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Published on: February 22, 2017
Induction of proinflammatory cytokines in human osteoblastic cells by Chlamydia pneumoniae
Antonietta Rizzo1, Marina Di Domenico, Caterina Romano Carratelli
1Department of Experimental Medicine, Section of Microbiology and Clinical Microbiology, Faculty of Medicine and Surgery-Second University of Naples, Naples, Italy.
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.
Insights
Chlamydia pneumoniae infects human osteoblasts, triggering an inflammatory response. Controlling specific cytokines like IL-23 may prevent inflammatory bone diseases.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Chlamydia pneumoniae is an intracellular bacterium linked to chronic inflammation and diseases.
- Its role in bone health and osteoblast interaction is not fully understood.
Purpose of the Study:
- To investigate if Chlamydia pneumoniae can infect and survive in human osteoblasts.
- To determine if this infection stimulates the release of pro-inflammatory cytokines.
Main Methods:
- Infection of SaOS-2 osteoblastic cell line with Chlamydia pneumoniae.
- Time-dependent analysis of bacterial replication, cell viability, and cytokine production.
- Co-culture with monocytes to assess cytokine release dynamics.
Main Results:
- Chlamydia pneumoniae successfully infected and replicated within SaOS-2 osteoblasts.
- Infection led to increased osteoblast number and viability.
- A significant pro-inflammatory response was observed, with increased levels of IL-6, IL-8, IL-17, and IL-23.
- Cytokine production peaked 72 hours post-infection, especially after monocyte interaction.
Conclusions:
- Chlamydia pneumoniae can infect osteoblasts, survive, and induce a pro-inflammatory cytokine response.
- This suggests a potential mechanism linking C. pneumoniae infection to inflammatory bone diseases.
- Targeting cytokine release, particularly IL-23, could be a therapeutic strategy for inflammatory bone conditions.
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