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A组链球菌多糖的致水肿活性及其在细胞壁诱导的多关节炎发病机制中的可能作用。

Edema-producing activity of group A streptococcal polysaccharide and its possible role in the pathogenesis of cell wall-induced polyarthritis.

作者信息

Chetty C, Brown R R, Schwab J H

出版信息

J Exp Med. 1983 Apr 1;157(4):1089-100. doi: 10.1084/jem.157.4.1089.

Abstract

Edematous responses were induced in the limbs of Sprague-Dawley rats by intravenous, intraperitoneal, or intra-articular injections of group-specific polysaccharide (PS) isolated from the cell walls of group A streptococci. After intravenous injection of the edema-producing PS, vascular permeability increase (measured by 125I-human serum albumin) was detected in the limbs, but not in the heart, lungs, spleen, liver, thymus, kidney, skin, skeletal muscle, submandibular lymph nodes, mesenteric lymph nodes, or ascending colon. This indicates a selective effect on vascular endothelium of the joints. Evidence to suggest that the edema-producing activity of the PS might play an important role in the pathogenesis of cell wall-induced polyarthritis included the following: (a) the presence of edema-producing activity in arthropathogenic cell wall preparations; (b) cell wall preparations without edema-producing activity were significantly less active in inducing arthritis than were those which contained edema-producing activity; and (c) the addition of edema-producing PS to cell wall preparations increased both the incidence and the severity of arthritis.

摘要

通过静脉内、腹膜内或关节内注射从A组链球菌细胞壁分离出的群特异性多糖(PS),在斯普拉格-道利大鼠的肢体中诱导出水肿反应。静脉注射产生水肿的PS后,在肢体中检测到血管通透性增加(通过125I-人血清白蛋白测量),但在心脏、肺、脾脏、肝脏、胸腺、肾脏、皮肤、骨骼肌、下颌下淋巴结、肠系膜淋巴结或升结肠中未检测到。这表明对关节血管内皮有选择性作用。提示PS的产生水肿活性可能在细胞壁诱导的多关节炎发病机制中起重要作用的证据包括以下几点:(a)致关节病的细胞壁制剂中存在产生水肿的活性;(b)没有产生水肿活性的细胞壁制剂在诱导关节炎方面的活性明显低于含有产生水肿活性的制剂;(c)向细胞壁制剂中添加产生水肿的PS会增加关节炎的发病率和严重程度。

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