Chlamydia muridarum infection induces CD4+ T cells apoptosis via PI3K/AKT signal pathway.

Apoptosis is essential for the homeostatic control of the lymphocytes number during the development of an immune response to an invasive microorganism. CD4+ T cells play a major role in homeostasis of the immune system and are sufficient to confer protection against Chlamydia muridarum (Cm) infection in mice. The present study demonstrated that phosphatidylinositol 3-kinase (PI3K) p110δ mRNA and phosphorylation of protein kinase B (p-AKT) level were significantly increased in lung cells and spleen cells at day 3 and day 7 post-infection, p-AKT level was inhibited when adding PI3K inhibitor LY294002. Moreover, Cm infection induced high levels of IL-2/IL-2Rα in CD4+ T cells, which may relate to PI3K/AKT signal pathway activation. We observed that Cm infection significantly induced apoptosis of CD4+ T cells. The related apoptosis proteins Bcl-2 and Mcl-1 uneven expression levels were induced in CD4+ T cells by Cm infection. These findings provided in vivo and in vitro evidence that Cm infection induces CD4+ T cells apoptosis possibly via PI3K/AKT signal pathway.