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Rapid Production of Type Iii Interferons After Influenza Virus Infection in Allergic Asthma Restricts Th2 Inflammation and Enhances Antiviral Resistance
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A1273 - Rapid Production of Type Iii Interferons After Influenza Virus Infection in Allergic Asthma Restricts Th2 Inflammation and Enhances Antiviral Resistance
Author Block: H. Kim, Y. Jeon, S. An, A. Jo; Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, Korea, Republic of.
Rationale: Although asthmatics has been considered to be highly susceptible to respiratory viral infection and most studies have focused on exacerbation of asthma by influenza A virus (IAV) infection, few experimental evidences exist to directly demonstrate that asthmatic mice are actually resistant to IAV infection. Our goal is to assess the specific role of interferon (IFN)-λ in controlling antiviral innate immune response in the lung of IAV-infected asthmatic mouse. Material and Methods: Mice with allergic asthma were infected with IAV (WS/33: H1N1) and survival rate, body weight, viral titer, histopathologic findings of lung and cytokine profiles including IFNs were measured. Results: Notably, asthmatic mouse were significantly resistant to IAV and showed completely lower viral load until 7 days after infection. Further, IAV-infected asthmatic mouse exhibited decreased Th2-related inflammation in lung tissue within 7 days. These increased antiviral resistant mechanism and reduced Th2 inflammation were attributable to rapid induction of IFN-λ and blockade of IFN-λs in asthmatic lung led to aggravate IAV infection and to enhance the production of Th2 cytokines. Actually, asthmatic mouse showed higher morbidity beyond 7 days after infection but intranasal administration of IFN-λs completely protect IAV-caused lung infection. Conclusion: Taken together, our study indicates that the rapid induction of IFN-λ might be distinctive immunologic findings in IAV-infected asthmatic mice and crucial for control of higher viral load and antiviral resistant immune mechanism in vivo asthma accompanying with restriction of Th2 cytokine productions. These findings suggest new insights into strategies for reducing asthmatic exacerbation from respiratory viral infection.
Author Block: H. Kim, Y. Jeon, S. An, A. Jo; Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, Korea, Republic of.
Rationale: Although asthmatics has been considered to be highly susceptible to respiratory viral infection and most studies have focused on exacerbation of asthma by influenza A virus (IAV) infection, few experimental evidences exist to directly demonstrate that asthmatic mice are actually resistant to IAV infection. Our goal is to assess the specific role of interferon (IFN)-λ in controlling antiviral innate immune response in the lung of IAV-infected asthmatic mouse. Material and Methods: Mice with allergic asthma were infected with IAV (WS/33: H1N1) and survival rate, body weight, viral titer, histopathologic findings of lung and cytokine profiles including IFNs were measured. Results: Notably, asthmatic mouse were significantly resistant to IAV and showed completely lower viral load until 7 days after infection. Further, IAV-infected asthmatic mouse exhibited decreased Th2-related inflammation in lung tissue within 7 days. These increased antiviral resistant mechanism and reduced Th2 inflammation were attributable to rapid induction of IFN-λ and blockade of IFN-λs in asthmatic lung led to aggravate IAV infection and to enhance the production of Th2 cytokines. Actually, asthmatic mouse showed higher morbidity beyond 7 days after infection but intranasal administration of IFN-λs completely protect IAV-caused lung infection. Conclusion: Taken together, our study indicates that the rapid induction of IFN-λ might be distinctive immunologic findings in IAV-infected asthmatic mice and crucial for control of higher viral load and antiviral resistant immune mechanism in vivo asthma accompanying with restriction of Th2 cytokine productions. These findings suggest new insights into strategies for reducing asthmatic exacerbation from respiratory viral infection.
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