Exposure of adult mice to environmental tobacco smoke fails to enhance the immune response to inhaled antigen

Kimberly S. Bowles, David W. Horohov, Daniel B. Paulsen, Casey J. LeBlanc, Martha A. Littlefield-Chabaud, Terry Ahlert, Ken Ahlert, Susan S. Pourciau, Arthur Penn

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16 Scopus citations


Epidemiologic evidence supports a role for environmental tobacco smoke (ETS) in the occurrence and severity of allergies/asthma. However, neither the precise combination of ETS and allergen exposure nor the mechanism (or mechanisms) by which these factors interact and contribute to asthma induction is known. Animal model studies have failed to establish a convincing relationship between ETS exposure and asthma induction, perhaps because of methodological inadequacies. Here, we tested the hypothesis that ETS inhalation would provoke an asthmatic response by overcoming normal airway tolerance to inhaled antigens. Our protocol combined daily ETS exposure with nose-only sensitization to ovalbumin. Three strains of mice were tested, each with a different level of susceptibility to airway hypersensitivity. Immunological responses were assessed by immunoglobulin production. Airway inflammation was assessed by bronchoalveolar lavage differentials and lung histopathology. Airway hyperresponsiveness was determined by methacholine challenge. The mice produced ovalbumin-specific antibodies following ovalbumin exposure in a strain-dependent manner. Only the A/J mice produced detectable levels of ovalbumin-specific immunoglobulin (Ig) E. Both A/J and BALB/c mice produced ovalbumin-specific IgG1 antibodies. The C57Bl/6 mice did not produce detectable levels of antibodies. The A/J mice also exhibited airway inflammation following ovalbumin exposure. Neither the C57Bl/6 nor the BALB/c mice exhibited signs of airway inflammation. Exposure to ETS failed to enhance ovalbumin-specific antibody production, airway inflammation, or hyperresponsiveness. Together these results indicate that ETS exposure accompanied by nose-only allergen sensitization fails to overcome aerosol tolerance in adult mice.

Original languageEnglish
Pages (from-to)43-51
Number of pages9
JournalInhalation Toxicology
Issue number1
StatePublished - Jan 2005

Bibliographical note

Funding Information:
Received 28 June 2004; accepted 23 August 2004. This work was supported in part by a grant from the Phillip Morris External Research Program. Address correspondence to David W. Horohov, University of Kentucky, Department of Veterinary Science, Lexington, KY 40546-0099, USA.

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis


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