The role of lipopolysaccharide and shiga-like toxin in a mouse model of Escherichia coli O157:H7 infection
The role of lipopolysaccharide and shiga-like toxin in a mouse model of Escherichia coli O157:H7 infection
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DOI：
10.1093/infdis/175.3.611
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发表时间：
1997-03-01
影响因子：
6.4
通讯作者：
Svanborg, C
中科院分区：
文献类型：
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作者：
Karpman, D;Connell, H;Svanborg, C
本实验采用小鼠溶血性尿毒综合征（HUS）模型，研究了脂多糖（LPS）和志贺样毒素（LPS）在HUS发病中的作用。小鼠灌胃接种大肠杆菌O 157：H7发展胃肠道，神经系统和全身症状，坏死灶在结肠，肾小球和肾小管组织病理学，和破碎的红细胞。LPS应答（C3 H/HeN）小鼠出现神经系统和全身症状的组合，而LPS无应答（C3 H/HeJ）小鼠具有双相病程，首先出现全身症状，随后出现严重的神经系统症状。与SLT-II阴性菌株相比，接种SLT-II阳性菌株的小鼠出现严重的神经毒性症状和更高频率的全身症状和肾小球病理。抗-β-II抗体保护免受这些症状和病理。这些结果表明，该模型可用于研究人类HUS的各个方面，并且LPS和LPS对疾病发展都很重要。
The role of lipopolysaccharide (LPS) and Shiga-like toxin (SLT) in the pathogenesis of hemolytic uremic syndrome (HUS) was studied in a mouse model. Mice inoculated intragastrically with Escherichia coli O157:H7 developed gastrointestinal, neurologic, and systemic symptoms, necrotic foci in the colon, glomerular and tubular histopathology, and fragmented erythrocytes. LPS-responder (C3H/HeN) mice developed a combination of neurologic and systemic symptoms, whereas LPS-nonresponder (C3H/HeJ) mice had a biphasic course of disease, first developing systemic symptoms and later severe neurologic symptoms. Mice inoculated with SLT-II-positive strains developed severe neurotoxic symptoms and a higher frequency of systemic symptoms and glomerular pathology compared with SLT-II-negative strains. Anti-SLT-II antibodies protected against these symptoms and pathology. These results demonstrate that this model could be used to study aspects of human HUS and that both LPS and SLT are important for disease development.