Ursodeoxycholic Acid Inhibits Inflammatory Cytokine Expression in THP-1 Cells Infected with Aggregatibacter actinomycetemcomitans
송유리, 김세연, 박미희, 나희삼, 정진,
소속 상세정보
송유리 ( Song Yu-Ri ) - Pusan National University School of Dentistry Department of Oral Microbiology
김세연 ( Kim Se-Yeon ) - Pusan National University School of Dentistry Department of Oral Microbiology
박미희 ( Park Mee-Hee ) - Pusan National University School of Dentistry Department of Oral Microbiology
나희삼 ( Na Hee-Sam ) - Pusan National University School of Dentistry Department of Oral Microbiology
정진 ( Chung Jin ) - Pusan National University School of Dentistry Department of Oral Microbiology
KMID : 0848120170420010033
Abstract
Background: Periodontitis is an inflammatory disease characterized by the breakdown of tooth-supporting tissues, leading to tooth loss. Aggregatibacter actinomycetemcomitans are major etiologic bacterium causing aggressive periodontitis. Ursodeoxycholic acid (UDCA), a hydrophilic gall bladder acid, has been used as an effective drug for various diseases related to immunity. The aim of this study was to investigate the effect of UDCA on the inflammatory response induced by A. actinomycetemcomitans.
Methods: A human acute monocytic leukemia cell line (THP-1) was differentiated to macrophage- like cells by treatment with phorbol 12-mystristate 13-acetate (PMA) and used for all experiments. The cytotoxic effect of UDCA was examined by MTT assay. THP-1 cells were pretreated with UDCA for 30 min before A. actinomycetemcomitans infection and the culture supernatant was analyzed for various cytokine production by ELISA. The effect of UDCA on bacterial growth was examined by measuring optical densities using a spectrophotometer.
Results: UDCA showed no cytotoxic effect on THP-1 cells, up to 80 μM Ed highlight: Please confirm technical meaning. UDCA pretreatment inhibited the A. actinomycetemcomitansinduced IL-1β, TNF-?, and IL-17A secretion in a dosedependent manner. UDCA also inhibited IL-21 production at 60 μM. The production of IL-12 and IL-4 was not influenced by A. actinomycetemcomitans infection.
Conclusion: These findings indicate that UDCA inhibits the production of inflammatory cytokines involved in innate and Th17 immune responses in A. actinomycetemcomitansinfected THP-1- derived macrophages, which suggests its possible use for the control of aggressive periodontitis.
키워드
A. actinomycetemcomitans ; ursodeoxycholic acid ; macrophage ; IL-1β ; TNF-? ; IL-17A ; periodontitis
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