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Nitric oxide synthase type‐II is synthesized by human gingival tissue and cultured human gingival fibroblasts
Author(s) -
Kendall H. K.,
Haase H. R.,
Li H.,
Xiao Y.,
Bartold P. M.
Publication year - 2000
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1034/j.1600-0765.2000.035004194.x
Subject(s) - connective tissue , porphyromonas gingivalis , nitric oxide synthase , nitric oxide , periodontitis , lipopolysaccharide , immunohistochemistry , pathology , inflammation , chemistry , microbiology and biotechnology , biology , medicine , immunology , organic chemistry
Nitric oxide is known to be an important inflammatory mediator, and is implicated in the pathophysiology of a range of inflammatory disorders. The aim of this study was to determine the localization and distribution of endothelial NOS (NOSII) in human gingival tissue, and to ascertain if human gingival fibroblasts express NOS‐II when stimulated with interferon gamma (IFN‐γ) and bacterial lipopolysaccharide (LPS). The distribution of NOS‐II in inflamed and non‐inflamed specimens of human gingivae was studied using a monoclonal antibody against nitric oxide synthase II. Cultures of fibroblasts derived from healthy human gingivae were used for the cell culture experiments. The results from immunohistochemical staining of the tissues indicated an upregulation of NOS‐II expression in inflamed compared to non‐inflamed gingival tissue. Fibroblasts and inflammatory cells within the inflamed connective tissue were positively stained for NOS‐II. In addition, basal keratinocytes also stained strongly for NOS‐II, in both healthy and inflamed tissue sections. When cultured human gingival fibroblasts were stimulated by INF‐γ and Porphyromonas gingivalis LPS, NOS‐II was more strongly expressed than when the cells were exposed to LPS or IFN‐γ alone. These data suggest that, as for other inflammatory diseases, NO plays a role in the pathophysiology of periodontitis.