Sannomiya P, Anteghini H J, Vianna E S, Garcia-Leme J
Agents Actions. 1985 Sep;16(6):552-7. doi: 10.1007/BF01983662.
Leucopenia induced by the administration of methotrexate reduced the volume of inflammatory exudate and the number of cells entering the pleural cavity during a 4-h carrageenin pleurisy when compared with that of non-leucopenic controls. The depressed response was partially but markedly restored when leucopenic animals were intravenously injected, immediately before the initiation of pleurisy, with spleen lymphocytes (or their products) obtained from normal, adrenal-demedullated or mock-operated rats. In contrast spleen lymphocytes (or their products) obtained from adrenalectomized rats or from rats receiving metyrapone, an inhibitor of adrenal glucocorticoid biosynthesis, were completely inactive. It is concluded that in physiologic concentrations glucocorticoids are essential for the production of lymphocyte-derived factors involved in the development of acute, non-immune inflammation. In pharmacologic concentrations, however, glucocorticoids suppress the release of such pro-inflammatory factors.
与非白细胞减少的对照组相比，在角叉菜胶诱导的胸膜炎4小时期间，甲氨蝶呤给药引起的白细胞减少减少了炎症渗出液的量和进入胸腔的细胞数量。当白细胞减少的动物在胸膜炎开始前立即静脉注射从正常、肾上腺髓质切除或假手术大鼠获得的脾淋巴细胞（或其产物）时，这种抑制反应部分但明显恢复。相比之下，从肾上腺切除的大鼠或接受甲吡酮（一种肾上腺糖皮质激素生物合成抑制剂）的大鼠获得的脾淋巴细胞（或其产物）则完全无活性。结论是，在生理浓度下，糖皮质激素对于参与急性非免疫炎症发展的淋巴细胞衍生因子的产生至关重要。然而，在药理浓度下，糖皮质激素会抑制此类促炎因子的释放。
