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有丝分裂原或糖原刺激绵羊和兔的单核炎性细胞分泌一种诱导充血的部分。

Secretion of a hyperemia-inducing moiety by mitogen or glycogen stimulated mononuclear inflammatory cells of sheep and rabbit.

作者信息

Vadas P, Hay J B

出版信息

Int Arch Allergy Appl Immunol. 1980;62(2):142-51. doi: 10.1159/000232506.

DOI:10.1159/000232506
PMID:7372364
Abstract

A nonlymphokine mediator of hyperemia has been shown to be secreted by both rabbit peritoneal exudate cells stimulated with 5% glycogen and by concanavalin A treated cells from afferent lymph of sheep. This mediator is not stored in an active form in cells, but is either activated or synthesized de novo in response to antigenic or mitogenic stimuli. Secretion of the mediator is inhibited by culturing cells in the presence of dexamethasone but not indomethacin. However, expression of the activity is inhibited by pretreatment of the assay animals with indomethacin, suggesting a two-step induction of hyperemia. A similar mediator was found to be secreted by sheep and rabbit alveolar lavage cells, and rat peritoneal exudate cells. The presence of this hyperemia-inducing activity from diverse species suggests a fundamental role in controlling blood flow. Alteration of blood flow may modulate delivery of blood-borne cells and factors to sites of chronic inflammation.

摘要

一种非淋巴因子介导的充血已被证明可由用5%糖原刺激的兔腹膜渗出细胞以及用伴刀豆球蛋白A处理的绵羊传入淋巴中的细胞分泌。这种介质在细胞中不是以活性形式储存,而是在抗原或促有丝分裂刺激下被激活或重新合成。在地塞米松存在下培养细胞可抑制介质的分泌,但吲哚美辛不能。然而,用吲哚美辛预处理试验动物可抑制该活性的表达,提示充血诱导分两步进行。发现绵羊和兔肺泡灌洗细胞以及大鼠腹膜渗出细胞也分泌类似的介质。来自不同物种的这种充血诱导活性的存在表明其在控制血流中起基本作用。血流改变可能调节血源性细胞和因子向慢性炎症部位的输送。

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Secretion of a hyperemia-inducing moiety by mitogen or glycogen stimulated mononuclear inflammatory cells of sheep and rabbit.有丝分裂原或糖原刺激绵羊和兔的单核炎性细胞分泌一种诱导充血的部分。
Int Arch Allergy Appl Immunol. 1980;62(2):142-51. doi: 10.1159/000232506.
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引用本文的文献

1
The appearance and significance of phospholipase A2 in lymph draining tuberculin reactions.磷脂酶A2在引流结核菌素反应的淋巴液中的表现及意义
Am J Pathol. 1982 Jun;107(3):285-91.
2
Extracellular phospholipase A2: causative agent in circulatory collapse of septic shock?细胞外磷脂酶A2:脓毒症休克循环衰竭的致病因素?
Agents Actions. 1988 Jul;24(3-4):320-5. doi: 10.1007/BF02028289.