実験的鼻アレルギーの確立と鼻粘膜におけるβ-Adrenergic Receptorの検討
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The autonomic nervous system as well as the immunological system may contribute to the pathogenesis of nasal allergy. In this study, we established an experimental model of nasal allergy and then examined their immunological processes of the sensitization in them. Additionally, we measured the beta-adrenergic receptor (beta-receptor) densities in nasal mucosa of ovalbumin (OA) sensitized guinea pigs and compaired them with those of histamine(HIS) administered guinea pigs and a normal control group. Both OA sensitized and HIS administered guinea pigs showed similar symptoms with human nasal allergy (sneezing, stiffiness, and hyperrhinorrhea). The symptoms of OA sensitized animals continued longer than those of HIS administered ones. The medians of heatstable PCA (latent period, 4 hrs) titers and heatlabile PCA (latent period, 8 days) titers of 95 OA sensitized guinea pigs were 88.4 and 9.5, respectively. Seventy nine out of 95 (83.2%) in heatstable PCA and 50 out of 95 (52.7%) in heatlabile PCA of sensitized animals represented more than 1:8 PCA titer. Local sensitization in the nasal mucosa was determined by the nasal perfusion method (by Kojima et al.). Following the challenge of OA or rabbit anti-guinea pig IgE, sensitized animals showed a remarkably increased vascular permeability. In passively sensitized animals, similar changes of vascular permeability were also observed following OA challenge. Histologically, we observed numerous infiltrations of eosinophils, desquamation of cilliated epithelium and an edematous change in the nasal mucosa of sensitized guinea pigs. Furthermore, we recognized both IgE and IgGl forming plasma cells just below the nasal epithelium. We classified OA sensitized guinea pigs into 2 groups. Guinea pigs of group A were sacrificed immediately after sensitization and those of group B, 4 weeks later. Maximum binding (Bmax) of mucosal membrane preparation with 3H-DHA were 102±19.8, 121±25.6, 113±32.6, 132±22.4 and 13±22.3 (fmol/mg protein) in OA sensitized group A, group B, HIS group, saline nebulizer group and the normal controls, respectively. Decrease of Bmax in group A was statistically significant to those in group B (p<0.05), the saline nebulizer group (p<0.01) and normal controls (p<0.01). There were no statistically significant correlations between the Bmax and IgE or IgGl PCA titers. Furthermore the Bmax of HIS group was decreased in comparison with the normal controls. Affinity of beta-receptor was not changed in each group. These results indicated the beta-adrenergic dysfunction in nasal allergy is not congenital, but secondarily acquired by an allergic reaction. Immunological aspects cannot be thoroughly explained by beta-adrenergic hyporesponsiveness in experimental animals and further studies are needed.
- 札幌医科大学の論文
- 1986-04-01
札幌医科大学 | 論文
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