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Indoleamine 2,3‐Dioxygenase Expression and Regulation in Chronic Periodontitis
Author(s) -
Nisapakultorn Kanokwan,
Makrudthong Jittima,
SaArdIam Noppadol,
Rerkyen Pimprapa,
Mahada Rangsini,
Takikawa Osamu
Publication year - 2009
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2009.080315
Subject(s) - porphyromonas gingivalis , periodontitis , indoleamine 2,3 dioxygenase , chronic periodontitis , tumor necrosis factor alpha , medicine , immunohistochemistry , immunology , inflammation , biology , tryptophan , biochemistry , amino acid
Background: Indoleamine 2,3‐dioxygenase (IDO) is an intracellular tryptophan‐oxidizing enzyme with immunosuppressive characteristics. Its expression and regulation in periodontal tissues are unknown. The aim of this study was to determine IDO expression in healthy gingiva and chronic periodontitis lesions. In addition, the effect of inflammatory cytokines and bacterial products on the expression and activity of DOI in human gingival fibroblasts (HGFs) was assessed. Methods: Human gingival tissue samples were obtained from patients who underwent periodontal surgery. IDO expression in healthy gingiva and periodontitis lesions was determined by immunohistochemistry. HGF cells were treated with interferon‐gamma (IFN‐γ), interleukin (IL)‐1β, tumor necrosis factor‐alpha (TNF‐α), and lipopolysaccharides from Porphyromonas gingivalis ( Pg LPS). IDO mRNA expression was determined by reverse transcription‐polymerase chain reaction. The IDO enzymatic activity was determined by measuring the kynurenine level using a colorimetric method. Results: In gingival tissues, IDO expression was detected in epithelial cells, fibroblasts, endothelial cells, and inflammatory mononuclear cells. IDO expression was higher in periodontitis lesions than in healthy gingiva. HGFs did not constitutively express IDO. IFN‐γ strongly induced IDO expression and activity in HGFs, in a dose‐dependent manner. IL‐1β, TNF‐α, and Pg LPS were also able to induce IDO expression in HGF cells. IFN‐γ in combination with IL‐1β, TNF‐α, or Pg LPS showed enhanced IDO expression. Conclusions: IDO was expressed in human gingiva, and the expression was upregulated in chronic periodontitis. The increased IDO expression in periodontitis lesions may be due, in part, to the activation of HGFs by inflammatory cytokines and bacterial products.