PapG-dependent adherence breaks mucosal inertia and triggers the innate host response
PapG-dependent adherence breaks mucosal inertia and triggers the innate host response
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DOI：
10.1086/383278
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发表时间：
2004-05-01
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：
Bergsten, G;Samuelsson, M;Svanborg, C
粘膜病原体与正常菌群成分的不同之处在于，它们会引起宿主反应，破坏粘膜的完整性。我们研究了离散粘附因子的阐述是否足以打破粘膜屏障的惯性。选择papg介导的粘附作为一个例子，因为P毛表达是尿路致病性大肠杆菌的特征，因为粘附开始攻击粘膜屏障。患者体内接种表达功能性P菌毛（大肠杆菌pap(+)）或缺乏黏附素的突变菌毛（大肠杆菌DeltapapG）的转化无毒大肠杆菌菌株。大肠杆菌pap（+）被证明可以激活先天宿主反应，并且在排泄的尿上皮细胞上观察到粘附的gfp（+）细菌。大肠杆菌DeltapapG未能引起反应，并且不具有粘附性。我们得出结论，papg介导的粘附通过触发先天免疫打破了人类尿路中的粘膜惯性，并提出这一激活步骤可以区分无症状携带和感染。
Mucosal pathogens differ from normal flora constituents in that they provoke a host response that upsets mucosal integrity. We investigated whether the elaboration of discrete adherence factors is sufficient to break the inertia of the mucosal barrier. PapG-mediated adherence was selected as an example, because P fimbrial expression characterizes uropathogenic Escherichia coli and because adherence starts the attack on the mucosal barrier. Patients were inoculated intravesically with transformed nonvirulent E. coli strains expressing functional P fimbriae (E. coli pap(+)) or mutant fimbriae lacking the adhesin (E. coli DeltapapG). E. coli pap(+) was shown to activate the innate host response, and adherent gfp(+) bacteria were observed on excreted uroepithelial cells. E. coli DeltapapG failed to trigger a response and was nonadhesive. We conclude that PapG-mediated adherence breaks mucosal inertia in the human urinary tract by triggering innate immunity and propose that this activation step differentiates asymptomatic carriage from infection.