Effective macrophage redox defense against Chlamydia pneumoniae depends on L-type Ca²⁺ channel activation

Abstract.

Macrophage immune capability depends on their efficient redox potential expressed in the effective release of reactive oxygen species (ROS) and nitric oxide. In this study the effect of the activation of a specialized Ca²⁺ channel on macrophage redox function during Chlamydia pneumoniae infection was explored. C. pneumoniae exhibited a profound and sustained Ca²⁺ influx capacity, with evidence of activity attributable to their lipopolysaccharide (cLPS) content. Also the organism showed an additional Ca²⁺ influx signal in macrophages exposed to thapsigargin, and there was evidence for the operation of a single ion channel of the L type as demonstrated by the effect of L-type channel antagonists (methoxyverapamil and nimodipine) despite exposure to Ca²⁺-rich medium. C. pneumoniae or cLPS induced intracellular ROS and NO generation in a manner consistent with dependence on intracellular calcium. L-type Ca²⁺ channel blocking significantly prompted C. pneumoniae inclusion formation. These findings suggest that Ca²⁺ influx signal and redox function in C. pneumoniae-infected macrophages depend on L-type Ca²⁺ channel activation.