Chlamydia pneumoniae survival in macrophages is regulated by free Ca2+ dependent reactive nitrogen and oxygen species

Despite an efficient macrophage immune capability, Chlamydia pneumoniae infects host cells and causes chronic diseases. To gain better insights into C. pneumoniae survival mechanisms in macrophages, its growth in regular RAW-264.7 cells (nitric oxide sufficient NO (+)) and RAW-264.7 cells (nitric oxide insufficient NO (-)) were studied. Role of Ca(2+), NO and reactive oxygen species (ROS) during C. pneumoniae infection in macrophages were determined. RAW-264.7 NO (-) cells supported significantly Chlamydia growth, showing an upregulation of ROS, superoxide dismutase (SOD) and catalase activities as compared with RAW-264.7 NO (+) cell. Ascorbic acid, inducible nitric oxide synthase inhibitor and glutathione significantly prompted Chlamydia inclusion formation. Cytosolic Ca(2+) had regulatory effect on organism growth, NO generation, SOD and catalase activities in both cell types. These findings suggest that minimal Ca(2+) signaling in macrophages at early stages of infection, NO and ROS release have modulatory effects onC. pneumoniae survival, onset of persistence and chronicity, processes which are needed for the initiation of diseases in which C. pneumoniae has been implicated as a possible etiologic agent.