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尿毒症患者的宿主免疫状态。IV. 体内吞噬作用与炎症反应。

Host immune status in uremia. IV. Phagocytosis and inflammatory response in vivo.

作者信息

Nelson J, Ormrod D J, Miller T E

出版信息

Kidney Int. 1983 Feb;23(2):312-9. doi: 10.1038/ki.1983.21.

Abstract

Infection is a frequent complication and cause of death in renal failure, but the association between uremia, depressed immune status, and susceptibility to infection is far from proven. In the present studies, the effect of uremia on the inflammatory response and phagocytic ability was investigated in an animal model. The inflammatory response, as measured by the ability of leukocytes to mobilize into subcutaneous implanted sponges, was impaired at 6 hr but was normal 24 hr after implantation. The peripheral blood response of uremic animals to the leukocytosis promoting protein from Bordetella pertussis was similar to that of control animals. Reticuloendothelial clearance of labelled albumin was unimpaired but catabolism of this substance was reduced significantly in uremic animals. The ability of the uremic host to clear an intravenous challenge of virus was also depressed. Phagocytic and bactericidal capability of polymorphonuclear (PMN) leukocytes, measured in vitro by latex ingestion and phagocytosis and killing of Staphylococcus aureus, was normal. PMN phagocytic function in vivo was determined by the clearance of viable Escherichia coli from subcutaneously implanted sponges and no significant difference between control and uremic groups was found. These studies have further defined the effect of uremia on immune mechanisms and support our contention that uremia per se is not a major factor contributing to the compromised immune status in this host.

摘要

感染是肾衰竭常见的并发症和死亡原因,但尿毒症、免疫状态低下与易感性之间的关联尚未得到充分证实。在本研究中,我们在动物模型中研究了尿毒症对炎症反应和吞噬能力的影响。通过白细胞向皮下植入海绵中迁移的能力来衡量的炎症反应,在植入后6小时受损,但在24小时后恢复正常。尿毒症动物对外周血中百日咳杆菌白细胞增多促进蛋白的反应与对照动物相似。标记白蛋白的网状内皮系统清除功能未受损害,但尿毒症动物中该物质的分解代谢显著降低。尿毒症宿主清除静脉注射病毒的能力也受到抑制。通过体外乳胶摄取、吞噬和杀灭金黄色葡萄球菌来测量的多形核(PMN)白细胞的吞噬和杀菌能力正常。通过皮下植入海绵中活大肠杆菌的清除来测定体内PMN吞噬功能,对照组和尿毒症组之间未发现显著差异。这些研究进一步明确了尿毒症对免疫机制的影响,并支持了我们的观点,即尿毒症本身并不是导致该宿主免疫状态受损的主要因素。

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