Ozone increases airway hyperreactivity and mucus hyperproduction in mice previously exposed to allergen
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Ozone increases airway hyperreactivity and mucus hyperproduction in mice previously exposed to allergen. / Larsen, Søren T; Matsubara, Shigeki; McConville, Glen; Poulsen, Steen Seier; Gelfand, Erwin W.
In: Journal of Toxicology and Environmental Health. Part A, Vol. 73, No. 11, 01.01.2010, p. 738-47.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Ozone increases airway hyperreactivity and mucus hyperproduction in mice previously exposed to allergen
AU - Larsen, Søren T
AU - Matsubara, Shigeki
AU - McConville, Glen
AU - Poulsen, Steen Seier
AU - Gelfand, Erwin W
PY - 2010/1/1
Y1 - 2010/1/1
N2 - Acute exacerbations of asthma represent a common clinical problem with major economic impact. Air pollutants including ozone have been shown to contribute to asthma exacerbation, but the mechanisms underlying ozone-induced asthma exacerbation are only partially understood. The present study aimed to develop a mouse model to gain insight into the development of airway hyperresponsiveness (AHR) to methacholine (MCh) in mice after exposure to both allergen and ozone. Mice were exposed for 20 min per day for 10 consecutive days to an aerosol of 1% ovalbumin (OVA) or saline followed by a single 3-h exposure to clean air or 100, 250, or 500 ppb ozone. Ozone induced AHR in mice previously exposed to OVA when compared to non-exposed (saline) control mice. After a 10-d exposure to OVA, a single exposure to a low (100 ppb) ozone concentration was sufficient to induce AHR. The AHR response was associated with goblet-cell metaplasia. Even the lowest concentration of ozone tested, 100 ppb, which may be exceeded in urban environments and in the workplace, resulted in a significant increase in AHR, most prominent 24 h after exposure in the OVA-exposed mice.
AB - Acute exacerbations of asthma represent a common clinical problem with major economic impact. Air pollutants including ozone have been shown to contribute to asthma exacerbation, but the mechanisms underlying ozone-induced asthma exacerbation are only partially understood. The present study aimed to develop a mouse model to gain insight into the development of airway hyperresponsiveness (AHR) to methacholine (MCh) in mice after exposure to both allergen and ozone. Mice were exposed for 20 min per day for 10 consecutive days to an aerosol of 1% ovalbumin (OVA) or saline followed by a single 3-h exposure to clean air or 100, 250, or 500 ppb ozone. Ozone induced AHR in mice previously exposed to OVA when compared to non-exposed (saline) control mice. After a 10-d exposure to OVA, a single exposure to a low (100 ppb) ozone concentration was sufficient to induce AHR. The AHR response was associated with goblet-cell metaplasia. Even the lowest concentration of ozone tested, 100 ppb, which may be exceeded in urban environments and in the workplace, resulted in a significant increase in AHR, most prominent 24 h after exposure in the OVA-exposed mice.
KW - Air Pollutants
KW - Allergens
KW - Animals
KW - Asthma
KW - Biological Markers
KW - Bronchial Hyperreactivity
KW - Bronchoalveolar Lavage Fluid
KW - Disease Models, Animal
KW - Drug Interactions
KW - Inhalation Exposure
KW - Leukocyte Count
KW - Leukocytes
KW - Lung
KW - Methacholine Chloride
KW - Mice
KW - Mucus
KW - Ovalbumin
KW - Ozone
KW - Periodic Acid-Schiff Reaction
KW - Respiratory Function Tests
U2 - 10.1080/15287391003614034
DO - 10.1080/15287391003614034
M3 - Journal article
C2 - 20391116
VL - 73
SP - 738
EP - 747
JO - Journal of Toxicology and Environmental Health. Part A: Current Issues
JF - Journal of Toxicology and Environmental Health. Part A: Current Issues
SN - 1528-7394
IS - 11
ER -
ID: 33792584