While our data support the notion that M2 polarization favors survival and replication of C. pneumoniae, we did not find definite evidence that C. pneumoniae would interfere with M1 polarization or would induce an M2 phenotype in macrophages, since infection of M0 macrophages generated by cultivation of monocytes in the absence of stimuli for 9 days elicited an initial pro-inflammatory response with high release of TNF-α and IL-12, followed by high IL-10 release at later time points. The gene discussed is IL10; the disease is infection.