tetano
Editor, Senior Moderator
Am J Physiol Lung Cell Mol Physiol. 2014 Sep 26. pii: ajplung.00158.2014. [Epub ahead of print]
Cigarette Smoke Attenuates the RIG-I-initiated Innate Antiviral Response to Influenza Infection in Two Murine Models.
Wu W1, Zhang W1, More S2, Booth JL1, Duggan ES1, Liu L2, Zhao YD3, Metcalf JP4.
Author information
Abstract
Cigarette smoke (CS) exposure increases the frequency and severity of respiratory tract infections. Despite this association, the mechanisms underlying the increased susceptibility to respiratory virus infection are poorly understood. Retinoic acid-inducible gene I (RIG-I) is an important regulator of influenza virus-induced expression of antiviral cytokines, mainly interferons (IFNs), which are necessary to clear viral infections. In this study, we compared the innate cytokine responses of two mouse CS exposure models following a challenge with influenza A virus (IAV): 1) exposure of the mice to cigarette smoke extract (CSE) intratracheally, and 2) exposure of the mice to CS in a whole-body exposure chamber. Both intratracheal CSE treatment and whole-body CS exposure caused antiviral immunosuppression in these mice, and both CS exposure methods inhibited RIG-I induction. CS attenuated influenza-induced antiviral IFNs and IP-10 expression in vivo. However, we did not find that CS inhibited induction of the proinflammatory cytokines IL-6 and TNF-α, whose expression was induced by IAV. Interestingly, IAV infection also increased toll-like receptor 3 (TLR3) expression in mouse lung, but CS exposure did not impact TLR3 induction in these mice. Together, the results support our previous finding in a human lung organ culture model that the suppression of RIG-I induction and antiviral cytokine responses by CS is likely important in the enhanced susceptibility of smokers to influenza infection in the lung.
Copyright ? 2014, American Journal of Physiology - Lung Cellular and Molecular Physiology.
KEYWORDS:
RIG-I; cytokine; influenza; smoking; virus
PMID:
25260755
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25260755
Cigarette Smoke Attenuates the RIG-I-initiated Innate Antiviral Response to Influenza Infection in Two Murine Models.
Wu W1, Zhang W1, More S2, Booth JL1, Duggan ES1, Liu L2, Zhao YD3, Metcalf JP4.
Author information
Abstract
Cigarette smoke (CS) exposure increases the frequency and severity of respiratory tract infections. Despite this association, the mechanisms underlying the increased susceptibility to respiratory virus infection are poorly understood. Retinoic acid-inducible gene I (RIG-I) is an important regulator of influenza virus-induced expression of antiviral cytokines, mainly interferons (IFNs), which are necessary to clear viral infections. In this study, we compared the innate cytokine responses of two mouse CS exposure models following a challenge with influenza A virus (IAV): 1) exposure of the mice to cigarette smoke extract (CSE) intratracheally, and 2) exposure of the mice to CS in a whole-body exposure chamber. Both intratracheal CSE treatment and whole-body CS exposure caused antiviral immunosuppression in these mice, and both CS exposure methods inhibited RIG-I induction. CS attenuated influenza-induced antiviral IFNs and IP-10 expression in vivo. However, we did not find that CS inhibited induction of the proinflammatory cytokines IL-6 and TNF-α, whose expression was induced by IAV. Interestingly, IAV infection also increased toll-like receptor 3 (TLR3) expression in mouse lung, but CS exposure did not impact TLR3 induction in these mice. Together, the results support our previous finding in a human lung organ culture model that the suppression of RIG-I induction and antiviral cytokine responses by CS is likely important in the enhanced susceptibility of smokers to influenza infection in the lung.
Copyright ? 2014, American Journal of Physiology - Lung Cellular and Molecular Physiology.
KEYWORDS:
RIG-I; cytokine; influenza; smoking; virus
PMID:
25260755
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25260755