Helicobacter pylori-induced microvascular protein leakage in rats: role of neutrophils, mast cells, and platelets.
Helicobacter pylori-induced microvascular protein leakage in rats: role of neutrophils, mast cells, and platelets.
复制标题
幽门螺杆菌诱导的大鼠微血管蛋白渗漏：中性粒细胞、肥大细胞和血小板的作用。
DOI：
10.1016/0016-5085(94)90062-0
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发表时间：
1994
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：
Kurose,I;Granger,DN;EvansJr,DJ;Evans,DG;Graham,DY;Miyasaka,M;Anderson,DC;Wolf,RE;Cepinskas,G;Kvietys,PR
背景/目的：先前的研究表明，幽门螺杆菌（HPE）的水提取物可以促进体内和体外中性粒细胞-内皮细胞的相互作用。本研究的目的是评估HPE是否改变大鼠肠系膜微静脉的白蛋白渗漏率，并确定介导HPE诱导的微血管功能障碍的因素。方法：使用活体显微镜连续监测HPE输注期间大鼠肠系膜微静脉中白细胞的粘附和迁移以及白蛋白渗漏。结果：HPE增加了白细胞的粘附和迁移以及微血管白蛋白渗漏。增强的白蛋白泄漏可分为两个部分：早期（10 分钟内）和后期（30 分钟内）阶段。 HPE 还引起微静脉周围肥大细胞脱粒和毛细血管后微静脉内血小板白细胞聚集体的形成。 HPE 诱导的早期白蛋白渗漏可通过肥大细胞稳定剂预处理减弱。针对 CD11b/CD18 或细胞间粘附分子 1 的单克隆抗体可减少 HPE 诱导的后期白蛋白渗漏。针对 P-选择素的单克隆抗体也能抑制 HPE 诱导的血小板白细胞聚集，并减少后期白蛋白渗漏。结论：HPE 诱导的微血管功能障碍似乎是间质和血管内细胞间相互作用的结果。
Background/Aims:Previous studies indicate that a water extract ofHelicobacter pylori(HPE) can promote neutrophil-endothelial cell interactions in vivo and in vitro. The objectives of this study were to assess whether HPE alters the rate of albumin leakage in rat mesenteric venules and identify the factors that mediate the HPE-induced microvascular dysfunction.Methods:Intravital microscopy was used to continuously monitor leukocyte adherence and emigration and albumin leakage in rat mesenteric venules during superfusion with HPE.Results:HPE increased leukocyte adherence and emigration and microvascular albumin leakage. The enhanced albumin leak could be subdivided into two components: an early (within 10 minutes) and a later (within 30 minutes) phase. HPE also elicited perivenular mast cell degranulation and the formation of platelet-leukocyte aggregates within post-capillary venules. The HPE-induced early phase of albumin leakage was attenuated by pretreatment with a mast cell stabilizer. The HPE-induced late phase of albumin leakage was reduced by monoclonal antibodies directed against either CD11b/CD18 or intercellular adhesion molecule 1. A monoclonal antibody against P-selectin also inhibited the HPE-induced platelet-leukocyte aggregation and reduced the later phase of albumin leak.Conclusions:HPE-induced microvascular dysfunction appears to be a consequence of interstitial and intravascular cell-cell interactions.