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Background  Intracellular pathogens have devised various mechanisms to subvert the host immune response in order to survive and replicate in host cells. Here, we studied the infection of human blood monocytes with the intracellular pathogen  C. pneumoniae  and the effect on cytokine and chemokine profiles in comparison to stimulation with LPS.    Results  Monocytes purified from peripheral blood mononuclear cells by negative depletion were infected with  C. pneumoniae . While immunofluorescence confirmed the presence of chlamydial lipopolysaccharide (LPS) in the cytoplasm of infected monocytes, real-time PCR did not provide evidence for replication of the intracellular pathogen. Complementary to PCR,  C. pneumoniae  infection was confirmed by an oligonucleotide DNA microarray for the detection of intracellular pathogens. Raman microspectroscopy revealed different molecular fingerprints for infected and non-infected monocytes, which were mainly due to changes in lipid and fatty acid content. Stimulation of monocytes with  C. pneumoniae  or with LPS induced similar profiles of tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6, but higher levels of IL-1β, IL-12p40 and IL-12p70 for  C. pneumoniae  which were statistically significant.  C. pneumoniae  also induced release of the chemokines MCP-1, MIP-1α and MIP-1β, and CXCL-8, which correlated with TNF-α secretion.    Conclusion  Infection of human blood monocytes with intracellular pathogens triggers altered cytokine and chemokine pattern as compared to stimulation with extracellular ligands such as LPS. Complementing conventional methods, an oligonucleotide DNA microarray for the detection of intracellular pathogens as well as Raman microspectroscopy provide useful tools to trace monocyte infection.    Electronic supplementary material  The online version of this article (doi:10.1186/s12865-014-0060-1) contains supplementary material, which is available to authorized users.

Human blood monocytes support persistence, but not replication of the intracellular pathogen C. pneumoniae