title: Influenza A virus infection increases IgE production and airway responsiveness in aerosolized antigen-exposed mice.
abstract: BACKGROUND
  Respiratory viral infection is known clinically to promote sensitization to antigen inhalation and the development of asthma.
  
  
  OBJECTIVE
  The purpose of this investigation was 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 ovalbumin 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 A 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: First Department of Internal Medicine, Yokohama City University School of Medicine, Fukuura, Kanazawa-ky, Yokohama 236, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
authors.forename: Y
authors.initials: Y
authors.lastname: Suzuki
authors.forename: N
authors.initials: N
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Matsumoto
authors.forename: A
authors.initials: A
authors.lastname: Shirai
authors.forename: T
authors.initials: T
authors.lastname: Okubo
mesh_terms: D000210:Acute-Phase Reaction / Q000821:virology; D000336:Aerosols; D000403:Airway Resistance; D000818:Animals; D000941:Antigens / Q000494:pharmacology*; D016535:Bronchial Hyperreactivity / Q000276:immunology* / Q000503:physiopathology*; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology*; D002452:Cell Count; D007073:Immunoglobulin E / Q000096:biosynthesis*; D009980:Influenza A virus; D008168:Lung / Q000033:anatomy & histology; D008297:Male; D016210:Methacholine Chloride / Q000008:administration & dosage / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D009976:Orthomyxoviridae Infections / Q000276:immunology / Q000503:physiopathology*
chemical_list: D000336:Aerosols; D000941:Antigens; D016210:Methacholine Chloride; D007073:Immunoglobulin E