Superoxide release and superoxide dismutase expression by human gingival fibroblasts

Oxygen reactive intermediates released from phagocytic cells are important for microbicidal activity, but they may also be harmful to surrounding cells and matrix components at the inflammation site. In different forms of inflammatory periodontal disease, peripheral and crevicular polymorphonuclear leukocytes, as well-as mononuclear phagocytes and gingival fibroblasts, are exposed to bacterial cell wall components and cytokines. The aim of this study was to evaluate if some bacterial components and cytokines induce superoxide release and superoxide dismutase (SOD) expression in gingival fibroblasts. Lipopolysaccharide (LPS), streptococcal cell walls (SCW), and formyl-methionyl-leucyl-phenylalanine were found to stimulate O-2(-) release from gingival fibroblasts, which increased when Ca2+ was added. Phorbol myristate acetate, a potent activator of respiratory burst in phagocytes, was found to be a weak stimulator of O-2(-) release in gingival fibroblasts. Of the cytokines tested, tumor necrosis factor (TNF)-alpha was found to activate superoxide release in gingival fibroblasts. Gene expression for manganese superoxide dismutase (MnSOD), but not for copper/zinc superoxide dismutase (CuZnSOD), was demonstrated in fibroblasts exposed to LPS, SCW and TNF-alpha using Northern blot analysis. The production of MnSOD may be protective for these cells. We conclude that bacterial cell wall components and cytokines modulate O-2(-) release by gingival fibroblasts which may contribute to periodontal pathology.