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In a mouse model of severe influenza A pneumonia, we found the proinflammatory cytokine IL-6 was necessary for the development of muscle dysfunction. Treatment with a Food and Drug Administration\u2013approved Ab antagonist to the IL-6R (tocilizumab) attenuated the severity of influenza A\u2013induced muscle dysfunction. In cultured myotubes, IL-6 promoted muscle degradation via JAK\/STAT, FOXO3a, and atrogin-1 upregulation. Consistent with these findings, atrogin-1+\/\u2212 and atrogin-1\u2212\/\u2212 mice had attenuated muscle dysfunction following influenza infection. Our data suggest that inflammatory endocrine signals originating from the injured lung activate signaling pathways in the muscle that induce dysfunction. Inhibiting these pathways may limit morbidity in patients with influenza A pneumonia and adult respiratory distress syndrome.<\/jats:p>","DOI":"10.4049\/jimmunol.1701433","type":"journal-article","created":{"date-parts":[[2018,12,7]],"date-time":"2018-12-07T15:49:24Z","timestamp":1544197764000},"page":"484-493","source":"Crossref","is-referenced-by-count":56,"title":["Influenza A Virus Infection Induces Muscle Wasting via IL-6 Regulation of the E3 Ubiquitin Ligase Atrogin-1"],"prefix":"10.1093","volume":"202","author":[{"given":"Kathryn A","family":"Radigan","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Medicine, Feinberg School of Medicine, Northwestern University , Chicago, IL 60611"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3187-1493","authenticated-orcid":false,"given":"Trevor T","family":"Nicholson","sequence":"additional","affiliation":[{"name":"Division of Pulmonary 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