{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T13:38:10Z","timestamp":1786541890055,"version":"build-2736575974"},"reference-count":85,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T00:00:00Z","timestamp":1786492800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T00:00:00Z","timestamp":1786492800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100007155","name":"Medical Research Council","doi-asserted-by":"publisher","award":["MR\/N013840\/1"],"award-info":[{"award-number":["MR\/N013840\/1"]}],"id":[{"id":"10.13039\/501100007155","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","award":["105570\/Z\/14\/A"],"award-info":[{"award-number":["105570\/Z\/14\/A"]}],"id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000268","name":"Biotechnology and Biological Sciences Research Council","doi-asserted-by":"publisher","award":["BB\/M011151\/1"],"award-info":[{"award-number":["BB\/M011151\/1"]}],"id":[{"id":"10.13039\/501100000268","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007155","name":"Medical Research Council","doi-asserted-by":"publisher","award":["MR\/J009156\/1"],"award-info":[{"award-number":["MR\/J009156\/1"]}],"id":[{"id":"10.13039\/501100007155","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007155","name":"Medical Research Council","doi-asserted-by":"publisher","award":["MR\/Z505948\/1"],"award-info":[{"award-number":["MR\/Z505948\/1"]}],"id":[{"id":"10.13039\/501100007155","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001320","name":"Wolfson Foundation","doi-asserted-by":"publisher","award":["WLR\\R1\\170024"],"award-info":[{"award-number":["WLR\\R1\\170024"]}],"id":[{"id":"10.13039\/501100001320","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2026,8,12]]},"abstract":"ABSTRACT<\/jats:title>\n \n \n \n Candida albicans<\/jats:italic>\n is a human commensal that can cause life-threatening invasive infection in immunocompromised individuals. Human immunity to\n C. albicans<\/jats:italic>\n infection is thought to be largely dependent on neutrophil reactive oxygen and nitrogen species (ROS\/RNS) generation by neutrophils. Despite this, our understanding of innate immune killing and escape by\n C. albicans<\/jats:italic>\n is primarily studied in macrophages, and the precise mechanisms of evasion are unclear in neutrophils. Here, we sought to determine the importance of neutrophil reactive nitrogen species (RNS) production during\n C. albicans<\/jats:italic>\n infection\n in vivo<\/jats:italic>\n . Using a zebrafish model, we found that\n C. albicans<\/jats:italic>\n rapidly downregulated neutrophil RNS below basal levels during the first day post-infection, a time at which neutrophil RNS is upregulated in bacterial infections as an important host-defense mechanism, indicating fungal evasion of host neutrophils. We confirmed the downregulation of RNS in human primary neutrophils and with clinical\n Candida<\/jats:italic>\n isolates, including emerging human pathogens\n Candida auris<\/jats:italic>\n and\n Candida glabrata<\/jats:italic>\n . Inducible nitric oxide synthase (iNOS; Nos2 in zebrafish), the enzyme responsible for RNS production, competes with the arginase enzyme for a shared substrate, L-arginine. Using a zebrafish\n arginase2<\/jats:italic>\n transgenic line and a\n C. albicans car1<\/jats:italic>\n \u0394 mutant, we showed that both host and fungal arginase contribute to the reduction in neutrophil RNS. Despite pathogen downregulation, upregulation of neutrophil RNS via hypoxia-inducible factor 1\u03b1 (Hif-1\u03b1) stabilization was sufficient to improve host survival following\n C. albicans<\/jats:italic>\n infection. Inhibition of Nos2 blocked the host protective effect of Hif-1\u03b1 stabilization. Finally, restoration of neutrophil RNS via Hif-1\u03b1 stabilization was additive to clinically relevant antifungal treatment, increasing survival and clearance of\n C. albicans<\/jats:italic>\n infections. Together, these data demonstrate that restoration of the neutrophil RNS response in\n C. albicans<\/jats:italic>\n infection improves infection outcomes, highlighting the potential of targeting Hif-1\u03b1 and RNS in host-directed therapies against fungal infections.\n <\/jats:p>\n \n IMPORTANCE<\/jats:title>\n \n Candida albicans<\/jats:italic>\n is a fungus that normally lives harmlessly in the human body but can cause life-threatening infections in people with weakened immune systems. A key part of the body\u2019s defense against this fungus is neutrophils, immune cells that kill microbes using toxic molecules. However, how\n Candida<\/jats:italic>\n avoids neutrophil defense is not well understood. Here, we used zebrafish and human immune cells to show that\n Candida<\/jats:italic>\n suppresses an important neutrophil defense, reactive nitrogen species (RNS), during infection. Unlike bacteria, which trigger RNS,\n Candida<\/jats:italic>\n reduces these protective molecules to below normal levels, helping its survival. This effect was also observed with other disease-causing\n Candida<\/jats:italic>\n species. We went on to show that both the host and\n Candida<\/jats:italic>\n contribute to this suppression. Importantly, boosting the neutrophil response improved survival and helped clear infection, especially when combined with standard antifungal drugs. These findings suggest new ways to support the immune system alongside existing treatments.\n <\/jats:p>\n <\/jats:sec>\n <\/jats:sec>","DOI":"10.1128\/mbio.00202-26","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T13:24:14Z","timestamp":1783344254000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Candida<\/i>\n spp. suppress neutrophil reactive nitrogen species to evade killing"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5757-7909","authenticated-orcid":false,"given":"Thomas B.","family":"Burgess","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05krs5044","id-type":"ROR","asserted-by":"publisher"}],"name":"Bateson Centre for Disease Mechanisms and Florey Institute of Infection, School of Medicine and Population Health, The University of Sheffield","place":["Sheffield, United 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and Florey Institute of Infection, School of Medicine and Population Health, The University of Sheffield","place":["Sheffield, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tihana","family":"Bicanic","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04cw6st05","id-type":"ROR","asserted-by":"publisher"}],"name":"Institute for Infection and Immunity, City St George's University of London","place":["London, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lynne R.","family":"Prince","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05krs5044","id-type":"ROR","asserted-by":"publisher"}],"name":"Bateson Centre for Disease Mechanisms and Florey Institute of Infection, School of Medicine and Population Health, The University of Sheffield","place":["Sheffield, United 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