","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4617-7552","authenticated-orcid":false,"given":"Savini U","family":"Thrikawala","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, Clemson University , Clemson, SC"},{"name":"Eukaryotic Pathogens Innovation Center, Clemson University , Clemson, SC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Molly H","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Clemson University , Clemson, SC"},{"name":"Eukaryotic Pathogens Innovation Center, Clemson University , Clemson, SC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6761-1098","authenticated-orcid":false,"given":"Emily E","family":"Rosowski","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Clemson University , Clemson, SC"},{"name":"Eukaryotic Pathogens Innovation Center, Clemson University , Clemson, SC"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,8,23]]},"reference":[{"key":"2025012305170748000_r1","doi-asserted-by":"crossref","first-page":"233","DOI":"10.1038\/nri.2017.1","article-title":"Immune regulation by glucocorticoids","volume":"17","author":"Cain","year":"2017","journal-title":"Nat. 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