title: Effect of BSA antigen sensitization during the acute phase of influenza A viral infection on CD11c+ pulmonary antigen presenting cells.
abstract: BACKGROUND
  Influenza A viral infection is concerned with induction of asthma. CD11c+ pulmonary antigen presenting cells (APCs) play a central role in sensitization with inhaled antigens during the acute phase of influenza A viral infection and also reside on bronchial epithelium for the long term after sensitization. To investigate the role of CD11c+ pulmonary APCs in the inhaled antigen sensitization during the acute phase of influenza A viral infection, we analyzed their function.
  
  
  METHODS
  Mice were infected with influenza A virus and were sensitized intranasally with BSA/alum during the acute phase of influenza A viral infection. Expression of surface antigens on CD11c+ pulmonary APCs was analyzed by FACS. Cytokine production from CD11c+ pulmonary APCs, and interaction between CD11c+ pulmonary APCs and naïve CD4+ T cells was assessed by ELISA. Ability of antigen presentation by CD11c+ pulmonary APCs was measured by proliferation assay.
  
  
  RESULTS
  BSA antigen sensitization during the acute phase of influenza A viral infection induced eosinophil recruitment into the lungs after BSA antigen challenge and moderately increased expression of MHC class II molecules on CD11c+ pulmonary APCs. The interaction between the CD11c+ pulmonary APCs and naïve CD4+ T cells secreted large amounts of IL-10.
  
  
  CONCLUSIONS
  BSA antigen sensitization during the acute phase of influenza A viral infection enhanced IL-10 production from naïve CD4+ T cell interaction with CD11c+ pulmonary APCs. The IL-10 secretion evoked Th2 responses in the lungs with downregulation of Th1 responses and was important for the eosinophil recruitment into the lungs after BSA antigen challenge.
authors.affiliation: Department of Immunology, Yokohama City University School of Medicine, Kanagawa, Japan.
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Sato
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Nakazawa
authors.forename: Shinichi
authors.initials: S
authors.lastname: Yamamiya
authors.forename: Chizuru
authors.initials: C
authors.lastname: Tamura
authors.forename: Naomi
authors.initials: N
authors.lastname: Hongo
authors.forename: Chie
authors.initials: C
authors.lastname: Hotta
authors.forename: Mutsuhiko
authors.initials: M
authors.lastname: Minami
mesh_terms: D000208:Acute Disease; D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology*; D000941:Antigens / Q000276:immunology; D001249:Asthma / Q000276:immunology*; D039521:CD11c Antigen / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D005802:Genes, MHC Class II / Q000276:immunology; D006801:Humans; D007114:Immunization; D053118:Influenza A Virus, H1N1 Subtype; D007251:Influenza, Human / Q000150:complications / Q000276:immunology*; D016753:Interleukin-10 / Q000096:biosynthesis; D008168:Lung / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D010047:Ovalbumin / Q000276:immunology; D012710:Serum Albumin, Bovine / Q000276:immunology*
chemical_list: D000941:Antigens; D039521:CD11c Antigen; D016753:Interleukin-10; D012710:Serum Albumin, Bovine; D010047:Ovalbumin