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Lung inflammation by fungus, Bjerkandera adusta isolated from Asian sand dust (ASD) aerosol and enhancement of ovalbumin-induced lung eosinophilia by ASD and the fungus in mice

Boying LiuDepartment of Health Sciences, Oita University of Nursing and Health Sciences, 870-1201, Oita, JapanTakamichi IchinoseDepartment of Health Sciences, Oita University of Nursing and Health Sciences, 870-1201 Oita, Japan. [email protected]Miao HeDepartment of Health Sciences, Oita University of Nursing and Health Sciences, 870-1201, Oita, JapanFumihisa KobayashiCollege of Science and Engineering, Kanazawa University, 920-1192, Ishikawa, JapanTeruya MakiCollege of Science and Engineering, Kanazawa University, 920-1192, Ishikawa, JapanSeiichi YoshidaDepartment of Health Sciences, Oita University of Nursing and Health Sciences, 870-1201, Oita, JapanYasuhiro YoshidaDepartment of Immunology and Parasitology, School of Medicine, University of Occupational and Environmental Health, Japan, 807-8555, Fukuoka, JapanKeiichi ArashidaniDepartment of Immunology and Parasitology, School of Medicine, University of Occupational and Environmental Health, Japan, 807-8555, Fukuoka, JapanHirohisa TakanoEnvironmental Health Division, Department of Environmental Engineering, Graduate School of Engineering, Kyoto University, 615-8530, Kyoto, JapanMasataka NishikawaEnvironmental Chemistry Division, National Institute for Environmental Studies, 305-8506, Ibaraki, JapanGuifan SunEnvironment and Chronic Non-communicable Disease Research Center, College of Public Health, China Medical University, 11001, Shenyang, ChinaTakayuki ShibamotoDepartment of Environmental Toxicology, University of California, Davis, CA, 95616, USA
2014en
ABI

Аннотация

BACKGROUND: Bjerkandera adusta (B. adusta) is one of the most important etiological fungi associated with chronic cough. However, precise details of the inflammatory response to exposure are not well understood yet. B. adusta was recently identified in Asian sand dust (ASD) aerosol. Therefore, in the present study the exacerbating effects of ASD on B. adusta-induced lung inflammation and B. adusta + ASD on ovalbumin (OVA)-induced murine lung eosinophilia were investigated using experimental mice. METHODS: In order to prepare testing samples, B. adusta obtained from ASD aerosol was inactivated by formalin and ASD collected from the atmosphere was heated to remove toxic organic substances (H-ASD). CD-1 mice were instilled intratracheally with 12 different samples prepared with various combinations of B. adusta, H-ASD, and OVA in a normal saline solution. The lung pathology, cytological profiles in bronchoalveolar lavage fluid (BALF), and the levels of inflammatory cytokines/chemokines in BALF were investigated. RESULTS: H-ASD aggravated the lung eosinophilia induced by B. adusta alone, which also aggravated the lung eosinophilia induced by OVA. The mixture of OVA, H-ASD, and B. adusta caused serious fibrous thickening of the subepithelial layer, eosinophil infiltration, and proliferation of goblet cells in the airways along with remarkable increases of IL-13, eotaxin, IL-5, and MCP-3 in BALF. CONCLUSIONS: The results of the present study demonstrated that B. adusta isolated from ASD aerosol induces allergic lung diseases. H-ASD enhanced allergic reactions caused by OVA or B. adusta. A mixture of B. adusta, H-ASD, and OVA caused the most remarkable exacerbation to the allergic airway inflammation via remarkable increases of pro-inflammatory mediators.

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