van Ierssel G J, van der Sluys Veer A, Verspaget H W, Griffioen G, van Hogezand R A, Lamers C B
Department of Gastroenterology and Hepatology, University Hospital Leiden, Netherlands.
Immunopharmacology. 1995 Feb;29(1):11-7. doi: 10.1016/0162-3109(95)00039-v.
We recently showed that patients with active ileocecal Crohn's disease (CD) have a temporarily suppressed peripheral blood natural killer (NK) cell activity during treatment with oral budesonide or prednisolone. This suppression was caused by a decrease in the number of CD16+ NK cells in the circulation. In the present study we evaluated the contribution of cortisol in plasma to this suppressed NK cell activity. The CD patients took part in a controlled study where they received either oral budesonide or prednisolone for 10 weeks. Before treatment, and at 4 and 10 weeks of treatment, peripheral blood NK cell activity, numbers of circulating CD16+ NK cells, and plasma cortisol levels were analysed. These parameters were determined both before and 30 min after administration of adrenocorticotropic hormone (ACTH). The ACTH-induced plasma cortisol increase was accompanied by a stimulated NK cell activity, when both are suppressed by corticosteroid treatment, without changing the number of CD16+ NK cells. Therefore, a low plasma cortisol level contributes to the corticosteroid mediated NK cell suppression in active ileocecal CD.
我们最近发现,患有活动性回盲部克罗恩病(CD)的患者在接受口服布地奈德或泼尼松龙治疗期间,其外周血自然杀伤(NK)细胞活性会暂时受到抑制。这种抑制是由循环中CD16+NK细胞数量减少所致。在本研究中,我们评估了血浆中皮质醇对这种NK细胞活性抑制的作用。CD患者参与了一项对照研究,他们接受口服布地奈德或泼尼松龙治疗10周。在治疗前、治疗第4周和第10周,分析外周血NK细胞活性、循环CD16+NK细胞数量以及血浆皮质醇水平。这些参数在给予促肾上腺皮质激素(ACTH)之前和之后30分钟均进行了测定。当二者均因皮质类固醇治疗而受到抑制时,ACTH诱导的血浆皮质醇增加伴随着NK细胞活性的增强,且CD16+NK细胞数量未发生变化。因此,低血浆皮质醇水平促成了皮质类固醇介导的活动性回盲部CD患者NK细胞抑制。