Immunohistochemical study of E-cadherin and ZO-1 in allergic nasal epithelium of the guinea pig
Immunohistochemical study of E-cadherin and ZO-1 in allergic nasal epithelium of the guinea pig
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DOI：
10.1159/000023945
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发表时间：
1998-07-01
影响因子：
2.8
通讯作者：
Konno, A
中科院分区：
文献类型：
--
作者：
Kobayashi, N;Dezawa, M;Konno, A
本实验采用卵清蛋白（ovalbumin，OA）致敏豚鼠鼻变态反应模型，通过观察细胞粘附分子E-cadherin和紧密连接蛋白ZO-1在鼻粘膜中的分布，探讨了过敏性炎症对鼻粘膜上皮细胞的损伤。在对照上皮，E-钙粘蛋白免疫反应连续沿着相邻上皮细胞边界检测。ZO-1斑点样免疫反应检测在对应于紧密连接（TJ）位置的上皮细胞的顶侧部分，但没有发现对照和挑战上皮细胞之间的免疫反应性的变化。在致敏动物的激发上皮中，同时观察到显著的嗜酸性粒细胞浸润和结构变化，如细胞间隙变宽和相邻上皮细胞脱离。另外。在上皮中观察到E-钙粘蛋白免疫反应性阴性的斑点，与嗜酸性粒细胞颗粒蛋白的细胞外沉积有关。免疫电镜显示E-钙粘蛋白免疫反应性的减少或消失，这不仅发生在细胞间隙宽和相邻的上皮细胞分离的区域，而且在浸润性嗜酸性粒细胞和上皮细胞之间的接触点。约87%的嗜酸性粒细胞中观察到的挑战上皮细胞与这种损失的E-钙粘蛋白免疫反应性。这些结果表明，密切的上皮细胞接触介导的E-钙粘蛋白松动的嗜酸性粒细胞浸润的结果，这可能会触发随后的上皮细胞在过敏状态下破坏的初始步骤。
Nasal epithelial damage during allergic inflammation was studied by observing the distribution of cell adhesion molecule E-cadherin and tight junction (zonula occludens) cell-cell contact associated protein ZO-1, The guinea pig model of nasal allergy, sensitized with intraperitoneally administered ovalbumin (OA) and subsequently challenged with OA intranasally, was used. In control epithelium, E-cadherin immunoreactivity was detected continuously along neighboring epithelial cell borders. ZO-1 spot-like immunoreactivity was detected in the apicolateral portion of epithelial cells corresponding to the tight junction (TJ) position, but no changes in immunoreactivity were found between control and challenged epithelia. In the challenged epithelium of sensitized animals, marked infiltration eosinophils and structural changes, such as widening of the intercellular spaces and detachment of adjacent epithelial cells, were observed concurrently. In addition. spots negative for E-cadherin immunoreactivity were noted in the epithelium, associated with the extracellular deposition of eosinophil granule proteins. Immunoelectron microscopy revealed a decrease or disappearance of E-cadherin immunoreactivity, which took place not only in regions where intercellular spaces were wide and adjacent epithelial cells were detached, but also at the point of contact between infiltrating eosinophils and epithelial cells. Approximately 87% of eosinophils observed in the challenged epithelium were associated with such loss of E-cadherin immunoreactivity. These results suggest that the intimate epithelial cell contact mediated by E-cadherin is loosened as a consequence of eosinophil infiltration, which may trigger the initial step of subsequent epithelial destruction in allergic states.