Strain-Specific Phenotypes of Airway Inflammation and Bronchial Hyperresponsiveness Induced by Epicutaneous Allergen Sensitization in BALB/c and C57BL/6 MiceKodama M. · Asano K. · Oguma T. · Kagawa S. · Tomomatsu K. · Wakaki M. · Takihara T. · Ueda S. · Ohmori N. · Ogura H. · Miyata J. · Tanaka K. · Kamiishi N. · Fukunaga K. · Sayama K. · Ikeda E. · Miyasho T. · Ishizaka A.
aDivision of Pulmonary Medicine, Department of Medicine, and bDepartment of Pathology, Keio University School of Medicine, Tokyo, and cLaboratory of Veterinary Biochemistry, Rakuno Gakuen University, Ebetsu, Japan
Background: Allergen sensitization through a disrupted skin barrier appears to play a prominent role in the development of atopic diseases, including allergic asthma. The role of the genetic background in immunological and physiological phenotypes induced by epicutaneous sensitization is undetermined. Methods: BALB/c and C57BL/6 mice were sensitized either epicutaneously by patch application of ovalbumin (OVA) or systemically by intraperitoneal injection of OVA with alum before exposure to aerosolized OVA. The concentrations of OVA-specific immunoglobulin in serum and cytokines in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay. The severity of airway inflammation was evaluated by cell counts in BALF, and bronchial responsiveness to methacholine was measured by the flexiVent system. Results: The production of OVA-specific IgG1 and IgE was greater in the epicutaneously sensitized BALB/c than C57BL/6 mice. In contrast, both eosinophilic airway inflammation and bronchial responsiveness to methacholine were more prominent in the C57BL/6 than in the BALB/c mice. The concentrations of interleukin-4 increased significantly in the BALF from C57BL/6 mice only. No between-strain differences were observed after intraperitoneal sensitization. Conclusions: The C57BL/6 mouse is a more appropriate model than the BALB/c mouse to study the relationship between skin barrier dysfunction and the pathogenesis of allergic asthma.
Correspondence to: Dr. Koichiro Asano
Division of Pulmonary Medicine, Department of Medicine
Keio University School of Medicine
35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582 (Japan)
Tel. +81 3 3353 1211, Fax +81 3 3353 2502, E-Mail firstname.lastname@example.org
Published online: June 4, 2010
Number of Print Pages : 8
Number of Figures : 4, Number of Tables : 0, Number of References : 18
International Archives of Allergy and Immunology
Vol. 152, No. Suppl. 1, Year 2010 (Cover Date: June 2010)
Journal Editor: Valenta R. (Vienna)
ISSN: 1018-2438 (Print), eISSN: 1423-0097 (Online)
For additional information: http://www.karger.com/IAA