title: Exposure to diesel exhaust exacerbates allergen-induced airway responses in guinea pigs.
abstract: Diesel exhaust (DE) is a major air pollutant in urban areas. To clarify the effects of DE on the exacerbation of asthma, guinea pigs were exposed 12 h daily to 3 mg/m(3) DE or air for 8 wk with or without sensitization to ovalbumin (OVA). In the DE-exposed sensitized animals, both immediate (IAR) and late (LAR) airway responses were enhanced after the inhalation challenge by OVA, compared with the DE-unexposed sensitized animals. Mucus was greatly accumulated in the airways of DE-exposed sensitized animals during IAR. The number of eosinophils and level of sialic acid concentration in bronchial lavage fluids were also significantly higher in the DE-exposed sensitized animals than in the DE-unexposed control animals. During LAR, intercellular spaces of the bronchial epithelium became enlarged in the DE-exposed sensitized animals, showing infiltration by numerous eosinophils. Albumin concentration was significantly higher in the bronchial lavage fluids from the DE-exposed sensitized animals than in those from the DE-unexposed control animals. These results suggest that exposure to DE enhances mucus hypersecretion and eosinophilic inflammation during IAR. DE exposure also increases airway permeability and airway inflammation during LAR. Thus, DE exposure exacerbates allergen-induced airway responses in guinea pigs.
authors.affiliation: Department of Respiratory Medicine, University of Tsukuba, Ibaraki, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hashimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Ishii
authors.forename: Y
authors.initials: Y
authors.lastname: Uchida
authors.forename: T
authors.initials: T
authors.lastname: Kimura
authors.forename: K
authors.initials: K
authors.lastname: Masuyama
authors.forename: Y
authors.initials: Y
authors.lastname: Morishima
authors.forename: K
authors.initials: K
authors.lastname: Hirano
authors.forename: A
authors.initials: A
authors.lastname: Nomura
authors.forename: T
authors.initials: T
authors.lastname: Sakamoto
authors.forename: H
authors.initials: H
authors.lastname: Takano
authors.forename: M
authors.initials: M
authors.lastname: Sagai
authors.forename: K
authors.initials: K
authors.lastname: Sekizawa
mesh_terms: D000485:Allergens / Q000009:adverse effects*; D000704:Analysis of Variance; D000818:Animals; D001249:Asthma / Q000097:blood / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology / Q000276:immunology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology; D005260:Female; D006168:Guinea Pigs; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D007249:Inflammation; D019570:Inhalation Exposure / Q000009:adverse effects*; D007958:Leukocyte Count; D009093:Mucus / Q000502:physiology; D019158:N-Acetylneuraminic Acid / Q000032:analysis; D010047:Ovalbumin / Q000276:immunology; D013997:Time Factors; D001335:Vehicle Emissions / Q000009:adverse effects*
chemical_list: D000485:Allergens; D007074:Immunoglobulin G; D001335:Vehicle Emissions; D007073:Immunoglobulin E; D010047:Ovalbumin; D019158:N-Acetylneuraminic Acid