Cyclosporin A inhibits the in vivo production of interleukin-1beta and tumour necrosis factor alpha, but not interleukin-6, by a T-cell-independent mechanism.
Cyclosporin A inhibits the in vivo production of interleukin-1beta and tumour necrosis factor alpha, but not interleukin-6, by a T-cell-independent mechanism.
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发表时间：
1996
期刊：
影响因子：
3.8
通讯作者：
J. Dawson;U. Hurtenbach;A. MacKenzie
中科院分区：
文献类型：
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作者：
J. Dawson;U. Hurtenbach;A. MacKenzie
观察了环孢素A（CsA）对急性炎症组织室模型中细胞因子产生的影响。CsA在正常小鼠和无胸腺小鼠中均引起白细胞介素1 β（IL-1 β）产生的剂量相关抑制，证实了早期的结论，即这种作用不是T细胞依赖性的（ED 50为40和53 mg/kg p.o.，分别）。40和58 mg/kg p.o.的ED 50对肿瘤坏死因子α（TNF-α）水平的影响相似。分别用于正常和无胸腺小鼠。相比之下，CsA仅在正常小鼠中抑制白细胞介素6（IL-6）的产生（ED 50 27 mg/kg p.o.）在正常和无胸腺小鼠的三种细胞因子的绝对生产的差异也被注意到。IL-1 β和IL-6水平在无胸腺小鼠中高出两倍，而TNF-α在两组之间没有差异。目前的研究结果支持了作者最初的假设，即CsA对IL-1 β的抑制机制不是通过T细胞介导的。同样的机制似乎也负责抑制TNF-α的产生，但不负责IL-6，其中CsA的抑制似乎需要T细胞的存在。
The effect of cyclosporin A (CsA) on cytokine production in the tissue chamber model of acute inflammation was investigated. CsA caused a dose-related inhibition of interleukin 1beta(IL-1beta) production in both normal and athymic mice, confirming earlier conclusions that this effect is not T cell dependent (ED50s 40 and 53 mg/kg p.o., respectively). Tumour necrosis factor alpha (TNF-alpha) levels were similarly affected with ED50s of 40 and 58 mg/kg p.o. for normal and athymic mice, respectively. By contrast, CsA inhibited interleukin 6 (IL-6) production only in normal mice (ED50 27 mg/kg p.o.) Differences in the absolute production of the three cytokines in normal and athymic mice were also noted. IL-1beta and IL-6 levels were two-fold higher in athymic mice, while for TNF-alpha, there was no difference between the two groups. The present findings support the authors' original hypothesis, that the inhibitory mechanism of CsA on IL-1beta is not mediated via T cells. The same mechanism also seems responsible for the inhibition of TNF-alpha production, but not for IL-6, where inhibition by CsA appears to require the presence of T cells.