ナギ サチヨ
  凪 幸世
   所属   医学部 医学科
   職種   助教
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages.
掲載誌名 正式名:Nature Scientific reports
略  称:Sci Rep
ISSNコード:20452322/20452322
掲載区分国外
巻・号・頁 30(8(1)),pp.6736
著者・共著者 Inoue Manabu, Niki Mamiko, Ozeki Yuriko, Nagi Sachiyo, Chadeka Evans Asena, Yamaguchi Takehiro, Osada-Oka Mayuko, Ono Kenji, Oda Tetsuya, Mwende Faith, Kaneko Yukihiro, Matsumoto Makoto, Kaneko Satoshi, Ichinose Yoshio, Njenga Sammy M, Hamano Shinjiro, Matsumoto Sohkichi
発行年月 2018/04
概要 Immune responses to parasitic pathogens are affected by the host physiological condition. High-density lipoprotein (HDL) and low-density lipoprotein (LDL) are transporters of lipids between the liver and peripheral tissues, and modulate pro-inflammatory immune responses. Pathogenic mycobacteria are parasitic intracellular bacteria that can survive within macrophages for a long period. Macrophage function is thus key for host defense against mycobacteria. These basic facts suggest possible effects of HDL and LDL on mycobacterial diseases, which have not been elucidated so far. In this study, we found that HDL and not LDL enhanced mycobacterial infections in human macrophages. Nevertheless, we observed that HDL remarkably suppressed production of tumor necrosis factor alpha (TNF-α) upon mycobacterial infections. TNF-α is a critical host-protective cytokine against mycobacterial diseases. We proved that toll-like receptor (TLR)-2 is responsible for TNF-α production by human macrophages infected with mycobacteria. Subsequent analysis showed that HDL downregulates TLR2 expression and suppresses its intracellular signaling pathways. This report demonstrates for the first time the substantial action of HDL in mycobacterial infections to human macrophages.
DOI 10.1038/s41598-018-24233-1
PMID 29712918