Exposure of pregnant mice to an air pollutant aerosol increases asthma susceptibility in offspring.
Air pollution contributes to both exacerbation and development of bronchial asthma. Studies showed that coexposure to air pollution directly promotes sensitization to inhaled allergen in neonatal mice. The aim of this study was to investigate whether prenatal exposure to air pollution could also increase susceptibility to development of asthma in early life. Pregnant female BALB/c mice were exposed to aerosolized leachate of residual oil fly ash (ROFA, 50 mg/ml, 30 min) at 5, 3, and 1 d before delivery. Offspring were treated once at 3 d of age with ovalbumin (OVA, 5 mug) and alum (ip), an intentionally suboptimal dose for sensitization, exposed to aerosolized OVA (1%, 10 min) at 12-14 d or 32-35 d of age, and evaluated 2 d after the final exposure. The offspring of ROFA-exposed mothers (ROFA group) revealed increasing airway hyperresponsiveness (higher enhanced pause [Penh] to methacholine challenge) and elevated substantial numbers of eosinophils in the bronchoalveolar lavage flued (BALF). Histopathology revealed prominent inflammation in the lungs of ROFA group and showed increased allergen-specific IgE and IgG1 levels. Their cultured splenocytes showed an enhanced interleukin (IL)-4/interferon (IFN)-gamma cytokine, indicating Th2 skewed immunity. Data indicate that exposure of pregnant female mice to an air pollutant aerosol increased asthma susceptibility in their offspring.
Hamada
Kaoru
K
Department of Internal Medicine II, Nara Medical University, Kashihara, Nara, Japan. khamada@naramed-u.ac.jp
Suzaki
Yasue
Y
Leme
Adriana
A
Ito
Toshihiro
T
Miyamoto
Kenichi
K
Kobzik
Lester
L
Kimura
Hiroshi
H
D000280:Administration, Inhalation; D000336:Aerosols; D000393:Air Pollutants / Q000633:toxicity*; D000485:Allergens / Q000633:toxicity*; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000139:chemically induced / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D016085:Bronchoconstrictor Agents; D002244:Carbon / Q000633:toxicity*; D002478:Cells, Cultured; D060729:Coal Ash; D004198:Disease Susceptibility / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D004804:Eosinophils / Q000187:drug effects / Q000473:pathology; D005260:Female; D007073:Immunoglobulin E / Q000378:metabolism; D007074:Immunoglobulin G / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D016210:Methacholine Chloride; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D052638:Particulate Matter / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012130:Respiratory Hypersensitivity / Q000139:chemically induced* / Q000276:immunology; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000276:immunology / Q000378:metabolism
D000336:Aerosols; D000393:Air Pollutants; D000485:Allergens; D016085:Bronchoconstrictor Agents; D060729:Coal Ash; D007074:Immunoglobulin G; D052638:Particulate Matter; D016210:Methacholine Chloride; D007073:Immunoglobulin E; D002244:Carbon; D010047:Ovalbumin