Wandall J H, Binder V
Gut. 1982 Mar;23(3):173-80. doi: 10.1136/gut.23.3.173.
Leucocyte function was evaluated by mobilisation to skin windows with chambers and by the chemotactic, phagocytic, and nitro blue tetrazolium (NBT) reducing activity of circulating leucocytes in vitro in 20 patients with Crohn's disease, 21 healthy volunteers, and nine patients with sarcoidosis or tuberculosis. Leucocytes had been mobilised in significantly reduced numbers at 12, 24, 36, and 48 hours in Crohn's disease compared with healthy volunteers (P less than 0.01) and patients with sarcoidosis/tuberculosis (P less than 0.01). The leucocyte migration rate showed that mobilisation in Crohn's disease begins after a prolonged lag phase and is reduced compared with healthy volunteers (P less than 0.01) and patients with sarcoidosis/tuberculosis (P less than 0.02). The reduced mobilisation was not correlated with disease activity. In vitro random migration by leucocytes was slightly lower in Crohn's disease (P less than 0.05) than in healthy volunteers, but there was no difference after removal of the autologous plasma. Chemotactic response to casein did not differ between the groups studied. Serum independent and dependent phagocytosis did not differ from control groups. Serum independent phagocytosis was positively and significantly correlated to the disease activity (rho 0.4812, P less than 0.05). Resting leucocyte NBT reduction was increased in Crohn's disease and sarcoidosis/tuberculosis (P less than 0.01), but during phagocytosis a lower NBT reduction was found in Crohn's disease than in healthy volunteers (P less than 0.02). The inflammatory response in Crohn's disease, with reduced leucocyte accumulation, differs from patients with other granulomatous reactions and is independent of the disease activity. Our data suggest that the defect is not cellular. They support the hypothesis that a pathogenic factor in Crohn's disease may be foreign material that is normally eliminated remaining in the tissue and eliciting a chronic inflammatory response.
通过在小室内将白细胞动员至皮肤窗口，以及检测20例克罗恩病患者、21名健康志愿者和9例结节病或结核病患者外周血白细胞的趋化、吞噬及硝基蓝四氮唑（NBT）还原活性，来评估白细胞功能。与健康志愿者相比，克罗恩病患者在12、24、36和48小时时动员的白细胞数量显著减少（P<0.01），与结节病/结核病患者相比亦显著减少（P<0.01）。白细胞迁移率显示，克罗恩病患者的动员在经过较长的延迟期后开始，且与健康志愿者相比降低（P<0.01），与结节病/结核病患者相比也降低（P<0.02）。动员减少与疾病活动度无关。克罗恩病患者白细胞的体外随机迁移略低于健康志愿者（P<0.05），但去除自体血浆后无差异。各研究组对酪蛋白的趋化反应无差异。血清非依赖性和依赖性吞噬与对照组无差异。血清非依赖性吞噬与疾病活动度呈正相关且具有显著性（rho 0.4812，P<0.05）。克罗恩病、结节病/结核病患者静息白细胞的NBT还原增加（P<0.01），但在吞噬过程中，克罗恩病患者的NBT还原低于健康志愿者（P<0.02）。克罗恩病中白细胞聚集减少的炎症反应与其他肉芽肿反应患者不同，且与疾病活动度无关。我们的数据表明缺陷并非细胞性的。它们支持这样一种假说，即克罗恩病的致病因素可能是通常会被清除但仍残留在组织中并引发慢性炎症反应的外来物质。
