Attenuation of butyric acid-induced T cell apoptosis by human gingival fibroblast

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(1) Although butyric acid exhibited a dose-dependent inhibition in F41-G and Ca 9-22 cells, their effect was not prominent compared to the data with T-, B- and monocytic cells. Furthermore, the results of DNA fragmentation assay indicated that butyric acid did not induced apoptosis in human gingival fibroblasts (Gin 1, F41G and H.pulp).(2) When the culture supernatants of gingival fibroblasts were assayed for IL-1α, IL-1β, IL-6, IL-8, IL-11, TNF α and TGF β by use of ELISA kits, butyric acid significautly increased IL-6, IL-8 and IL-11 production. Maximum levels of these cytokines were noted by the addition of 5 mM butyric acid in Gin 1, F41-G and H.pulp cells. These levels were 1,500 to 1,900 pg/ml (IL-6), ca.4,000 to 5,000 pg/ml (IL-8), and ca.900 to 1,100 pg/ml (IL-11).(3) Co-culturing Jurkat cells with F41G or Gin 1 cells using intercup partially rescued butyric acid- or Fas-induced Jurkat cell apoptosis, suggest a role for a soluble factor released from fibroblasts in preventing T cell-apoptosis.(4) IL-6 and IL-8 slightly stimulated butyric acid- or Fas-induced Jurkat cell apoptosis in a dose-dependent manner, in contrast, IL-11 significantly suppressed these Jurkat cell apoptosis dose-dependently. These results suggest that the sum of their effects of the inflammatory cytokines such as IL-6, IL-8 and IL-11, produced in fibroblast by the addition of butyric acid, are concernted in the attenuation of T cell apoptosis by gingival fibroblast.(5) Furthemore, the direct cell-cell interaction indicated that the apoptosis of Jurkat T cells attached on the gingival fibroblasts was significantly rescued. CD47, CD44 and CD58 expression on the fibroblasts was increased by the addition of butyric acid, suggest that the increase of these cell surface molecule was concerned with the suppression of T cell apoptosis induced by butyric acid.