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 naive 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 naive 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 naive 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.