Grimm M C, Pullman W E, Bennett G M, Sullivan P J, Pavli P, Doe W F
Division of Clinical Sciences, John Curtin School of Medical Research, Australian National University, Canberra, Australia.
J Gastroenterol Hepatol. 1995 Jul-Aug;10(4):387-95. doi: 10.1111/j.1440-1746.1995.tb01589.x.
Alterations in phenotype and function of intestinal macrophages occur in inflammatory bowel disease (IBD) but it is unclear whether these changes result from the recruitment of circulating monocytes to the intestine or from proliferation of resident intestinal macrophages. We sought to demonstrate the arrival of blood monocytes, the precursors of macrophages, in IBD mucosa. Peripheral blood mononuclear cells were isolated from 23 patients with clinically active intestinal inflammation (13 Crohn's disease, eight ulcerative colitis, two infective colitis), then radiolabelled with 99mtechnetium (Tc)-stannous colloid (n = 13) or 111indium (In)-oxine (n = 10) before re-injection and abdominal scanning. Four patients had demonstrable intestinal monocyte uptake using [99mTc]-stannous colloid, while six [111In]-oxine-labelled monocyte scans were positive. Uptake sites correlated with actively inflamed regions. Patients demonstrating monocyte uptake had been treated with corticosteroids for a significantly (P < 0.02) shorter duration (median 3 vs 20 days) than those with negative scans. There was no significant difference between positive and negative scans for disease category, clinical or histological disease, activity, or radioisotope used. Biopsies of inflamed mucosa from two patients suffering ulcerative colitis who had positive scans showed a high proportion of CD14-positive macrophages, 4-9% of which contained autoradiographic grains. These results demonstrate that blood monocytes are recruited to the mucosa of actively inflamed bowel, and suggest that this process may be inhibited by corticosteroids. Moreover, the phenotype of the recently-arrived monocytes indicates their susceptibility to stimulation by lipopolysaccharide, and suggests a mechanism for the continuing inflammation in the bacterial product-rich milieu of IBD.
炎症性肠病（IBD）中肠道巨噬细胞的表型和功能会发生改变，但尚不清楚这些变化是由于循环单核细胞募集至肠道，还是由于常驻肠道巨噬细胞增殖所致。我们试图证明巨噬细胞的前体——血液单核细胞在IBD黏膜中的抵达情况。从23例临床活动期肠道炎症患者（13例克罗恩病、8例溃疡性结肠炎、2例感染性结肠炎）中分离出外周血单核细胞，然后用99m锝（Tc）-锡胶体（n = 13）或111铟（In）-奥克辛（n = 10）进行放射性标记，之后再注射并进行腹部扫描。4例患者使用[99mTc]-锡胶体显示出肠道单核细胞摄取，而6例[111In]-奥克辛标记的单核细胞扫描呈阳性。摄取部位与活跃炎症区域相关。显示单核细胞摄取的患者接受皮质类固醇治疗的时间（中位数3天对20天）明显（P < 0.02）短于扫描阴性的患者。疾病类别、临床或组织学疾病、活动度或所用放射性同位素在阳性和阴性扫描之间无显著差异。对2例溃疡性结肠炎且扫描阳性患者的炎症黏膜活检显示，CD14阳性巨噬细胞比例较高，其中4 - 9%含有放射自显影片颗粒。这些结果表明血液单核细胞被募集至活跃炎症肠道的黏膜，提示该过程可能受到皮质类固醇的抑制。此外，最近抵达的单核细胞的表型表明它们易受脂多糖刺激，提示了IBD富含细菌产物环境中持续炎症的一种机制。
