Yoshida N, Granger D N, Evans D J, Evans D G, Graham D Y, Anderson D C, Wolf R E, Kvietys P R
Department of Physiology, Louisiana State University Medical Center, Shreveport.
Gastroenterology. 1993 Nov;105(5):1431-40. doi: 10.1016/0016-5085(93)90148-6.
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.
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).
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.
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.
幽门螺杆菌感染与黏膜炎症相关。本研究的目的是评估幽门螺杆菌水提取物是否能促进中性粒细胞（多形核白细胞[PMN]）与内皮细胞的黏附，并确定这种黏附相互作用的分子基础。
采用活体显微镜原位研究大鼠肠系膜小静脉中的白细胞黏附相互作用。使用人PMN和人脐静脉内皮细胞（HUVEC）单层在体外研究PMN-内皮细胞黏附相互作用。
在体内，用幽门螺杆菌提取物灌注大鼠肠系膜可增加小静脉中的白细胞黏附和迁移。在体外，幽门螺杆菌提取物以浓度依赖的方式增加人PMN与HUVEC的黏附。单独用幽门螺杆菌提取物预处理HUVEC对PMN黏附无影响，而单独预处理PMN则显著增加其与HUVEC的黏附。针对中性粒细胞上的CD11a、CD11b或CD18的单克隆抗体（MAb）以及针对内皮细胞上的细胞间黏附分子-1（ICAM-1）而非E或P选择素的MAb可显著减少提取物诱导的黏附。
这些研究表明，幽门螺杆菌产物通过促进PMN与内皮细胞通过CD11a/CD18和CD11b/CD18依赖的与ICAM-1的相互作用而黏附，从而引发胃肠道炎症。
