Analyzes of periodontitis status from changes in gingival fibroblasts subpopulation

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Tumor necrosis factor (TNF-alpha) has been known to stimulate prostaglandin production in gingival fibroblasts. In this study, we showed that, by the addition of interleukin-1beta (IL-1beta) into the culture, this enhancement was further augmented. IL-1beta decreased the number of TNF-alpha receptor and affinity to its ligand in gingival fibroblasts. We therefore examined the expression profile of IL-1 receptor mRNA and that of TNF-alpha receptor subtype mRNA under the absence or presence of IL-1beta to understand the underlying mechanisms by which IL-1beta modulate the responsiveness of gingival fibroblasts to TNF-alpha.Both type I and II TNF-alpha receptor mRNA were detected in gingival fibroblasts, but the expression of type I receptor was much more than that of type II.When gingival fibroblasts was stimulated by IL-1beta, the expression of type I TNF-alpha receptor was markedly depressed, while type II receptor was not affected.These results indicate that the initial observation that IL-1beta enhances the affinity of TNF-alpha to gingival fibrolasts (leading to increase of PGE_2 synthesis) can not be explained solely by the expression profile of TNF-alpha receptors.