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Strain-Specific Phenotypes of Airway Inflammation and Bronchial Hyperresponsiveness Induced by Epicutaneous Allergen Sensitization in BALB/c and C57BL/6 MiceKodama M.a · Asano K.a · Oguma T.a · Kagawa S.a · Tomomatsu K.a · Wakaki M.a · Takihara T.a · Ueda S.a · Ohmori N.a · Ogura H.a · Miyata J.a · Tanaka K.a · Kamiishi N.a · Fukunaga K.a · Sayama K.a · Ikeda E.b · Miyasho T.c · Ishizaka A.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.
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