title: Differences in allergic inflammatory responses between urban PM2.5 and fine particle derived from desert-dust in murine lungs.
abstract: The biological and chemical natures of materials adsorbed onto fine particulate matter (PM2.5) vary by origin and passage routes. The exacerbating effects of the two samples-urban PM2.5 (U-PM2.5) collected during the hazy weather in a Chinese city and fine particles (ASD-PM2.5) collected during Asian sand dust (ASD) storm event days in Japan-on murine lung eosinophilia were compared to clarify the role of toxic materials in PM2.5. The amounts of β-glucan and mineral components were higher in ASD-PM2.5 than in U-PM2.5. On the other hand, organic chemicals, including polycyclic aromatic hydrocarbons (PAHs), were higher in U-PM2.5 than in ASD-PM2.5. When BALB/c mice were intratracheally instilled with U-PM2.5 and ASD-PM2.5 (total 0.4 mg/mouse) with or without ovalbumin (OVA), various biological effects were observed, including enhancement of eosinophil recruitment induced by OVA in the submucosa of the airway, goblet cell proliferation in the bronchial epithelium, synergic increase of OVA-induced eosinophil-relevant cytokines and a chemokine in bronchoalveolar lavage fluid, and increase of serum OVA-specific IgG1 and IgE. Data demonstrate that U-PM2.5 and ASD-PM2.5 induced allergic inflammatory changes and caused lung pathology. U-PM2.5 and ASD-PM2.5 increased F4/80(+) CD11b(+) cells, indicating that an influx of inflammatory and exudative macrophages in lung tissue had occurred. The ratio of CD206 positive F4/80(+) CD11b(+) cells (M2 macrophages) in lung tissue was higher in the OVA+ASD-PM2.5 treated mice than in the OVA+U-PM2.5 treated mice. These results suggest that the lung eosinophilia exacerbated by both PM2.5 is due to activation of a Th2-associated immune response along with induced M2 macrophages and the exacerbating effect is greater in microbial element (β-glucan)-rich ASD-PM2.5 than in organic chemical-rich U-PM2.5.
authors.affiliation: Environment and Non-communicable Disease Research Center, School of Public Health, China Medical University, Shenyang 110122, China; Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita 870-1201, Japan. Electronic address: hemiao@mail.cmu.edu.cn.
authors.forename: Miao
authors.initials: M
authors.lastname: He
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita 870-1201, Japan. Electronic address: ichinose@oita-nhs.ac.jp.
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.affiliation: Department of Respiratory Medicine, Kanazawa Medical University, Ishikawa 920-0293, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Kobayashi
authors.affiliation: Department of Immunology and Parasitology, School of Medicine, University of Occupational and Environmental Health, Fukuoka 807-8555, Japan.
authors.forename: Keiichi
authors.initials: K
authors.lastname: Arashidani
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita 870-1201, Japan.
authors.forename: Seiichi
authors.initials: S
authors.lastname: Yoshida
authors.affiliation: Environmental Chemistry Division, National Institute for Environmental Studies, Ibaraki 305-8506, Japan.
authors.forename: Masataka
authors.initials: M
authors.lastname: Nishikawa
authors.affiliation: Environmental Health Division, Department of Environmental Engineering, Graduate School of Engineering, Kyoto University, Kyoto 615-8530, Japan.
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.affiliation: Environment and Non-communicable Disease Research Center, School of Public Health, China Medical University, Shenyang 110122, China.
authors.forename: Guifan
authors.initials: G
authors.lastname: Sun
authors.affiliation: Department of Environmental Toxicology, University of California, Davis, CA 95616, USA.
authors.forename: Takayuki
authors.initials: T
authors.lastname: Shibamoto
mesh_terms: D000393:Air Pollutants / Q000737:chemistry / Q000633:toxicity*; D000485:Allergens / Q000276:immunology; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D002452:Cell Count; D002681:China; D016207:Cytokines / Q000276:immunology; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D007564:Japan; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008297:Male; D008670:Metals / Q000032:analysis; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D052638:Particulate Matter / Q000737:chemistry / Q000633:toxicity*; D011657:Pulmonary Eosinophilia / Q000276:immunology* / Q000473:pathology; D047071:beta-Glucans / Q000032:analysis
chemical_list: D000393:Air Pollutants; D000485:Allergens; D016207:Cytokines; D007074:Immunoglobulin G; D008670:Metals; D052638:Particulate Matter; D047071:beta-Glucans; D007073:Immunoglobulin E; D010047:Ovalbumin
keywords: Eosinophilia; Fine particulate matter; M2 macrophages; Microbial element; PM2.5; Th2 immune response