NASAL CHALLENGE WITH ALLERGEN UP-REGULATES THE LOCAL EXPRESSION OF VASCULAR ENDOTHELIAL ADHESION MOLECULES

NASAL CHALLENGE WITH ALLERGEN UP-REGULATES THE LOCAL EXPRESSION OF VASCULAR ENDOTHELIAL ADHESION MOLECULES
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DOI:
10.1016/0091-6749(94)90119-8
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发表时间:
1994-12-01
影响因子:
14.2
通讯作者:
BAROODY, FM
BAROODY, FM
中科院分区:
医学1区
文献类型:
--
作者:
LEE, BJ;NACLERIO, RM;BAROODY, FM

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为了了解选择性嗜酸性粒细胞迁移到过敏性炎症部位的事件,我们研究了鼻粘膜血管内皮粘附分子的表达。10例无症状的季节性变应性鼻炎患者和13例非变应性鼻炎患者接受了单侧下鼻甲局部过敏原激发试验。24小时后;从季节性过敏受试者的双侧和非过敏对照受试者的单侧下鼻甲获得活检标本。将标本分开,切片,染色鉴定嗜酸性粒细胞或化学分析细胞间粘附分子-1,E-选择素,血管细胞粘附分子-1(VCAM-1)和血管性血友病因子。所有粘膜标本中均观察到细胞间粘附分子-1表达,组间无显著差异。E-选择素显示最小的基线表达,并且与非过敏受试者相比,在过敏受试者的激发粘膜上显著诱导低水平(p < 0.05)。VCAM-2在基底表达,并且与未激发侧和非过敏对照受试者相比,通过过敏原激发显著上调(p < 0.05)。与非过敏性对照组相比,过敏性受试者抗原激发后24小时粘膜下嗜酸性粒细胞显著增加,与VCAM-1表达弱相关(r(s)= 0.33,p = 0.06)。我们的研究结果表明,内皮细胞活化伴随过敏性炎症。此外,因为VCAM-1的反配体,极晚期活化抗原-4,存在于嗜酸性粒细胞上,VCAM-1上调可能有助于这些细胞选择性募集到鼻粘膜。
To understand the events involved in selective eosinophil migration into allergic inflammatory sites, we studied the expression of vascular endothelial adhesion molecules in the nasal mucosa. Ten subjects with asymptomatic seasonal allergic rhinitis and 13 nonallergic subjects underwent localized allergen challenge of one inferior turbinate. Twenty-four hours later; biopsy specimens were obtained from the inferior turbinates, bilaterally in the seasonally allergic subjects and unilaterally in the nonallergic control subjects. The specimens were divided, sectioned, and either stained for identification of eosinophils or analyzed immunohistochemically for intercellularlar adhesion molecule-1, E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and von Willebrand's factor. Intercellular adhesion molecule-1 expression was observed in all mucosal specimens, with no significant difference among groups. E-selectin showed minimal baseline expression, and low levels were significantly induced on the challenged mucosa of the allergic compared with nonallergic subjects (p < 0.05). VCAM-2 was expressed basally and was significantly upregulated by allergen challenge compared with the nonchallenged side and nonallergic control subjects (p < 0.05). Submucosal eosinophils increased significantly in allergic subjects 24 hours after antigen challenge, compared with nonallergic control subjects and weakly correlated with VCAM-1 expression (r(s) = 0.33, p = 0.06). Our results suggest that endothelial activation accompanies allergic inflammation. Furthermore because the counter ligand for VCAM-1, very late activation antigen-4, is present on eosinophils, VCAM-1 upregulation may contribute to the selective recruitment of these cells to the nasal mucosa.