淋巴因子对人外周血单个核细胞β-肾上腺素能受体功能的影响。
Effect of lymphokines on beta-adrenoceptor function of human peripheral blood mononuclear cells.
作者信息
van Oosterhout A J, Nijkamp F P
机构信息
Department of Pharmacology, Faculty of Pharmacy, University of Utrecht, The Netherlands.
出版信息
Br J Clin Pharmacol. 1990;30 Suppl 1(Suppl 1):150S-152S. doi: 10.1111/j.1365-2125.1990.tb05490.x.
Pathological induced changes in beta-adrenoceptor function occur in diseases such as asthma and hypertension. The mechanism(s) of this dysfunction is at present unclear. In the present study, the effect of lymphokines on beta-adrenoceptor agonist induced cAMP production in peripheral blood mononuclear cells (PBMC) is investigated. Pre-incubation of PBMC during 20 h with interleukin-2 (IL-2, 100 u ml-1) and granulocyte/macrophage-colony stimulating factor (GM-CSF, 100 u ml-1) significantly decreases beta-adrenoceptor agonist induced cAMP production by 35 +/- 8% and 37 +/- 11% respectively. IL-3 and IL-4 do not affect beta-adrenoceptor agonist induced cAMP production in PBMC. It can be concluded that IL-2 and GM-CSF, mediators derived from T-lymphocytes, can induce beta-adrenoceptor dysfunction in PBMC.
在诸如哮喘和高血压等疾病中会出现病理性诱导的β-肾上腺素能受体功能变化。目前这种功能障碍的机制尚不清楚。在本研究中，研究了淋巴因子对外周血单核细胞（PBMC）中β-肾上腺素能受体激动剂诱导的环磷酸腺苷（cAMP）产生的影响。将PBMC与白细胞介素-2（IL-2，100 U/ml）和粒细胞/巨噬细胞集落刺激因子（GM-CSF，100 U/ml）预孵育20小时，可使β-肾上腺素能受体激动剂诱导的cAMP产生分别显著降低35±8%和37±11%。IL-3和IL-4不影响PBMC中β-肾上腺素能受体激动剂诱导的cAMP产生。可以得出结论，源自T淋巴细胞的介质IL-2和GM-CSF可诱导PBMC中的β-肾上腺素能受体功能障碍。
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