Blocking IL-10 receptor signaling ameliorates Mycobacterium tuberculosis infection during influenza-induced exacerbation
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Authors
Ring, SarahEggers, Lars
Behrends, Jochen
Wutkowski, Adam
Schwudke, Dominik
Kröger, Andrea
Hierweger, Alexandra Maximiliane
Hölscher, Christoph
Gabriel, Gülsah
Schneider, Bianca E.
Issue Date
2019-01-01
Metadata
Show full item recordAbstract
Epidemiological findings indicate that coinfection with influenza viruses is associated with an increased risk of death in patients suffering from tuberculosis but the underlying pathomechanisms are not well understood. In this study, we demonstrate that influenza A virus (IAV) coinfection rapidly impairs control of Mycobacterium tuberculosis (Mtb) in C57BL/6 mice. IAV coinfection was associated with significantly increased bacterial loads, reduced survival and a substantial modulation of innate and adaptive immune defenses including an impaired onset and development of Mtb-specific CD4+ T cell responses and the accumulation of macrophages with increased arginase-1 production in the lungs. Our findings strongly indicate that IAV coinfection compromises the host's ability to control Mtb infection via the production of IL-10 which was rapidly induced upon viral infection. The blockade of IL-10 receptor signaling reduced the bacterial load in coinfected mice to a level comparable with that in Mtb-only-infected animals. Taken together, our data suggest that IL-10 signaling constitutes a major pathway that enhances susceptibility to Mtb during concurrent IAV infectionCitation
JCI Insight. 2019 Apr 18;5. pii: 126533. doi: 10.1172/jci.insight.126533.Affiliation
HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.Journal
JCI InsightURI
https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85070660696&origin=inwardhttp://hdl.handle.net/10033/621928
PubMed ID
30998505Type
ArticleLanguage
enSeries/Report no.
10ae974a485f413a2113503eed53cd6c53
10.1172/jci.insight.126533
Scopus Count
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- Creative Commons
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