title: Diesel exhaust particle-induced airway responses are augmented in obese rats.
abstract: Air pollutants and obesity are important factors that contribute to asthma. The aim of this study was to assess the airway responsiveness and inflammation in Otsuka-Long Evans Tokushima Fatty (OLETF) obese rats and Long Evans Tokushima-Otsuka (LETO) nonobese rats exposed to diesel exhaust particles (DEPs). Otsuka Long Evans Tokushima fatty rats and LETO rats were exposed intranasally to DEP and then challenged with aerosolized DEP on days 6 to 8. Body plethysmography, bronchoalveolar lavage (BAL), and histology were performed. Enhanced pause (Penh) was measured as an indicator of airway resistance on day 9 and samples were collected on day 10. After exposure to DEP, the OLETF group exhibited a greater increase in Penh compared to that in the LETO group. Moreover, the BAL fluid in mice showed an increase in the total and differential cell counts in the DEP-exposed OLETF group compared to that in the DEP-exposed LETO group. Histological assessment of lung tissue from each group revealed that the DEP-exposed OLETF group tended to have increased inflammatory cell infiltrations in the prebronchial area. Increased peroxisome proliferator-activated receptor γ, coactivator 1β messenger RNA was observed in the lungs of obese rats compared to that in nonobese rats following DEP exposure. These data indicate that the DEP-exposed OLETF group had increased airway responses and inflammation compared to the DEP-exposed LETO group, indicating that diesel particulates and obesity may be co-contributors to asthma.
authors.affiliation: Department of Internal Medicine, Division of Allergy and Respiratory Diseases, Soonchunhyang University Hospital, 170 Jomaru-ro, Wonmi-gu, Bucheon, Gyeonggi-Do, 420-767, Republic of Korea. Email: jas877@schmc.ac.kr.
authors.forename: Kuk-Young
authors.initials: KY
authors.lastname: Moon
authors.forename: Moo-Kyun
authors.initials: MK
authors.lastname: Park
authors.forename: George D
authors.initials: GD
authors.lastname: Leikauf
authors.forename: Choon-Sik
authors.initials: CS
authors.lastname: Park
authors.forename: An-Soo
authors.initials: AS
authors.lastname: Jang
mesh_terms: D000403:Airway Resistance / Q000187:drug effects*; D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000209:etiology*; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology / Q000276:immunology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009765:Obesity / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D052638:Particulate Matter / Q000633:toxicity*; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D010993:Plethysmography, Whole Body; D051381:Rats; D020334:Rats, Inbred OLETF; D020318:Rats, Long-Evans; D020545:Respiratory Mucosa / Q000187:drug effects* / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D013047:Specific Pathogen-Free Organisms; D014157:Transcription Factors / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects*; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D052638:Particulate Matter; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; C501429:Ppargc1a protein, rat; D014157:Transcription Factors; D001335:Vehicle Emissions
keywords: air pollution; asthma; obesity