{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T08:27:21Z","timestamp":1791188841225,"version":"4.1.0"},"reference-count":55,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2011,2,1]],"date-time":"2011-02-01T00:00:00Z","timestamp":1296518400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Staphylococcus aureus is a significant cause of hospital and community acquired pneumonia and causes secondary infection after influenza A. Recently, patients with hyper-IgE syndrome, who often present with S. aureus infections of the lung and skin, were found to have mutations in STAT3, required for Th17 immunity, suggesting a potential critical role for Th17 cells in S. aureus pneumonia. Indeed, IL-17R\u2212\/\u2212 and IL-22\u2212\/\u2212 mice displayed impaired bacterial clearance of S. aureus compared with that of wild-type mice. Mice challenged with influenza A PR\/8\/34 H1N1 and subsequently with S. aureus had increased inflammation and decreased clearance of both virus and bacteria. Coinfection resulted in greater type I and II IFN production in the lung compared with that with virus infection alone. Importantly, influenza A coinfection resulted in substantially decreased IL-17, IL-22, and IL-23 production after S. aureus infection. The decrease in S. aureus-induced IL-17, IL-22, and IL-23 was independent of type II IFN but required type I IFN production in influenza A-infected mice. Furthermore, overexpression of IL-23 in influenza A, S. aureus-coinfected mice rescued the induction of IL-17 and IL-22 and markedly improved bacterial clearance. These data indicate a novel mechanism by which influenza A-induced type I IFNs inhibit Th17 immunity and increase susceptibility to secondary bacterial pneumonia.<\/jats:p>","DOI":"10.4049\/jimmunol.1002194","type":"journal-article","created":{"date-parts":[[2010,12,22]],"date-time":"2010-12-22T22:47:49Z","timestamp":1293058069000},"page":"1666-1674","source":"Crossref","is-referenced-by-count":330,"title":["Influenza A Inhibits Th17-Mediated Host Defense against Bacterial Pneumonia in Mice"],"prefix":"10.1093","volume":"186","author":[{"given":"Anupa","family":"Kudva","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erich V","family":"Scheller","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keven M","family":"Robinson","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chris R","family":"Crowe","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sun Mi","family":"Choi","sequence":"additional","affiliation":[{"name":"Department of Genetics, Lousiana State University Health Sciences Center , New Orleans, LA 70112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samantha R","family":"Slight","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shabaana A","family":"Khader","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricia J","family":"Dubin","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard I","family":"Enelow","sequence":"additional","affiliation":[{"name":"Department of Medicine, Dartmouth Medical School , Lebanon, NH 03756"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay K","family":"Kolls","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224"},{"name":"Department of Genetics, Lousiana State University Health Sciences Center , New Orleans, LA 70112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John F","family":"Alcorn","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Children\u2019s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2011,2,1]]},"reference":[{"key":"2025032411015522600_r1","doi-asserted-by":"crossref","first-page":"25","DOI":"10.1016\/S1473-3099(01)00170-0","article-title":"Estimates of world-wide distribution of child deaths from acute respiratory infections","volume":"2","author":"Williams","year":"2002","journal-title":"Lancet Infect. 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