Induction of proinflammatory cytokines in human osteoblastic cells by Chlamydia pneumoniae
Abstract
Chlamydia pneumoniae is an obligate intracellular Gram-negative bacterium that causes recurrent pharyngitis, pneumonia and chronic inflammation induced by cycles of persistence and productive infection that might also explain the association with chronic diseases. The aim of this study was to determine whether C. pneumoniae can invade and survive within human osteoblasts and whether this infection elicits the secretion of proinflammatory cytokines. Our results demonstrated that C. pneumoniae was able to infect the SaOS-2 osteoblastic cell line and to replicate in the osteoblasts in a time-dependent manner and was associated to an increase in the cell number and cell viability. In addition, infection of the SaOS-2 cell line with C. pneumoniae at MOI of 4 is correlated to a proinflammatory response. Infected osteoblasts produced increased levels of cytokines IL-6, IL-8, IL-17, and IL-23. The production of cytokines increased with subsequent interaction between osteoblasts and monocytes and the maximum levels of cytokines released were detected 72 h after infection with C. pneumoniae. Thus, controlling the release of chemokines, e.g., IL-23, may be a therapeutic strategy for preventing inflammatory bone disease and counteract inflammation and bone destruction.
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