Chlamydia pneumoniae inhibits apoptosis in human peripheral blood mononuclear cells through induction of IL-10

Chlamydia pneumoniae is a common cause of pulmonary infection, with serum p ositivity in at least 50 % of the general population. In this study, we rep ort that human PBMCs exposed to C, pneumoniae are resistant to apoptosis in duced by the potent photoactivated chemotherapeutic agents 8-methoxypsorale n and hypericin, In contrast, PBMCs treated with a heat-inactivated inoculu m exhibit normal susceptibility to apoptosis, We also observed that human P BMCs are responsive to C, pneumoniae infection by secretion of key immune r egulatory cytokines, including IL-12 and n-10, While IL-12 may play an impo rtant role in limiting C. pneumoniae proliferation within cells, IL-10 serv es an anti-inflammatory function by down-regulating proinflammatory cytokin es such as IL-12 and TNF-alpha. Depletion of endogenous IL-10, but not of I L-12, abolished the apoptosis resistance of C, pneumoniae-infected PBMCs, F urthermore, addition of exogenous IL-10, but not IL-12, significantly incre ased the resistance of control inoculum-treated PBMCs to photoactivated 8-m ethoxypsoralen- and hypericin-induced apoptosis, Therefore, we conclude tha t C. pneumoniae possesses an antiapoptotic mechanism. The resistance to apo ptosis observed in PBMCs exposed to C. pneumoniae is due, at least partiall y, to the IL-10 induced during C. pneumoniae infection.