title: PM2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways.
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-1β 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.
authors.affiliation: Department of Environmental Health, National Institute of Public Health, 2-3-6 Minami, Wako-shi, Saitama, 351-0197, Japan.
authors.forename: Kanae
authors.initials: K
authors.lastname: Bekki
authors.affiliation: 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.
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Ito
authors.affiliation: Department of Immunology, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahata-nishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Yoshida
authors.affiliation: Department of Immunology, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahata-nishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
authors.forename: Cuiying
authors.initials: C
authors.lastname: He
authors.affiliation: Department of Immunology, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahata-nishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
authors.forename: Keiichi
authors.initials: K
authors.lastname: Arashidani
authors.affiliation: 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.
authors.forename: Miao
authors.initials: M
authors.lastname: He
authors.affiliation: 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.
authors.forename: Guifan
authors.initials: G
authors.lastname: Sun
authors.affiliation: Center for Health and Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki, 305-8506, Japan.
authors.forename: Yang
authors.initials: Y
authors.lastname: Zeng
authors.affiliation: Center for Health and Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, Ibaraki, 305-8506, Japan.
authors.forename: Hideko
authors.initials: H
authors.lastname: Sone
authors.affiliation: Department of Environmental Health, National Institute of Public Health, 2-3-6 Minami, Wako-shi, Saitama, 351-0197, Japan.
authors.forename: Naoki
authors.initials: N
authors.lastname: Kunugita
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, 2944-9 Megusuno, Oita City, Oita Prefecture, 870-1201, Japan.
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
mesh_terms: D000393:Air Pollutants / Q000032:analysis / Q000633:toxicity*; D000818:Animals; D002470:Cell Survival / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D002681:China; D051546:Cyclooxygenase 2 / Q000235:genetics; D004784:Environmental Monitoring / Q000379:methods*; D053583:Interleukin-1beta / Q000235:genetics; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics; D018384:Oxidative Stress / Q000187:drug effects* / Q000235:genetics / Q000276:immunology; D010316:Particle Size; D052638:Particulate Matter / Q000032:analysis / Q000633:toxicity*; D000067996:RAW 264.7 Cells; D015398:Signal Transduction / Q000187:drug effects; D051195:Toll-Like Receptor 2 / Q000235:genetics; D051197:Toll-Like Receptor 4 / Q000235:genetics; D014507:Urbanization
chemical_list: D000393:Air Pollutants; D053583:Interleukin-1beta; C507780:Myd88 protein, mouse; D053594:Myeloid Differentiation Factor 88; D052638:Particulate Matter; C493486:Tlr2 protein, mouse; C493487:Tlr4 protein, mouse; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2
keywords: Inflammation; Macrophage; Oxidative stress; PM(2.5)