凪 幸世
   Department   School of Medicine, School of Medicine
   Position   Assistant Professor
Article types Original article
Language English
Peer review Peer reviewed
Title High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages.
Journal Formal name:Nature Scientific reports
Abbreviation:Sci Rep
ISSN code:20452322/20452322
Domestic / ForeginForegin
Volume, Issue, Page 30(8(1)),pp.6736
Author and coauthor 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
Publication date 2018/04
Summary 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