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

机译:肾盂肾炎宿主防御的细胞基础。 I.慢性感染。

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摘要

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.
机译:在慢性肾盂肾炎中感染会持续很长时间,但是对宿主-寄生虫关系的细胞基础了解甚少。我们已经获得了有关病原体(大肠杆菌)与细胞防御机制之间关系的定量数据。使用全身照射,甲基强的松龙,环磷酰胺或角叉菜胶和二氧化硅颗粒进行细胞成分的消耗。然后开发了通过使用缓释载体以及分级照射剂量来给予环磷酰胺和甲基强的松龙的系统,以控制细胞能力的降低。在患有慢性肾盂肾炎和正常细胞防御储备的宿主中进行的定量研究表明,在严重损害宿主防御机制之前,有必要大量消耗粒细胞。这一发现与微生物在肾脏中存活并长期存在的观察结果相矛盾。另外,非细胞因子也可能限制细菌的生长。

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