Abstract
Background: Asthmatics in particular have a need for influenza vaccines because influenza infection is a frequent cause of hospitalization of patients with bronchial asthma. Currently, only inactivated influenza vaccines are recommended for influenza prevention in asthma sufferers. Objective: The aim of our study was to analyze and compare the effects of influenza infection and vaccination with live attenuated influenza vaccine (LAIV) on different phases of experimental murine allergic bronchial asthma (acute asthma and remission phase) and on subsequent exposure to allergen in sensitized animals. Methods: Ovalbumin (OVA)-specific serum IgE levels, IL-4 production by spleen and lung lymphocytes, and histological changes in the lungs of mice infected with pathogenic virus or LAIV were studied at two phases of OVA-induced bronchial asthma (acute asthma and remission). Results: Infection with pathogenic virus both in acute asthma and remission led to asthma exacerbation associated with the production of OVA-specific IgE, IL-4 and significant inflammatory infiltration in airways. Infection, even after complete virus clearance, induced the aggravation of lung inflammation and IgE production in asthmatic mice additionally exposed to OVA. Immunization with LAIV at remission did not enhance allergic inflammatory changes in the lung, OVA-specific IgE or IL-4 production. Then after additional OVA exposure, histological and immunological changes in these mice were the same as in the control group. Conclusion: Influenza infection provokes asthma exacerbation regardless of the disease phase. Immunization with LAIV during the remission phase of bronchial asthma is safe and does not interfere upon subsequent contact of asthma sufferers with allergen. © Journal compilation © 2008 Blackwell Publishing Ltd.
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Chirkova, T., Petukhova, G., Korenkov, D., Naikhin, A., & Rudenko, L. (2008). Immunization with live influenza viruses in an experimental model of allergic bronchial asthma: Infection and vaccination. Influenza and Other Respiratory Viruses, 2(5), 165–174. https://doi.org/10.1111/j.1750-2659.2008.00061.x
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