title: Deficiency of tenascin C attenuates allergen-induced bronchial asthma in the mouse.
abstract: Tenascin C (TN-C) is an extracellular matrix glycoprotein whose expression is increased in several inflammatory diseases of the lung, including bronchial asthma. However, the exact function of TN-C in the pathogenesis of lung inflammation remains unclear. In the present study, we compared the degree of bronchial asthma in wild-type and TN-C-deficient (-/-) BALB/c mice. Bronchial asthma was induced by sensitization and challenge with ovalbumin. Littermates treated with saline were used as controls. Cytokines in bronchoalveolar lavage fluid and plasma were measured by enzyme immunoassays. The number of eosinophils in the lung was significantly increased in wild-type mice compared with TN-C-knockout mice. Airway hyperreactivity, NF-kappaB activation and concentrations of monocyte chemoattractant protein-1, IL-5, IL-13, metalloproteinase-9 and immunoglobulin-E in the bronchoalveolar lavage fluid were significantly decreased in ovalbumin-sensitized/challenged TN-C-knockout mice compared with their wild-type counterparts. In vitro experiments disclosed that TN-C significantly stimulates the secretion of IL-5, IL-13, IFN-gamma and immunoglobulin-E from spleen lymphocytes. These observations suggest that TN-C is involved in the pathogenesis of bronchial asthma.
authors.affiliation: Department of Pulmonary and Critical Care Medicine, Mie University Graduate School of Medicine, Tsu-city, Japan.
authors.forename: Hiroki
authors.initials: H
authors.lastname: Nakahara
authors.forename: Esteban C
authors.initials: EC
authors.lastname: Gabazza
authors.forename: Hajime
authors.initials: H
authors.lastname: Fujimoto
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Nishii
authors.forename: Corina N
authors.initials: CN
authors.lastname: D'Alessandro-Gabazza
authors.forename: Nelson E
authors.initials: NE
authors.lastname: Bruno
authors.forename: Takehiro
authors.initials: T
authors.lastname: Takagi
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Hayashi
authors.forename: Junko
authors.initials: J
authors.lastname: Maruyama
authors.forename: Kazuo
authors.initials: K
authors.lastname: Maruyama
authors.forename: Kyoko
authors.initials: K
authors.lastname: Imanaka-Yoshida
authors.forename: Koji
authors.initials: K
authors.lastname: Suzuki
authors.forename: Toshimichi
authors.initials: T
authors.lastname: Yoshida
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Adachi
authors.forename: Osamu
authors.initials: O
authors.lastname: Taguchi
mesh_terms: D000485:Allergens / Q000008:administration & dosage* / Q000276:immunology*; D000818:Animals; D001249:Asthma / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D008168:Lung / Q000276:immunology / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D019063:Tenascin / Q000172:deficiency* / Q000235:genetics* / Q000502:physiology; D018418:Th2 Cells / Q000378:metabolism
chemical_list: D000485:Allergens; D016207:Cytokines; D019063:Tenascin; D010047:Ovalbumin