title: Silica-carrying particulate matter enhances Bjerkandera adusta-induced murine lung eosinophilia.
abstract: Bjerkandera adusta (B. adusta) causes fungus-associated chronic cough. However, the inflammatory response is not yet fully understood. Recently, B. adusta was identified in Asian sand dust (ASD) aerosol. This study investigated the enhancing effects of ASD on B. adusta-induced lung inflammation. B. adusta was inactivated by formalin. ASD was heated to remove toxic organic substances. ICR mice were intratracheally instilled with saline, B. adusta 0.2 µg, or B. adusta 0.8 µg with or without heated ASD 0.1 mg (H-ASD), four times at 2-week intervals. Two in vitro experiments were conducted to investigate any enhancing effects using bone marrow-derived macrophages (BMDM) from Toll-like receptor (TLR) knockout mice and ICR mice. Co-exposure to H-ASD and B. adusta, especially at high doses, caused eosinophil infiltration, proliferation of goblet cells in the airway, and fibrous thickening of the subepithelial layer, and remarkable increases in expression of Th2 cytokines and eosinophil-related cytokine and chemokine expression in bronchoalveolar lavage fluid. In the in vitro study using BMDM from wild-type, TLR2-/-, and TLR4-/- mice, the TLR-signaling pathway for cytokine production caused by B. adusta was predominantly TLR2 rather than TLR4. H-ASD increased the expression of NF-κB and cytokine production by B. adusta in BMDM from ICR mice. The results suggest that co-exposure to H-ASD and B. adusta caused aggravated lung eosinophilia via remarkable increases of pro-inflammatory mediators. The aggravation of inflammation may be related, at least in part, to the activation of the TLR2-NF-κB signaling pathway in antigen presenting cells by H-ASD.
authors.affiliation: Environment and Chronic Non-Communicable Disease Research Center, School of Public Health, China Medical University, 11001, Shenyang, China.|Department of Health Sciences, Oita University of Nursing and Health Sciences, 870-1201, Oita, Japan.
authors.forename: Miao
authors.initials: M
authors.lastname: He
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, 870-1201, Oita, Japan.
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.affiliation: Environment and Chronic Non-Communicable Disease Research Center, School of Public Health, China Medical University, 11001, Shenyang, China.|Department of Health Sciences, Oita University of Nursing and Health Sciences, 870-1201, Oita, Japan.
authors.forename: Boying
authors.initials: B
authors.lastname: Liu
authors.affiliation: Department of Immunology and Parasitology, School of Medicine, University of Occupational and Environmental Health, 807-8555, Fukuoka, Japan.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Song
authors.affiliation: Department of Immunology and Parasitology, School of Medicine, University of Occupational and Environmental Health, 807-8555, Fukuoka, Japan.
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Yoshida
authors.affiliation: Faculty of Natural System, College of Science and Engineering, Kanazawa University, 920-1192, Ishikawa, Japan.
authors.forename: Fumihisa
authors.initials: F
authors.lastname: Kobayashi
authors.affiliation: Faculty of Chemistry, Institute of Science and Engineering, Kanazawa University, 920-1192, Ishikawa, Japan.
authors.forename: Teruya
authors.initials: T
authors.lastname: Maki
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, 870-1201, Oita, Japan.
authors.forename: Seiichi
authors.initials: S
authors.lastname: Yoshida
authors.affiliation: Division of Environmental Chemistry, National Institute for Environmental Studies, 305-8506, Ibaraki, Japan.
authors.forename: Masataka
authors.initials: M
authors.lastname: Nishikawa
authors.affiliation: Division of Environmental Health, Department of Environmental Engineering, Graduate School of Engineering, Kyoto University, 615-8530, Kyoto, Japan.
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.affiliation: Environment and Chronic Non-Communicable Disease Research Center, School of Public Health, China Medical University, 11001, Shenyang, China.
authors.forename: Guifan
authors.initials: G
authors.lastname: Sun
mesh_terms: D000818:Animals; D001854:Bone Marrow Cells / Q000166:cytology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D018925:Chemokines / Q000378:metabolism; D055453:Coriolaceae / Q000737:chemistry* / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D024202:Electrophoretic Mobility Shift Assay; D008070:Lipopolysaccharides / Q000032:analysis; D008264:Macrophages / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D018345:Mice, Knockout; D016328:NF-kappa B / Q000378:metabolism; D052638:Particulate Matter / Q000633:toxicity*; D010936:Plant Extracts / Q000737:chemistry / Q000633:toxicity*; D011657:Pulmonary Eosinophilia / Q000139:chemically induced* / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects; D012822:Silicon Dioxide / Q000633:toxicity*; D051195:Toll-Like Receptor 2 / Q000172:deficiency / Q000235:genetics; D051197:Toll-Like Receptor 4 / Q000172:deficiency / Q000235:genetics
chemical_list: D018925:Chemokines; D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D052638:Particulate Matter; D010936:Plant Extracts; C493486:Tlr2 protein, mouse; C493487:Tlr4 protein, mouse; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D012822:Silicon Dioxide
keywords: Asian sand dust; Bjerkandera adusta; NF-κB; bone marrow-derived macrophages; lung eosinophilia; toll-like receptor knockout mice