Quick Search:

uzh logo
Browse by:

Zurich Open Repository and Archive 

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.

Accepted Version


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.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Dental Medicine > Institute of Oral Biology
DDC: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
Publisher DOI:10.1007/s10753-010-9216-1
PubMed ID:20446027
Citations:Web of Science®. Times Cited: 11
Google Scholar™
Scopus®. Citation Count: 11

Users (please log in): suggest update or correction for this item

Repository Staff Only: item control page