Abstract
It has been proposed that 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which activates glucocorticoids, plays a role in chronic inflammatory diseases including metabolic diseases, rheumatoid arthritis, and ulcerative colitis. We have recently reported that the expression of 11β-HSD1 is increased in the gingiva of patients with chronic periodontitis and in that of rats with ligature-induced periodontitis. In this study, to further demonstrate the involvement of 11β-HSD1 in chronic periodontitis, the expression of 11β-HSD1 was investigated in another rat model of experimental periodontitis induced by intragingival injection of lipopolysaccharide from Porphyromonas gingivalis (LPS-PG). Alveolar bone loss was observed two weeks after intragingival injection of LPS-PG. The level of 11β-HSD1 mRNA assessed by real-time reverse transcriptase-polymerase chain reaction was significantly elevated in LPS-PG-induced periodontitis compared with controls. The expression of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which inactivates glucocorticoids, was not significantly different between control and LPS-PG-induced periodontitis. The expression of 11β-HSD1 was significantly correlated with that of TNF in LPS-PG-induced periodontitis. The increased expression of 11β-HSD1 protein in LPS-PG-induced periodontitis was confirmed by immunohistochemistry using anti-11β-HSD1 antibody. These results further suggest a role for 11β-HSD1 in the pathogenesis of chronic periodontitis.
Highlights
It is well known that glucocorticoids play various roles in the metabolism of nutrients and immune responses [1]
Experimental periodontitis was induced by intragingival injection of LPS from Porphyromonas gingivalis (LPS-PG) in rats
The expression levels of 11β-HSD1, 11β-HSD2, and tumor necrosis factor (TNF) mRNA in rat gingiva were analyzed using real-time Reverse Transcription-Polymerase Chain Reaction (RT-PCR) methods as described above
Summary
It is well known that glucocorticoids play various roles in the metabolism of nutrients and immune responses [1]. It has been proposed that 11β-HSDs play a pivotal role in the intracellular regulation of glucocorticoids. The involvement of 11β-HSD1 in metabolic diseases including obesity and diabetes mellitus has been reported [4] [5] [6]. The expression of 11β-HSD1 was elevated in adipocytes in the visceral fat of patients with obesity. Animal studies revealed that 11β-HSD1-deficient mice were protected against overnutrition [7]. Transgenic mice overexpressing 11β-HSD1 selectively in adipose tissue developed metabolic phenotypes including visceral fat obesity, dyslipidemia, insulin resistance, and hypertension [8] [9]. Since several inhibitors of 11β-HSD1 ameliorate metabolic diseases in animal models [10] [11], selective and potent 11β-HSD1 inhibitors have been developed for the treatment of metabolic diseases [12] [13]
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