Journal
SCIENTIFIC REPORTS
Volume 12, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41598-022-08066-7
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Funding
- Oklahoma Shared Clinical and Translational Resource (OSCTR) [U54GM104938]
- Merit Review Program of the Department of Veterans Affairs [I01 BX001937]
- National Institute of General Medical Sciences [5P20GM103648]
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In smokers, early administration of IFN-beta can improve survival during influenza infection, while late administration does not alter mortality. In addition, IFN-beta treatment increases inflammation and lung injury induced by IAV infection, especially in nonsmokers.
During influenza A virus (IAV) infection, it is unclear whether type I interferons (IFNs) have defensive antiviral effects or contribute to immunopathology in smokers. We treated nonsmoking (NS) and cigarette smoke (CS)-exposed mice intranasally with early (prophylactic) or late (therapeutic) IFN-beta. We compared the mortality and innate immune responses of the treated mice following challenge with IAV. In NS mice, both early and late IFN-beta administration decreased the survival rate in mice infected with IAV, with late IFN-beta administration having the greatest effect on survival. In contrast, in CS-exposed mice, early IFN-beta administration significantly increased survival during IAV infection while late IFN-beta administration did not alter mortality. With regards to inflammation, in NS mice, IFN-beta administration, especially late administration, significantly increased IAV-induced inflammation and lung injury. Early IFN-beta administration to CS-exposed mice did not increase IAV-induced inflammation and lung injury as occurred in NS mice. Our results demonstrate, although IFN-beta administration worsens the susceptibility of NS mice to influenza infection with increased immunopathology, early IFN-beta administration to CS-exposed mice, which have suppression of the intrinsic IFN response, improved outcomes during influenza infection.
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