[ODP-174] Analysis of Card9 function in pulmonary mycobacterial infection
Card9 is known to play an essential role in innate immune signaling via C-type lectin receptors. Card9-deficient mice were shown to be highly susceptible to Mycobacterium tuberculosis, died early after aerosol infection, and showed a higher mycobacterial burden. In Card9-deficient mice, the antigen-specific T cell response after infection is comparable to that of wild-type (WT) mice, and it is thus considered that Card9 deficiency affects innate immunity rather than acquired T cell responses during infection. However, the contribution of Card9 to early mycobacterial infection is poorly understood. To clarify the role of Card9 in the early stages of mycobacterial infection, Card9-deficient mice were infected intraperitoneally with M. tuberculosis var. BCG. Seven days after infection, production of IFNγ in the peritoneal cavity was observed in WT mice, but was decreased in Card9-deficient mice while their intraperitoneal bacterial burdens were increased. We further performed infection through airways, and found that bacterial loads in the lungs were comparable between WT and Card9-deficient mice 7 and 21 days after infection. These results suggest that Card9 might not contribute to the elimination of bacteria in the early stages of pulmonary BCG infection. Therefore, we are now examining the effect of Card9 deficiency on the later stages of pulmonary mycobacterial infection.