Induction of proinflammatory cytokines in human osteoblastic cells by Chlamydia pneumoniae

► Chlamydia pneumoniae infects and replicates within the human SaOS-2 osteoblastic cell line. ► C. pneumoniae infection stimulates an inflammatory cytokine response. ► Infection is associated with increased IL-6, IL-8, IL-17, and IL-23 cytokine levels. Chlamydia pneumoniae is an obligate intracellul...

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Veröffentlicht in:Cytokine (Philadelphia, Pa.) Pa.), 2011-11, Vol.56 (2), p.450-457
Hauptverfasser: Rizzo, Antonietta, Di Domenico, Marina, Carratelli, Caterina Romano, Mazzola, Nello, Paolillo, Rossella
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Sprache:eng
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Zusammenfassung:► Chlamydia pneumoniae infects and replicates within the human SaOS-2 osteoblastic cell line. ► C. pneumoniae infection stimulates an inflammatory cytokine response. ► Infection is associated with increased IL-6, IL-8, IL-17, and IL-23 cytokine levels. 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 72h 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.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2011.06.027