NDLI: PM2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways.

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PM2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways.

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PM2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Bekki, Kanae Ito, Tomohiro Yoshida, Yasuhiro He, Cuiying Arashidani, Keiichi He, Miao Sun, Guifan Zeng, Yang Sone, Hideko Kunugita, Naoki Ichinose, Takamichi
Description	Country affiliation: Japan Author Affiliation: Bekki K ( Department of Environmental Health, National Institute of Public Health, 2-3-6 Minami, Wako-shi, Saitama, 351-0197, Japan.); Ito T ( Center for Health and Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki, 305-8506, Japan. Electronic address: itotomo@nies.go.jp.); Yoshida Y ( Department of Immunology, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahata-nishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.); He C ( Department of Immunology, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahata-nishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.); Arashidani K ( Department of Immunology, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahata-nishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.); He M ( Environment and Non-Communicable Disease Research Center, School of Public Health, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, PR China.); Sun G ( Environment and Non-Communicable Disease Research Center, School of Public Health, China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, PR China.); Zeng Y ( Center for Health and Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki, 305-8506, Japan.); Sone H ( Center for Health and Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki, 305-8506, Japan.); Kunugita N ( Department of Environmental Health, National Institute of Public Health, 2-3-6 Minami, Wako-shi, Saitama, 351-0197, Japan.); Ichinose T ( Department of Health Sciences, Oita University of Nursing and Health Sciences, 2944-9 Megusuno, Oita City, Oita Prefecture, 870-1201, Japan.)
Abstract	Air pollution continues to increase in East Asia, particularly in China, and is considered to cause serious health problems. In this study, we investigated the toxicological properties of particulate matter ≤2.5mm (PM2.5) collected in an urban area in China (Shenyang), focusing on inflammation and oxidative stress tightly linked to respiratory diseases. Exposure to PM2.5 significantly increased the expression levels of inflammatory (interleukin-1ß and cyclooxygenase-2) and oxidative stress (heme oxygenase1) genes in the mouse macrophages. PM2.5-caused inflammatory response was strongly suppressed by endotoxin neutralizer (polymyxin B) and knock-out of toll-like receptor 4, while oxidative stress was not. On the other hand, an antioxidant (N-acetylcystein) suppressed oxidative stress, but not inflammatory response. These results suggest that PM2.5 in the atmospheric environment of China causes inflammation and oxidative stress in macrophages via separate pathways.
File Format	HTM / HTML
ISSN	13826689
Journal	Environmental Toxicology and Pharmacology
Volume Number	45
e-ISSN	18727077
Language	English
Publisher	Elsevier
Publisher Date	2016-07-01
Publisher Place	Netherlands
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Environmental Health Discipline Pharmacology
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Medicine Toxicology Pharmacology

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