Influenza A virus infection increases IgE production and airway responsiveness in aerosolized antigen-exposed mice

Background: Respiratory viral infection is known clinically to promote sensitization to antigen inhalation and the development of asthma. Objective: The purpose of this investigation mas to determine whether influenza type A virus infection enhances inhalation sensitization and increases airway responsiveness in mice. Methods: Mice were infected by intranasal inoculation with influenza A viruses (strains: H1N1 and H3N2) or PBS. Animals were exposed to aerosols of of albumin on day 3. Two weeks after ovalbumin sensitization, mice were challenged with ovalbumin aerosols: 24 hours later, airway responsiveness (AR) to inhaled methacholine, levels of ovalbumin-specific IgE, and bronchoalveolar lavage fluid (BALF) were examined. Results: Neither influenza virus (H1N1 nor H3N2) alone nor ovalbumin sensitization alone caused changes in AR or IgE. However, ovalbumin sensitization after inoculation with either influenza A virus increased AR and levels of ovalbumin-specific IgE. On BALF-cell analysis, ovalbumin sensitization after inoculation with influenza virus A increased the number of lymphocytes but not the number of eosinophils. No difference in AR or IgE levels was observed between the 2 strains of influenza A viruses. Immmunostaining of BALF cells showed an increase in T cells, especially CD8(+) cells, with ovalbumin sensitization after inoculation with influenza virus A. Conclusion: Infection by influenza A virus enhances sensitization to inhaled antigens and airway responsiveness in mice by means of mechanisms including CD8(+) cells and antigen-specific IgE.