The Peroxisome Proliferator-Activated Receptor alpha- Agonist Gemfibrozil Promotes Defense Against Mycobacterium abscessus Infections
- 주제(키워드) PPAR alpha , Mycobacterium abscessus , gemfibrozil , TFEB , inflammation
- 주제(기타) Cell Biology
- 설명문(일반) [Kim, Yi Sak; Kim, Jin Kyung; Kim, Hyeon Ji; Kim, Young Jae; Jeon, Sang Min; Park, Cho Rong; Jo, Eun-Kyeong] Chungnam Natl Univ, Dept Microbiol, Sch Med, Daejeon 35015, South Korea; [Kim, Yi Sak; Kim, Jin Kyung; Kim, Hyeon Ji; Kim, Young Jae; Jeon, Sang Min; Park, Cho Rong; Jo, Eun-Kyeong] Chungnam Natl Univ, Infect Control Convergence Res Ctr, Sch Med, Daejeon 35015, South Korea; [Bui Thi Bich Hanh; Jang, Jichan] Gyeongsang Natl Univ, Res Inst Life Sci, Div Life Sci, Mol Mech Antibiot, Jinju 52828, South Korea; [Bui Thi Bich Hanh; Jang, Jichan] Gyeongsang Natl Univ, BK21plus Program, Div Appl Life Sci, Jinju 52828, South Korea; [Kim, Soo Yeon] Korea Basic Sci Inst, Div Bioconvergence Anal, Drug & Dis Target Res Team, Cheongju 28119, South Korea; [Oh, Goo Taeg] Ewha Womans Univ, Dept Life Sci, Seoul 03760, South Korea; [Park, June-Woo] Korea Inst Toxicol, Environm Risk Assessment Res Div, Jinju 52834, South Korea; [Park, June-Woo] Korea Univ Sci & Technol UST, Human & Environm Toxicol Program, Daejeon 34113, South Korea; [Kim, Jin-Man] Chungnam Natl Univ, Dept Pathol, Sch Med, Daejeon 35015, South Korea
- 등재 SCIE, SCOPUS
- OA유형 gold, Green Published
- 발행기관 MDPI
- 발행년도 2020
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000172082
- 본문언어 영어
- Published As https://dx.doi.org/10.3390/cells9030648
- PubMed https://pubmed.ncbi.nlm.nih.gov/32155958
초록/요약
Peroxisome proliferator-activated receptor alpha (PPAR alpha) shows promising potential to enhance host defenses against Mycobacterium tuberculosis infection. Herein we evaluated the protective effect of PPAR alpha against nontuberculous mycobacterial (NTM) infections. Using a rapidly growing NTM species, Mycobacterium abscessus (Mabc), we found that the intracellular bacterial load and histopathological damage were increased in PPAR alpha-null mice in vivo. In addition, PPAR alpha deficiency led to excessive production of proinflammatory cytokines and chemokines after infection of the lung and macrophages. Notably, administration of gemfibrozil (GEM), a PPAR alpha activator, significantly reduced the in vivo Mabc load and inflammatory response in mice. Transcription factor EB was required for the antimicrobial response against Mabc infection. Collectively, these results suggest that manipulation of PPAR alpha activation has promising potential as a therapeutic strategy for NTM disease.
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