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Tamm-Horsfall糖蛋白可干扰细菌对人肾细胞的黏附。

Tamm Horsfall glycoprotein interferes with bacterial adherence to human kidney cells.

作者信息

Dulawa J, Jann K, Thomsen M, Rambausek M, Ritz E

机构信息

Department of Internal Medicine, University of Heidelberg, FRG.

出版信息

Eur J Clin Invest. 1988 Feb;18(1):87-91. doi: 10.1111/j.1365-2362.1988.tb01171.x.

Abstract

The effect of Tamm Horsfall protein (THP) of 18 healthy subjects and 14 diabetics on adherence of Escherichia coli (06:K13) 2699 strain to human kidney cells (HUK) was studied. Adhesion of bacteria (without additions: 100 bacteria per cell) was reduced dose-dependently by THP, half maximal inhibition occurring with 250 micrograms THP ml-1. Maximal inhibition (-84% at 1000 micrograms ml-1) exceeded inhibition by alpha-methyl-mannoside (36% at 50 mM), was specific (not reproduced by other glycoproteins, e.g. ovalbumin, mucin or thyroglobulin) and reversible (abolished by washing THP off HUK cells). Anti-adherence property of THP was not abolished by neuraminidase treatment. No significant difference of anti-adherence activity of THP was found between controls and diabetics, despite altered carbohydrate composition of THP in diabetes.

摘要

研究了18名健康受试者和14名糖尿病患者的Tamm-Horsfall蛋白(THP)对大肠杆菌(06:K13)2699菌株黏附于人肾细胞(HUK)的影响。THP可使细菌的黏附(未添加时:每个细胞100个细菌)呈剂量依赖性降低,在250微克THP/ml时出现半数最大抑制。最大抑制(在1000微克/ml时为-84%)超过了α-甲基甘露糖苷的抑制作用(在50 mM时为36%),具有特异性(其他糖蛋白如卵清蛋白、黏蛋白或甲状腺球蛋白不能重现)且可逆(通过将THP从HUK细胞上洗去而消除)。神经氨酸酶处理并未消除THP的抗黏附特性。尽管糖尿病患者THP的碳水化合物组成发生了改变,但在对照组和糖尿病患者之间未发现THP抗黏附活性的显著差异。

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