ENDURANCE RUN INCREASES CIRCULATING IL-6 AND IL-1RA BUT DOWN-REGULATES EX-VIVO TNF-ALPHA AND IL-1-BETA PRODUCTION

ENDURANCE RUN INCREASES CIRCULATING IL-6 AND IL-1RA BUT DOWN-REGULATES EX-VIVO TNF-ALPHA AND IL-1-BETA PRODUCTION
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DOI:
10.1152/jappl.1995.79.5.1497
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发表时间:
1995-11-01
影响因子:
3.3
通讯作者:
VANDERMEER, JWM
VANDERMEER, JWM
中科院分区:
医学2区
文献类型:
--
作者:
DRENTH, JPH;VANUUM, SHM;VANDERMEER, JWM

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我们研究了是否6小时耐力跑改变细胞因子血浆浓度和脂多糖(LPS)刺激的细胞因子在全血培养的19名训练有素的运动员离体生产。平均覆盖距离为65.1 +/- 8.64(SD)km。运动结束时,血浆白细胞介素1受体激动剂(IL-1 ra)浓度由运动前24 h的188 pg/ml上升到886 pg/ml(P < 0.0005)。平均血浆白细胞介素-g浓度从18.5 +/- 4.2增加到71.5 +/- 33.3 pg/ml(P < 0.0001)。中性粒细胞的增加与IL-1 ra浓度的增加相关(r = 0.58,P < 0.005)。我们无法检测到运动对白细胞介素-1 β(IL-1 β)或肿瘤坏死因子-α(TNF-α)血浆浓度的影响。运动员在跑步前24小时的离体LPS刺激的IL-1 β的产生显著高于久坐的对照组。运动诱导LPS刺激的IL-1 β和TNF-α的产生减少,而IL-1 α的产生没有变化。这些结果表明,长时间的运动eleves的促炎细胞因子的产生和细胞因子IL-1 ra和白细胞介素-6的上调的选择性下调。
We investigated whether a 6-h endurance run changes cytokine plasma concentrations and lipopolysaccharides (LPS) stimulated ex vivo production of cytokines in a whole blood culture of 19 well-trained athletes. The average distance covered was 65.1 +/- 8.64 (SD) km. At the end of the exercise, the mean plasma concentration of interleukin-1-receptor agonist (IL-1ra), which was 188 pg/ml 24 h before finish, increased to 886 pg/ml (P < 0.0005). The mean plasma interleukin-g concentration increased from 18.5 +/- 4.2 to 71.5 +/- 33.3 pg/ml (P < 0.0001). The increase of neutrophils correlated with the increase of IL-1ra concentrations (r = 0.58, P < 0.005). We could not detect an effect of exercise on plasma concentrations of interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha: (TNF-alpha). The ex vivo LPS-stimulated production of IL-1 beta in athletes 24 h before the run was significantly higher than in sedentary controls. Exercise induced a decrease of LPS-stimulated production of IL-1 beta and TNF-alpha, whereas production of IL-1 alpha was unchanged. These results show that prolonged exercise elicits a selective downregulation of the proinflammatory cytokine production and upregulation of the cytokines IL-1ra and interleukin-6.