High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages

Abstract 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 mycobact...

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Autores principales:	Manabu Inoue, Mamiko Niki, Yuriko Ozeki, Sachiyo Nagi, Evans Asena Chadeka, Takehiro Yamaguchi, Mayuko Osada-Oka, Kenji Ono, Tetsuya Oda, Faith Mwende, Yukihiro Kaneko, Makoto Matsumoto, Satoshi Kaneko, Yoshio Ichinose, Sammy M. Njenga, Shinjiro Hamano, Sohkichi Matsumoto
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/24ac1e4da1684968ba9bb16119a34aa4
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spelling	oai:doaj.org-article:24ac1e4da1684968ba9bb16119a34aa42021-12-02T15:08:40ZHigh-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages10.1038/s41598-018-24233-12045-2322https://doaj.org/article/24ac1e4da1684968ba9bb16119a34aa42018-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-24233-1https://doaj.org/toc/2045-2322Abstract 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.Manabu InoueMamiko NikiYuriko OzekiSachiyo NagiEvans Asena ChadekaTakehiro YamaguchiMayuko Osada-OkaKenji OnoTetsuya OdaFaith MwendeYukihiro KanekoMakoto MatsumotoSatoshi KanekoYoshio IchinoseSammy M. NjengaShinjiro HamanoSohkichi MatsumotoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-11 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Manabu Inoue Mamiko Niki Yuriko Ozeki Sachiyo Nagi Evans Asena Chadeka Takehiro Yamaguchi Mayuko Osada-Oka Kenji Ono Tetsuya Oda Faith Mwende Yukihiro Kaneko Makoto Matsumoto Satoshi Kaneko Yoshio Ichinose Sammy M. Njenga Shinjiro Hamano Sohkichi Matsumoto High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages
description	Abstract 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.
format	article
author	Manabu Inoue Mamiko Niki Yuriko Ozeki Sachiyo Nagi Evans Asena Chadeka Takehiro Yamaguchi Mayuko Osada-Oka Kenji Ono Tetsuya Oda Faith Mwende Yukihiro Kaneko Makoto Matsumoto Satoshi Kaneko Yoshio Ichinose Sammy M. Njenga Shinjiro Hamano Sohkichi Matsumoto
author_facet	Manabu Inoue Mamiko Niki Yuriko Ozeki Sachiyo Nagi Evans Asena Chadeka Takehiro Yamaguchi Mayuko Osada-Oka Kenji Ono Tetsuya Oda Faith Mwende Yukihiro Kaneko Makoto Matsumoto Satoshi Kaneko Yoshio Ichinose Sammy M. Njenga Shinjiro Hamano Sohkichi Matsumoto
author_sort	Manabu Inoue
title	High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages
title_short	High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages
title_full	High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages
title_fullStr	High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages
title_full_unstemmed	High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages
title_sort	high-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/24ac1e4da1684968ba9bb16119a34aa4
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High-density lipoprotein suppresses tumor necrosis factor alpha production by mycobacteria-infected human macrophages

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