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Interleukin\u20106 (IL\u20106) drives pathological inflammation in viral infections such as COVID\u201019, but its role in influenza, particularly with secondary AF infection, remains unclear. Using a mouse model of post\u2010influenza AF infection, including IL\u20106 knockout mice, we found that IL\u20106 signaling promotes neutrophilic lung inflammation but is not required for pathogen clearance of either influenza or AF. However, IL\u20106 deficiency increases epithelial cell damage, as indicated by elevated RAGE levels in bronchoalveolar lavage fluid. In contrast, lung capillary permeability (measured by IgM levels in BAL) and tissue injury (assessed histologically) remain unaffected in the absence of IL\u20106 signaling. These findings reveal a nuanced role for IL\u20106 in post\u2010influenza AF infection, underscoring its contribution to lung inflammation and epithelial integrity.<\/jats:p>","DOI":"10.14814\/phy2.70372","type":"journal-article","created":{"date-parts":[[2025,5,27]],"date-time":"2025-05-27T03:00:52Z","timestamp":1748314852000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["<scp>IL<\/scp>\u20106 signaling regulates the inflammatory response without impacting pathogen burden during influenza\u2010associated pulmonary aspergillosis"],"prefix":"10.14814","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3040-9029","authenticated-orcid":false,"given":"Lokesh","family":"Sharma","sequence":"first","affiliation":[{"name":"Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine University of Pittsburgh  Pittsburgh Pennsylvania 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