Effect of BSA antigen sensitization during the acute phase of influenza A viral infection on CD11c+ pulmonary antigen presenting cells.

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.