Chlamydia pneumoniae induces Interleukin-6 and Interleukin-10 in human gingival fibroblasts

Chlamydia pneumoniae is an obligate intracellular Gram-negative bacterium with a unique biphasic developmental cycle that can cause persistent infections. In humans, Chlamydia causes airway infection and has been implicated in chronic inflammatory diseases, such as asthma and atherosclerosis. In addition, recent studies demonstrated that patientswith severe periodontitis can harbor C. pneumoniae, which can increase the risk for a host inflammatory response with weighty clinical sequelae. Previous studies have established that periodontal pathogenic bacteria (i.e. Gram-negative bacteria) can induce the synthesis and release of cytokines and other inflammatory mediators in human gingival fibroblasts. HGFare resident cells of the periodontium that respond to receptor stimulation by producing a variety of substances including cytokines and growth factors.Ourresults demonstrate that after 48 hr of incubation with viable C. pneumoniae HGFshowed a proliferative response, as seen by both colorimetricMTT assay and direct cell count (30% and 35%, respectively). In addition, HGF incubated with viable or UV lightinactivated C. pneumoniae organisms showed an increase in the levels of IL-6 and IL-10, but not IL-4; on the contrary, HGF infected with heat-killed bacteria did not show a significant production of any of the cytokines considered. In conclusion, the present study suggests that C. pneumoniae maymodulate the expression of IL-6 and IL-10 by human gingival fibroblasts. Further studies are warranted to clarify the molecular mechanisms of C. pneumoniae in the regulation of cytokine expression by host cells and to elaborate the relevant clinical implications.