Ursodeoxycholic Acid Inhibits Inflammatory Cytokine Expression in THP-1 Cells Infected with Aggregatibacter actinomycetemcomitans

서지정보

ㆍ발행기관 : 대한구강생물학회 ㆍ수록지정보 : International Journal of Oral Biology / 42권 / 1호
ㆍ저자명 : YuRi Song, SeYeon Kim, Mee Hee Park, Hee Sam Na, Jin Chung

목차

Introduction
Materials and Methods
Reagents
Bacterial culture
Cell culture and treatment
Cell cytotoxicity assay
Bacteria of growth curve
Cytokine analysis
Statistics
Results
1. Effect of UDCA on the viability of THP- 1-derivedmacrophages and the growth of A. actinomycetemcomitans
2. Effect of UDCA on the production of proinflammatorycytokines in A. actinomycetemcomitansinfectedTHP-1-derived macrophages
Discussion
Acknowledgements
Conflict of interest
References

영어 초록

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.

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