Zoellner H, Cebon J, Layton J E, Stanton H, Hamilton J A
University of Melbourne, Department of Medicine, Royal Melbourne Hospital, Parkville, Vic., Australia.
Lymphokine Cytokine Res. 1993 Apr;12(2):93-9.
Endothelial cells (EC) may regulate both local and systemic aspects of inflammation through the synthesis of cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), macrophage colony-stimulating factor (M-CSF), and interleukin-6 (IL-6). EC are known to synthesize these cytokines in response to interleukin-1 (IL-1 alpha), tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS). In this paper, we illustrate the effect of interleukin-4 (IL-4) in reducing the synthesis of GM-CSF by EC stimulated with IL-1 alpha, TNF-alpha, or LPS. This is compared with the previously reported strong synergy between IL-4 and IL-1 alpha, TNF-alpha, or LPS in the synthesis of IL-6 by EC. No clear effect of IL-4 was seen in the synthesis of G-CSF or M-CSF. The range of concentrations of IL-4 at which these effects were seen was identical for both reduced GM-CSF synthesis and increased IL-6 synthesis. The effect of IL-4 on IL-6 synthesis was seen by 4 h of treatment, while that on GM-CSF was apparent between 4 and 8 h. It is suggested that these contrasting effects of IL-4 may reflect a biological role for this cytokine in the regulation of leukocytosis and the acute phase response.
内皮细胞（EC）可通过合成细胞因子来调节炎症的局部和全身反应，这些细胞因子包括粒细胞-巨噬细胞集落刺激因子（GM-CSF）、粒细胞集落刺激因子（G-CSF）、巨噬细胞集落刺激因子（M-CSF）和白细胞介素-6（IL-6）。已知内皮细胞会在白细胞介素-1（IL-1α）、肿瘤坏死因子-α（TNF-α）和脂多糖（LPS）的刺激下合成这些细胞因子。在本文中，我们阐述了白细胞介素-4（IL-4）对经IL-1α、TNF-α或LPS刺激的内皮细胞合成GM-CSF的抑制作用。将其与之前报道的IL-4与IL-1α、TNF-α或LPS在内皮细胞合成IL-6过程中的强烈协同作用进行比较。未观察到IL-4对G-CSF或M-CSF的合成有明显影响。观察到这些作用的IL-4浓度范围在抑制GM-CSF合成和增加IL-6合成方面是相同的。IL-4对IL-6合成的作用在处理4小时后即可观察到，而对GM-CSF的作用在4至8小时之间较为明显。提示IL-4的这些相反作用可能反映了该细胞因子在调节白细胞增多和急性期反应中的生物学作用。
