Enhancing effects of Mycoplasma pneumoniae antigens on Th2-attracting chemokine responses by murine splenocytes.

Mycoplasma pneumoniae is an aetiologic agent responsible for primary atypical pneumonia mainly in children and early teens. The pathogenic mechanisms for M. pneumoniae pneumonia is thought to be multifactorial with contribution from an excessive host immune response. In this report, we isolated splenocytes, CD4+ CD62L+ cells and CD90.2- cells from mouse spleen. These cells were stimulated by M. pneumoniae sonicated antigens in vitro and immunological analyses to examine the Th2 response induction were performed. It was shown that M. pneumoniae antigen stimulation did not induce IL-13 production from CD4+ CD62L+ cells. However, under Th2 dominant conditions in the presence of IL-4, M. pneumoniae antigen sensitization did induce IL-13 production from CD4+ CD62L+ cells. M. pneumoniae antigens also induced macrophage-derived chemokine (MDC) production from mouse splenocytes, and up-regulated MDC mRNA gene expression from CD90.2- cells in the presence of anti-CD40 antibodies. These results suggest that M. pneumoniae antigen stimulation may be involved in the pathological mechanisms of allergic conditions by inducing IL-13 production from Th2 cells, and by transition and localization of Th2 cells by MDC production from CD90.2- cells.