Role IL-17A and IL-10 in the antigen induced inflammation model by Mycoplasma pneumoniae

Background: Mycoplasma pneumoniae is one of the causative organisms of community-acquired pneumonia which is found commonly in younger patients. Extrapulmonary complications similar to autoimmune disease are caused by M. pneumoniae following the initial infection. The mechanism and pathology of onset is not clear, but it is considered that excessive host immunoreactions play a part in the onset of mycoplasmal pneumonia and its extrapulmonary complications. In this study, we investigated the participation of the immune response, excluding the participation of Th1 and Th2 which has previously been investigated. Results: In this study, the host immune response of an antigen induced inflammation model using SPF mice repeatedly sensitized with M. pneumoniae antigens was analyzed. The specificity of M. pneumoniae antigens in the Th17 response of murine lymphocytes in vitro was also examined. Frequent and concentrated sensitization induced exacerbation of lung inflammation immunologically and pathologically, and evoked intrapulmonary IL-17A and IL-10 production. M. pneumoniae antigen stimulation induced proliferation of mouse lymphocytes and caused production of IL-17A and IL-10. In addition, it was shown that IL-17A and IL-10 production was increased in the presence of IL-6 and TGF-beta 1. Conclusions: It was shown that M. pneumoniae antigens induced potent immunoreaction and enhanced the Th17 cell response both in vivo and in vitro, and that both Treg and IL-10 are involved in the suppression of IL-17A production. This raises the possibility that breakdown of the immune balance may be part of the process leading to subsequent development of extrapulmonary mycoplasmal pneumonia.