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Persistent Inflammatory Responses Enhance the Proinflammatory Activity of Lymphocytes

机译:持续的炎症反应增强淋巴细胞的促炎活性

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摘要

Intravenous administration to leucopenic rats of lymphocyte suspensions, or lymphocyte products, restored the depressed inflammatory responses of these animals to various inflammatory stimuli. Utilizing carrageenin to induce inflammatory responses in leucopenic animals, an enhanced restorative effect of lymphocytes, or of their products, was observed when the cells were collected from donor rats in which a persistent inflammatory lesion was previously induced in the paw by the local injection of complete Freund's adjuvant (CFA). The enhancement of cell activity was gradual with the age of the lesion: cells collected from donors bearing 3-day-old lesions were less effective than cells from donors in which the persistent inflammatory lesion was induced 18 days before. Steroidal and non-steroidal anti-inflammatory drugs (e.g. hydrocortisone, aspirin, sodium salicylate and indomethacin), administered to donor animals, were capable of blocking the restorative effect of lymphocytes. This blocking action affected also cells rendered hyperactive by the stimulus of CFA-induced lesions, but was reverted by the interruption of drug administration to donors. When cells rendered inactive by the action of anti-inflammatory drugs were disrupted before injection into leucopenic animals, the resulting cell products were capable of restoring the depressed inflammatory responses of these animals to carrageenin. Aspirin was an exception, because it rendered inactive the cell products besides the intact cells. It is concluded that persistent inflammatory responses induced by CFA enhance the proinflammatory function of lymphocytes in the rat which, in turn, might contribute to the persistency of the response. Antiinflammatory drugs may interrupt this sort of vicious circle by decreasing the amounts of the available active cell products.
机译:向白细胞减少症大鼠静脉内施用淋巴细胞悬液或淋巴细胞产物可恢复这些动物对各种炎症刺激的抑制性炎症反应。利用角叉菜胶在白血球缺乏症动物中诱发炎症反应,当从供体大鼠中收集细胞时,观察到淋巴细胞或其产物的增强的恢复作用,其中先前通过局部注射全脂素诱导了足爪中的持续性炎性病变弗氏佐剂(CFA)。细胞活性的增强随着病变的年龄逐渐增加:从携带3天大病变的供体中收集的细胞效果不如在18天前诱发持续性炎性病变的供体中。给供体动物服用的类固醇和非类固醇抗炎药(例如氢化可的松,阿司匹林,水杨酸钠和消炎痛)可以阻断淋巴细胞的修复作用。这种阻断作用还影响了通过CFA诱导的病变刺激而变得过度活跃的细胞,但由于中断了对供体的药物施用而被恢复。当在注射入白血球减少的动物中通过抗炎药作用而失活的细胞被破坏时,所得的细胞产物能够恢复这些动物对角叉菜胶的抑制的炎性反应。阿司匹林是一个例外,因为它使除完整细胞外的细胞产物失活。结论是,CFA诱导的持续性炎症反应增强了大鼠淋巴细胞的促炎功能,进而可能促进了反应的持续性。抗炎药可能会通过减少可用活性细胞产物的数量来打断这种恶性循环。

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