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猪链球菌2型刺激后人THP-1单核细胞上ICAM-1、CD11a/CD18和CD11c/CD18的上调

Up-regulation of ICAM-1, CD11a/CD18 and CD11c/CD18 on human THP-1 monocytes stimulated by Streptococcus suis serotype 2.

作者信息

Al-Numani D, Segura M, Doré M, Gottschalk M

机构信息

Groupe de Recherche sur les Maladies Infectieuses du Porc (GREMIP), Faculté de médecine vétérinaire, Université de Montréal, St-Hyacinthe, Québec, Canada.

出版信息

Clin Exp Immunol. 2003 Jul;133(1):67-77. doi: 10.1046/j.1365-2249.2003.02189.x.

Abstract

Streptococcus suis serotype 2 is known to be a major pathogen of swine, causing mainly meningitis. It is also a zoonotic agent leading predominantly to meningitis in humans working in close contact with pigs. In this study, we investigated the ability of S. suis to up-regulate the expression of adhesion molecules involved in inflammation, using an enzyme-linked immunosorbent assay. S. suis serotype 2 stimulated the up-regulation of the expression of intercellular adhesion molecule-1 (ICAM-1, CD54), CD11a/CD18 and CD11c/CD18 on human THP-1 monocytes, but did not change that of ICAM-1, vascular cell adhesion molecule-1 (VCAM-1, CD106) and E-selectin (CD62E) on human endothelial cells. The up-regulation of adhesion molecules was time- and bacterial concentration-dependent, and cell wall components were largely responsible for such stimulation. To a lesser extent, purified haemolysin of S. suis also stimulated adhesion molecule expression. Stimulation of monocytes with strains of different origin showed that there was no clear tendency for human strains to induce a higher expression of adhesion molecules than strains from diseased pigs. Finally, monocytes stimulated with S. suis also showed an increase in adherence to endothelial cells. Hence, S. suis is capable of up-regulating important adhesion molecules involved in inflammation, which may result in an increased leucocyte recruitment into sites of infection, thus providing a possible mechanism for some of the inflammatory features of meningitis caused by this pathogen.

摘要

猪链球菌2型是猪的主要病原体,主要引起脑膜炎。它也是一种人畜共患病原体,主要导致与猪密切接触的人类患脑膜炎。在本研究中,我们使用酶联免疫吸附测定法研究了猪链球菌上调参与炎症的粘附分子表达的能力。猪链球菌2型刺激人THP-1单核细胞上细胞间粘附分子-1(ICAM-1,CD54)、CD11a/CD18和CD11c/CD18的表达上调,但对人内皮细胞上ICAM-1、血管细胞粘附分子-1(VCAM-1,CD106)和E-选择素(CD62E)的表达没有影响。粘附分子的上调具有时间和细菌浓度依赖性,细胞壁成分在很大程度上负责这种刺激。在较小程度上,猪链球菌的纯化溶血素也刺激粘附分子表达。用不同来源的菌株刺激单核细胞表明,人源菌株诱导粘附分子表达高于患病猪源菌株没有明显趋势。最后,用猪链球菌刺激的单核细胞对内皮细胞的粘附也增加。因此,猪链球菌能够上调参与炎症的重要粘附分子,这可能导致白细胞向感染部位募集增加,从而为该病原体引起的脑膜炎的一些炎症特征提供了一种可能的机制。

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