Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-42993
Belibasakis, G N; Bostanci, N; Reddi, D (2011). Porphyromonas gingivalis induces RANKL in T-cells. Inflammation, 34(2):133-138.
View at publisher
Porphyromonas gingivalis is an oral pathogen highly implicated in chronic periodontitis, a disease characterized by inflammatory destruction of the tooth-supporting alveolar bone and eventually, tooth loss. T-cell innate immune responses are actively involved in this pathological process. Receptor activator of NF-kappaB Ligand (RANKL) is a cytokine that stimulates bone resorption, while its soluble decoy receptor osteoprotegerin (OPG) blocks its action. This study aimed to investigate in Jurkat T-cells the effects of P. gingivalis on the RANKL-OPG system and the major inflammatory mediator of bone resorption prostaglandin E(2) (PGE(2)). P. gingivalis caused concentration-dependent up-regulation of RANKL gene expression and protein production, assessed by quantitative PCR and ELISA, respectively. PGE(2) production was also enhanced. However, OPG was not detected. In conclusion, P. gingivalis induces RANKL and PGE(2) in T-cells, potentially favoring bone resorption. These T-cell responses to P. gingivalis may contribute to the pathogenesis of inflammatory alveolar bone destruction occurring in chronic periodontitis.
60 downloads since deposited on 22 Jan 2011
13 downloads since 12 months
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Center for Dental Medicine > Institute of Oral Biology|
|Dewey Decimal Classification:||610 Medicine & health|
|Deposited On:||22 Jan 2011 19:47|
|Last Modified:||28 Nov 2013 00:19|
|Additional Information:||The original publication is available at www.springerlink.com|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page