Abstract
P.gingivalis heat-shock-protein(HtpG) induces pro-inflammatory response in monocytes and gingival fibroblasts
Objective:
Heat-shock proteins are a group of evolutionary conserved proteins that are synthesized rapidly by most cells responding to stress-related events. They act as chaperons through interactions with other molecules to protect them from alterations during noxious processes. P.gingivalis produces a number of heat shock proteins that are essential tools in normal cellular processes and in response to environmental stresses during infection. The aim of this study was to examine immunomodulatory effects of P.gingivalis HtpG and its interaction with lipopolysaccharide.
Method:
P.gingivalis HtpG was cloned and purified using the full-length sequence and Ni-agarose chromatography. THP-1 cells and primary gingival fibroblasts were treated with different concentrations of HtpG for four hours and IL-8 and TNF-α production was measured by ELISA. Interaction between HtpG and P.gingivalis LPS was measured by binding assay.
Result:
P.gingivalis HtpG triggered significant pro-inflammatory response in monocytes and gingival fibroblasts measured by productions of IL-8 and TNF-α. In addition, immune response to P.gingivalis LPS was augmented when the cells were co-cultured with HtpG. Nevertheless, the binding assay revealed no physical interaction between HtpG and LPS.
Conclusion:
P.gingivalis HtpG is able to induce a strong inflammatory response in monocytes and gingival fibroblasts. This may have consequences in the pathogenesis of periodontitis through establishment and perpetuation of chronic inflammation.
Objective:
Heat-shock proteins are a group of evolutionary conserved proteins that are synthesized rapidly by most cells responding to stress-related events. They act as chaperons through interactions with other molecules to protect them from alterations during noxious processes. P.gingivalis produces a number of heat shock proteins that are essential tools in normal cellular processes and in response to environmental stresses during infection. The aim of this study was to examine immunomodulatory effects of P.gingivalis HtpG and its interaction with lipopolysaccharide.
Method:
P.gingivalis HtpG was cloned and purified using the full-length sequence and Ni-agarose chromatography. THP-1 cells and primary gingival fibroblasts were treated with different concentrations of HtpG for four hours and IL-8 and TNF-α production was measured by ELISA. Interaction between HtpG and P.gingivalis LPS was measured by binding assay.
Result:
P.gingivalis HtpG triggered significant pro-inflammatory response in monocytes and gingival fibroblasts measured by productions of IL-8 and TNF-α. In addition, immune response to P.gingivalis LPS was augmented when the cells were co-cultured with HtpG. Nevertheless, the binding assay revealed no physical interaction between HtpG and LPS.
Conclusion:
P.gingivalis HtpG is able to induce a strong inflammatory response in monocytes and gingival fibroblasts. This may have consequences in the pathogenesis of periodontitis through establishment and perpetuation of chronic inflammation.
Original language | English |
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Publication status | Published - 10 Sept 2013 |
Event | IADR British Division Meeting - Bath, United Kingdom Duration: 10 Sept 2013 → 10 Sept 2013 |
Conference
Conference | IADR British Division Meeting |
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Country/Territory | United Kingdom |
City | Bath |
Period | 10/09/2013 → 10/09/2013 |