Allison M C, Poulter L W
Gastroenterology Unit, Royal Infirmary, Glasgow, UK.
Clin Exp Immunol. 1991 Sep;85(3):504-9. doi: 10.1111/j.1365-2249.1991.tb05757.x.
Previous studies have demonstrated the presence of much more marked macrophage heterogeneity in colonic mucosa affected by the idiopathic inflammatory bowel diseases (ulcerative colitis and Crohn's disease) than in normal mucosa. This study examines the morphology, distribution and phenotypic expression of mucosal macrophage-like cells in biopsies from patients with idiopathic inflammatory bowel disease in comparison with disease control samples from patients with colonic infection or ischaemia. Approximately 80% of macrophage-like cells in histologically normal mucosa co-express the antigens recognized by the monoclonal antibodies RFD1 (an interdigitating cell marker) and RFD7 (a marker for mature tissue macrophages). In idiopathic inflammatory bowel disease, the normal colonic macrophage population is partly replaced by cells staining positively with RFD7 alone, and, to a lesser extent, with RFD1+ dendritic cells. Sections from patients with infections and ischaemia exhibited epithelial HLA-DR positivity and infiltration of the lamina propria by a more heterogeneous population of macrophages than that seen in histologically normal mucosa. However, the displacement of the normal colonic macrophage phenotype by RFD7+ tissue macrophages occurred to a significantly greater extent in idiopathic inflammatory bowel disease than in disease control mucosa. A pathognomonic feature of the ulcerative colitis and Crohn's colitis sections was the clustering of RFD9+ epithelioid cells at the bases of disrupted crypts and adjacent to areas of mucosal damage. It is concluded that a degree of macrophage heterogeneity and macrophage infiltration can occur as a non-specific response to colonic mucosal damage. The distinctive feature of idiopathic inflammatory bowel disease mucosa is the almost complete replacement of the normal colonic mucosal macrophage population by tissue macrophages and epithelioid cells, and this phenomenon may be important in promoting the development of a chronic inflammatory state.
先前的研究表明，与正常黏膜相比，受特发性炎症性肠病（溃疡性结肠炎和克罗恩病）影响的结肠黏膜中巨噬细胞的异质性更为显著。本研究检查了特发性炎症性肠病患者活检组织中黏膜巨噬细胞样细胞的形态、分布和表型表达，并与结肠感染或缺血患者的疾病对照样本进行了比较。在组织学正常的黏膜中，约80%的巨噬细胞样细胞共表达单克隆抗体RFD1（一种交错突细胞标志物）和RFD7（成熟组织巨噬细胞的标志物）所识别的抗原。在特发性炎症性肠病中，正常的结肠巨噬细胞群体部分被仅RFD7染色阳性的细胞取代，在较小程度上被RFD1+树突状细胞取代。感染和缺血患者的切片显示上皮细胞HLA-DR阳性，固有层有比组织学正常黏膜中更异质性的巨噬细胞浸润。然而，与疾病对照黏膜相比，RFD7+组织巨噬细胞对正常结肠巨噬细胞表型的取代在特发性炎症性肠病中更为显著。溃疡性结肠炎和克罗恩结肠炎切片的一个特征性表现是RFD9+上皮样细胞在隐窝破坏底部和黏膜损伤区域附近聚集。结论是，巨噬细胞异质性和巨噬细胞浸润程度可作为对结肠黏膜损伤的非特异性反应而出现。特发性炎症性肠病黏膜的独特特征是正常结肠黏膜巨噬细胞群体几乎完全被组织巨噬细胞和上皮样细胞取代，这种现象可能在促进慢性炎症状态的发展中起重要作用。
