• Motohiro Kodama, Koichiro Asano, Tsuyoshi Oguma, Shizuko Kagawa, Katsuyoshi Tomomatsu, Misa Wakaki, Takahisa Takihara, Soichiro Ueda, Nao Ohmori, Hiromi Ogura, Jun Miyata, Kyuto Tanaka, Nobufumi Kamiishi, Koichi Fukunaga, Koichi Sayama, Eiji Ikeda, Taku Miyasho, and Akitoshi Ishizaka.
• Division of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
• Int. Arch. Allergy Immunol. 2010 Jan 1; 152 Suppl 1: 67-74.

BackgroundAllergen 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.MethodsBALB/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.ResultsThe 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.ConclusionsThe 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.(c) 2010 S. Karger AG, Basel.

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