title: Alcohol reduces airway hyperresponsiveness (AHR) and allergic airway inflammation in mice.
abstract: There is very limited knowledge about the effects of alcohol on airway hyperresponsiveness and inflammation in asthma. Historical accounts of alcohol administration to patients with breathing problems suggest that alcohol may have bronchodilating properties. We hypothesized that alcohol exposure will alter airway hyperresponsiveness (AHR) and pulmonary inflammation in a mouse model of allergic asthma. To test this hypothesis, BALB/c mice were fed either 18% alcohol or water and then sensitized and challenged with ovalbumin (OVA). AHR was assessed by means of ventilation or barometric plethysmography and reported as either total lung resistance or enhanced pause, respectively. Airway inflammation was assessed by total and differential cell counts in bronchoalveolar lavage fluid (BALF), cytokine levels in BALF, lung histology, and serum immunoglobulin E (IgE) levels. Alcohol feeding significantly blocked methacholine-induced increases in AHR compared with water-fed controls. Alcohol feeding significantly reduced total cell numbers (64%) as well as the number of eosinophils (84%) recruited to the lungs of these mice. Modest changes in lung pathology were also observed. Alcohol exposure led to a reduction of IgE in the serum of the EtOH OVA mice. These data demonstrate that alcohol exposure blunts AHR and dampens allergic airway inflammation indices in allergic mice and suggest that there may be an important role for alcohol in the modulation of asthma. These data provide an in vivo basis for previous clinical observations in humans substantiating the bronchodilator properties of alcohol and for the first time demonstrates an alcohol-induced reduction of allergic inflammatory cells in a mouse model of allergic asthma.
authors: Nebraska Medical Center, Univ. of Nebraska Medical Ctr., Omaha, NE 68198-5910, USA.
authors: Peter J
authors: PJ
authors: Oldenburg
authors: Jill A
authors: JA
authors: Poole
authors: Joseph H
authors: JH
authors: Sisson
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001249:Asthma / Q000139:chemically induced* / Q000188:drug therapy / Q000517:prevention & control; D001992:Bronchoalveolar Lavage Fluid; D016084:Bronchoconstriction / Q000187:drug effects; D016085:Bronchoconstrictor Agents / Q000494:pharmacology; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D002452:Cell Count; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D004804:Eosinophils / Q000473:pathology; D000431:Ethanol / Q000494:pharmacology* / Q000627:therapeutic use; D020397:Goblet Cells / Q000187:drug effects / Q000473:pathology; D007073:Immunoglobulin E / Q000097:blood; D007249:Inflammation / Q000139:chemically induced* / Q000188:drug therapy / Q000517:prevention & control; D008168:Lung / Q000187:drug effects / Q000473:pathology*; D008297:Male; D008679:Metaplasia / Q000517:prevention & control; D016210:Methacholine Chloride / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin; D047495:PPAR gamma / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D016085:Bronchoconstrictor Agents; D016207:Cytokines; D047495:PPAR gamma; D016210:Methacholine Chloride; D007073:Immunoglobulin E; D000431:Ethanol; D010047:Ovalbumin; D015740:Calcitonin Gene-Related Peptide