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肾盂肾炎宿主防御的细胞基础。I. 慢性感染。

Cellular basis of host defence in pyelonephritis. I. Chronic infection.

作者信息

Miller T E, Findon G, Cawley S

出版信息

Br J Exp Pathol. 1986 Feb;67(1):13-23.

Abstract

Infection persists for long periods in chronic pyelonephritis, but the cellular basis of the host-parasite relationship is poorly understood. We have obtained quantitative data on the relationship between the pathogen (E. coli) and cellular defence mechanisms. Depletion of cellular components was carried out using whole body irradiation, methylprednisolone, cyclophosphamide or carrageenan and silica particles. A system of administering cyclophosphamide and methylprednisolone through the use of a slow release carrier, as well as graded doses of irradiation, was then developed to allow the controlled reduction of cellular competence. Quantitative studies in a host with chronic pyelonephritis and normal cellular defence reserves showed that severe depletion of granulocytic cells is necessary before host defence mechanisms are adversely affected. This finding conflicts with the observation that microorganisms survive and persist in the kidney for extended periods. Additionally, noncellular factors may also limit bacterial growth.

摘要

在慢性肾盂肾炎中,感染会长期持续存在,但宿主与寄生虫关系的细胞基础却知之甚少。我们已经获得了关于病原体(大肠杆菌)与细胞防御机制之间关系的定量数据。通过全身照射、甲基强的松龙、环磷酰胺或角叉菜胶及二氧化硅颗粒来消耗细胞成分。随后开发了一种通过使用缓释载体来施用环磷酰胺和甲基强的松龙以及分级剂量照射的系统,以实现对细胞能力的可控降低。对患有慢性肾盂肾炎且细胞防御储备正常的宿主进行的定量研究表明,在宿主防御机制受到不利影响之前,粒细胞的严重耗竭是必要的。这一发现与微生物在肾脏中长期存活和持续存在的观察结果相矛盾。此外,非细胞因素也可能限制细菌生长。

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