Miller T E, Findon G, Cawley S
Br J Exp Pathol. 1987 Jun;68(3):377-88.
Hosts were depleted of individual cellular components to determine the effects of these manipulations on cellular defence mechanisms in acute and chronic pyelonephritis. T-lymphocytes were found to have little or no involvement in host protection but cyclosporin A administration had a dramatic effect on the gross pathology and bacteriological status of experimentally induced pyelonephritis. This change represented a major depression of host defence status. Cyclosporin A also activated resolved lesions in chronic pyelonephritis, associated with an increase in bacterial numbers. Administration of antineutrophil serum also led to a 1000-fold increase in bacterial numbers in the acute phase but had little effect on the host-parasite balance in chronic pyelonephritis. Macrophage blockade, on the other hand, did not affect the course of either acute or chronic infection. These studies have provided additional information on the immunobiology of experimental pyelonephritis and have focussed attention on the role of neutrophils, and an unidentified mechanism, affected by cyclosporin A, in host defence to renal infection.
去除宿主的单个细胞成分,以确定这些操作对急性和慢性肾盂肾炎细胞防御机制的影响。发现T淋巴细胞在宿主保护中几乎没有或没有参与,但给予环孢素A对实验性诱导的肾盂肾炎的大体病理和细菌学状况有显著影响。这种变化代表宿主防御状态的严重抑制。环孢素A还激活了慢性肾盂肾炎中已消退的病变,伴有细菌数量增加。给予抗中性粒细胞血清在急性期也导致细菌数量增加1000倍,但对慢性肾盂肾炎中的宿主-寄生虫平衡影响很小。另一方面,巨噬细胞阻断不影响急性或慢性感染的进程。这些研究提供了关于实验性肾盂肾炎免疫生物学的更多信息,并将注意力集中在中性粒细胞的作用以及环孢素A影响的一种未知机制在宿主对肾脏感染的防御中的作用。