|Institution:||University of Louisville|
|Full text PDF:||http://ir.library.louisville.edu/etd/1495|
P. gingivalis is a major periodontal disease causing pathogen. Gingival epithelial cells being the first line of defense, interact and internalize the bacteria evoking a cell signaling response that finally leads to the release of cytokines. IL-6 is a potent pro- inflammatory cytokine, which is one of the responsible factors for bone resorption, a clinical manifestation of periodontitis. The experimental model study hypothesizes that P. gingivalis infection increases the production of IL-6 in telomerase immortalized gingival keratinocytes (TIGKs) through up-regulation of c-Jun (AP-1 reporter). We observed the IL-6 production post-infection with P. gingivalis WT ATCC33277 and mutants ?0482, ?Ndk and ?luxS. The ndk gene in P. gingivalis controls ATP scavenging and persistence of the bacterium intracellularly. The mutant was therefore expected to be less efficient in the intra cellular environment. The luxS gene in the bacterium plays a role in maintaining several physiological functions like hemin uptake, quorum sensing etc. The mutant was hence expected to show reduced activation of cell signaling pathways and IL-6 production. The cells were infected with bacteria at 4h and 24h time points and concluded that IL-6 production is increased in infected samples, compared to controls. Also, western blots indicated that c-Jun phosphorylation was up regulated in infected samples, providing a possible evidence that P. gingivalis stimulates IL-6 production through phosphorylation of c-Jun in gingival epithelial cells, finally leading to IL-6 secretion.