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痛风热:尿酸盐结晶激活人和兔单核吞噬细胞产生内源性致热原。

The fever of gout: urate crystals activate endogenous pyrogen production from human and rabbit mononuclear phagocytes.

作者信息

Duff G W, Atkins E, Malawista S E

出版信息

Trans Assoc Am Physicians. 1983;96:234-45.

PMID:6093311
Abstract

Acute gout may be associated with fever but activation of EP production by crystalline urate in vivo has not been previously reported. We found that crystalline urate or silica stimulated macrophages but not PMNs to produce EP, without mediation by lymphocytes. The activation process did not require ingestion of the urate crystals, was unaffected by colchicine, and was not due to incidental LPS. Additionally, the failure of ingested latex particles to stimulate EP release indicated that phagocytosis alone was not a sufficient stimulus for EP production. We suggest that since EP and IL 1 are probably the same, the known inflammatory effects of IL 1, apart from fever induction, may contribute to the pathogenesis of acute gout and other crystal-associated human diseases.

摘要

急性痛风可能伴有发热,但此前尚无关于体内尿酸盐结晶激活内源性致热原(EP)生成的报道。我们发现,尿酸盐结晶或二氧化硅可刺激巨噬细胞而非中性粒细胞产生EP,且该过程不受淋巴细胞介导。激活过程无需摄取尿酸盐结晶,不受秋水仙碱影响,也并非由偶然存在的脂多糖(LPS)所致。此外,摄取的乳胶颗粒未能刺激EP释放,这表明单纯吞噬作用并非EP产生的充分刺激因素。我们认为,由于EP和白细胞介素1(IL-1)可能是同一物质,因此除了引起发热外,IL-1已知的炎症作用可能在急性痛风及其他与晶体相关的人类疾病的发病机制中发挥作用。

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