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首页> 外文期刊>Digestive Diseases and Sciences >Fibrocytes are involved in inflammation as well as fibrosis in the pathogenesis of Crohn's disease
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Fibrocytes are involved in inflammation as well as fibrosis in the pathogenesis of Crohn's disease

机译：纤维细胞参与克罗恩病的发病过程中的炎症和纤维化

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Background: We previously showed that fibrocytes, a hematopoietic stem cell source of fibroblasts/myofibroblasts, infiltrated the colonic mucosa of a murine colitis model. Aim: We investigated whether fibrocytes were involved in the pathogenesis of Crohn's disease. Methods: Human surgical intestinal specimens were stained with anti-leukocyte-specific protein 1 and anti-collagen type-I (ColI) antibodies. Circulating fibrocytes in the human peripheral blood were quantified by fluorescence-activated cell sorting with anti-CD45 and anti-ColI antibodies. Cultured human fibrocytes were prepared by culturing peripheral CD14+ monocytes. Results: In the specimens of patients with Crohn's disease, the fibrocyte/total leukocyte percentage was significantly increased in inflammatory lesions (22.2 %, p 0.01) compared with that in non-affected areas of the intestine (2.5 %). Interestingly, the percentage in fibrotic lesions was similar (2.2 %, p = 0.87) to that in non-affected areas. The percentages of circulating fibrocytes/total leukocytes were significantly higher in patients with Crohn's disease than in healthy controls. Both CXC-chemokine receptor 4+ and intercellular adhesion molecule 1 + fibrocyte numbers were significantly increased in Crohn's disease, suggesting that circulating fibrocytes have a higher ability to infiltrate injured sites and traffic leukocytes. In cultured fibrocytes, lipopolysaccharide treatment remarkably upregulated tumor necrosis factor (TNF)-α mRNA (17.0 ± 5.7-fold) and ColI mRNA expression (12.8 ± 5.7-fold), indicating that fibrocytes stimulated by bacterial components directly augmented inflammation as well as fibrosis. Conclusions: Fibrocytes are recruited early in the inflammatory phase and likely differentiate into fibroblasts/ myofibroblasts until the fibrosis phase. They may enhance inflammation by producing TNF-α and can directly augment fibrosis by producing ColI.
机译：背景：我们先前显示，成纤维细胞/成肌纤维细胞的造血干细胞来源纤维细胞浸润了鼠结肠炎模型的结肠粘膜。目的：我们研究了纤维细胞是否参与了克罗恩病的发病机制。方法：用抗白细胞特异性蛋白1和抗I型胶原（ColI）抗体对人外科手术肠道标本进行染色。通过用抗CD45和抗ColI抗体进行荧光激活的细胞分选，定量测定人外周血中的循环纤维细胞。通过培养外周CD14 +单核细胞来制备培养的人纤维细胞。结果：在克罗恩病患者的标本中，与未受影响的肠道区域（2.5％）相比，炎性病变中的纤维细胞/总白细胞百分比显着增加（22.2％，p <0.01）。有趣的是，纤维化病变中的百分比与未受影响地区相似（2.2％，p = 0.87）。克罗恩病患者的循环纤维细胞/总白细胞百分比显着高于健康对照组。在克罗恩病中，CXC-趋化因子受体4+和细胞间粘附分子1+的纤维细胞数量均显着增加，这表明循环的纤维细胞具有更高的浸润损伤部位和交通白细胞的能力。在培养的纤维细胞中，脂多糖处理显着上调了肿瘤坏死因子（TNF）-αmRNA（17.0±5.7倍）和ColI mRNA表达（12.8±5.7倍），表明细菌成分刺激的纤维细胞直接增加了炎症以及纤维化。结论：纤维细胞在炎症期早期被募集，并可能分化为成纤维细胞/成肌纤维细胞，直到纤维化阶段。它们可能通过产生TNF-α增强炎症，并可以通过产生ColI直接增强纤维化。

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