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[肾盂肾炎的免疫病理学]

[Immunopathology of pyelonephritis].

作者信息

Rother K

出版信息

Klin Wochenschr. 1983 Oct 17;61(20):1011-7. doi: 10.1007/BF01537499.

Abstract

Urinary tract infection (as apposed to symptomless bacteriuria) begins with the binding of the bacterium to the epithelium lining the urinary tract. Immune SIgA2 may react with the bacterial ligands ("adhesins") thus blocking their attachment to the epithelium. In the absence of the protective blockade tissue lesions ensues. The pathomechanism of the circumscript interstitial inflammatory spots is assumed to depend on complement activation by immune complexes of bacterial antigens and antibodies: chemotactic activity is generated from the C-system, leucocytes are attracted and the lysosomal enzymes initiate tissue damage.

摘要

尿路感染(与无症状菌尿症相对)始于细菌与尿路衬里上皮细胞的结合。免疫分泌型免疫球蛋白A2(SIgA2)可能会与细菌配体(“粘附素”)发生反应,从而阻止它们附着在上皮细胞上。在没有这种保护性阻断的情况下,组织损伤就会发生。局限性间质性炎症灶的发病机制被认为取决于细菌抗原和抗体的免疫复合物激活补体:补体系统产生趋化活性,吸引白细胞,溶酶体酶引发组织损伤。

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