Streptococcus suis stimulates ICAM-1 shedding from microvascular endothelial cells
Streptococcus suis stimulates ICAM-1 shedding from microvascular endothelial cells
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DOI：
10.1111/j.1574-695x.2008.00476.x
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发表时间：
2008-11-01
影响因子：
--
通讯作者：
Bodet, Charles
中科院分区：
文献类型：
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作者：
Grenier, Daniel;Bodet, Charles
在这项研究中，我们假设，猪链球菌诱导脱落的粘附分子从人脑微血管内皮细胞（HBMEC）的表面，这可能有助于正在进行的病理生理过程的脑膜炎。当用S.在S735细胞中，可溶性细胞间粘附分子-1（sICAM-1）的分泌量显著增加，而可溶性E-钙粘蛋白和P-选择素的分泌量基本不变。在感染复数为1和10时，S. suis使sICAM-1浓度分别增加3.5倍和5倍。一株S. suis比亲本菌株诱导更多的脱落。此外，S.猪细胞壁制剂剂量依赖性地刺激ICAM-1脱落。酪氨酸激酶、丝裂原活化细胞外激酶1、2和c-JUN N-末端激酶的特异性抑制剂显著降低S。猪介导的ICAM-1释放。ICAM-1脱落也被基质金属蛋白酶的特异性抑制剂抑制。S.猪诱导ICAM-1脱落具有许多功能意义，可能有助于脑膜炎的病理生理过程。
In this study, we hypothesized that Streptococcus suis induces the shedding of adhesion molecules from the surface of human brain microvascular endothelial cells (HBMEC), which may contribute to the ongoing pathophysiological processes of meningitis. When HBMEC were stimulated with whole cells of S. suis S735, significantly larger amounts of soluble intercellular adhesion molecule-1 (sICAM-1) were shed into conditioned medium while basal levels of soluble E-cadherin and P-selectin were unaffected. At a multiplicity of infection of 1 and 10, S. suis increased the concentration of sICAM-1 3.5- and 5-fold, respectively. A capsule-deficient mutant of S. suis induced more shedding than the parental strain. In addition, an S. suis cell wall preparation dose-dependently stimulated ICAM-1 shedding. Specific inhibitors of tyrosine kinase, mitogen-activated extracellular kinase 1, 2, and c-JUN N-terminal kinase significantly reduced S. suis-mediated ICAM-1 release. ICAM-1 shedding was also inhibited by a specific inhibitor of matrix metalloproteinases. The capacity of S. suis to induce ICAM-1 shedding has many functional implications that may contribute to the pathophysiological process of meningitis.