Cell adhesion molecule expression in coronary artery aneurysms in acute Kawasaki disease
Cell adhesion molecule expression in coronary artery aneurysms in acute Kawasaki disease
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DOI：
10.1097/01.inf.0000142171.91235.fc
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发表时间：
2004-10-01
影响因子：
3.6
通讯作者：
Rowley, AH
中科院分区：
文献类型：
--
作者：
Miura, M;Garcia, FL;Rowley, AH
背景：急性川崎病（KD）冠状动脉瘤（CAA）形成的发病机制尚不清楚。细胞粘附分子介导细胞-细胞和细胞-基质相互作用，调节白细胞迁移、血管生成和组织重塑。我们假设细胞粘附分子在急性KD - CAA中表达。方法：在6例急性KD患者和7例对照组冠状动脉中免疫定位p -选择素、e-选择素、血管细胞粘附分子-1 （VCAM-1）和整合素β(1)。结果：6例患者KD - CAA外血管内皮细胞均表达p -选择素和整合素β(1)， 4例患者表达e -选择素和/或VCAM-1。对照组和非动脉瘤性KD冠状动脉内皮细胞表达p -选择素和整合素β(1)，但不表达e -选择素或VCAM-1。整合素β(1)在6个KD CAA中的5个浸润性白细胞上表达，在6个成纤维细胞上表达；在对照组和非动脉瘤性KD冠状动脉中没有这些发现。结论：急性KD冠状动脉内皮细胞缺乏e -选择素或VCAM-1的广泛表达令人惊讶，这表明炎症细胞浸润到KD冠状动脉并不仅仅是循环细胞因子广泛上调内皮细胞粘附分子的结果。更确切地说，炎症细胞可能被一种引起KD的病原体定向到冠状动脉的特定区域。我们的研究结果表明，e -选择素和VCAM-1在新生血管中的表达可能有助于新生血管生成和延长CAA炎症，整合素β(1)可能参与急性KD CAA的成纤维细胞重塑。
Background: The pathogenesis of coronary artery aneurysm (CAA) formation in acute Kawasaki disease (KD) remains unclear. Cell adhesion molecules mediate cell-cell and cell-matrix interactions and regulate leukocyte migration, angiogenesis and tissue remodeling. We hypothesized that cell adhesion molecules are expressed in acute KD CAA.Methods: P-selectin, E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and integrin beta(1) were immunolocalized in coronary arteries from 6 acute KD patients and 7 controls.Results: In endothelial cells of adventitial neovasculature in KD CAA, P-selectin and integrin beta(1) were expressed in all of 6 patients, and E-selectin and/or VCAM-1 were expressed in 4 of 6. Endothelial cells in controls and in nonaneurysmal KD coronary arteries expressed P-selectin and integrin beta(1), but not E-selectin or VCAM-1. Integrin beta(1) was expressed on infiltrating leukocytes in 5 of 6 KD CAA and on fibroblasts in 6 of 6; these findings were absent in controls and in nonaneurysmal KD coronary arteries.Conclusions: The lack of widespread expression of E-selectin or VCAM-1 on endothelial cells of acute KD coronary arteries was surprising and suggests that inflammatory cell infiltration into KD coronaries is not simply the result of widespread up-regulation of cell adhesion molecules on endothelial cells by circulating cytokines. Rather, inflammatory cells may be directed to specific areas of the coronary arteries targeted by a pathogen causing KD. Our results suggest that E-selectin and VCAM-1 expression on neovasculature may contribute to neoangiogenesis and prolonged CAA inflammation and that integrin beta(1) might be involved in fibroblastic remodeling of acute KD CAA.