MECHANISMS INVOLVED IN HELICOBACTER-PYLORI-INDUCED INFLAMMATION
MECHANISMS INVOLVED IN HELICOBACTER-PYLORI-INDUCED INFLAMMATION
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DOI：
10.1016/0016-5085(93)90148-6
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发表时间：
1993-11-01
期刊：
影响因子：
29.4
通讯作者：
KVIETYS, PR
中科院分区：
文献类型：
--
作者：
YOSHIDA, N;GRANGER, DN;KVIETYS, PR
背景：幽门螺杆菌感染与粘膜炎症有关。本研究的目的是评估幽门螺杆菌水提取物是否促进中性粒细胞（多形核白细胞[PMN]）粘附内皮细胞，并确定这种粘附相互作用的分子基础。方法：采用活体显微镜观察大鼠肠系膜小静脉内白细胞黏附相互作用。利用人脐静脉内皮细胞（HUVEC）单层膜与pmn细胞进行了体外粘附相互作用的研究。结果：在体内，幽门螺杆菌提取物在大鼠肠系膜内的灌注增加了小静脉内白细胞的粘附和迁移。在体外，幽门螺杆菌提取物以浓度依赖性的方式增加了人PMNs对HUVEC的粘附。单独使用幽门螺杆菌提取物预处理HUVEC对PMN的粘附性没有影响，而单独使用PMN预处理可显著增加HUVEC的粘附性。针对中性粒细胞的CD11a、CD11b或CD18的单克隆抗体（MAb）和针对内皮细胞的细胞间粘附分子-1 （ICAM-1）的单克隆抗体（MAb）显著降低了提取物诱导的粘附，但e-或p -选择素没有作用。结论：这些研究表明，幽门螺杆菌产物通过与ICAM-1的CD11a/ cd18和CD11b/ cd18依赖性相互作用促进PMN粘附内皮细胞，从而引发胃肠道炎症。
Background: Helicobacter pylori infection is associated with mucosal inflammation. The aims of the present study were to assess whether a water extract of H. pylori promotes neutrophil (polymorphonuclear leukocyte [PMN]) adherence to endothelial cells and define the molecular basis of this adhesive interaction. Methods: Intravital microscopy was used to study leukocyte adhesive interactions in rat mesenteric venules in situ. PMN-endothelial cell adhesive interactions were studied in vitro using human PMNs and monolayers of human umbilical vein endothelial cells (HUVEC). Results: In vivo, superfusion of rat mesentery with the H. pylori extract increased leukocyte adhesion and emigration in venules. In vitro, adhesion of human PMNs to HUVEC was increased by the H. pylori extract in a concentration-dependent manner. Pretreatment of HUVEC alone with H. pylori extract had no effect on PMN adherence, whereas pretreatment of PMN alone significantly increased their adherence to HUVEC. The extract-induced adhesion was significantly diminished by monoclonal antibodies (MAb) directed against either CD11a, CD11b, or CD18 on neutrophils, and by MAbs against intercellular adhesion molecule-1 (ICAM-1), but not E-or P-selectin, on endothelial cells. Conclusions: These studies suggest that products of H. pylori elicit gastrointestinal inflammation by promoting PMN adhesion to endothelial cells via CD11a/CD18-and CD11b/CD18-dependent interactions with ICAM-1.