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马肉芽肿性肠炎中小肠黏膜表面的 topography 及肠上皮细胞形态。(注:“topography”此处结合语境推测可能是指局部解剖结构之类的意思,但因专业语境中该词有多种含义,仅按字面翻译,具体含义需结合医学知识进一步确定)

Topography and enterocyte morphology of the small bowel mucosal surface in equine granulomatous enteritis.

作者信息

Lindberg R, Karlsson L

出版信息

J Comp Pathol. 1985 Jan;95(1):65-78. doi: 10.1016/0021-9975(85)90078-7.

Abstract

The jejunal mucosa of 4 cases of equine granulomatous enteritis and 2 control horses was investigated by light microscopy and by scanning and transmission electron microscopy. Attention was focused upon changes in mucosal topography and enterocyte morphology in the inflamed mucosa. Structural changes ranged in severity from only a slight thickening and shortening of villi to the appearance of a virtually flat mucosa, upon which crypts opened directly or through shallow cavities encircled by collars of epithelial cells. Between these extremes, the mucosa showed a variety of patterns, all characterized by distinctly abnormal villus projections. These were often united by epithelial bridges and were commonly markedly short, broad and irregular. Enterocytes of mildly changed mucosae showed a normal histology and fine structure, whereas more severely changed specimens displayed a flattened surface epithelium with ultrastructural abnormalities, the most consistent being a pronounced shortening of microvilli. In particular, greatly flattened cells showed evidence of cellular injury, such as prominence of cytolysosomes and degenerative changes of the rough endoplasmic reticulum, while other cells were chiefly characterized by an abundance of non-membrane-bound ribosomes and other features signifying an immature state. Cell-membrane-tight junctions of the surface epithelium appeared to be intact. No intracellular micro-organisms were detected. It is suggested that several factors are involved in the creation of the abnormal mucosal topography in this disease, including excessive enterocyte loss, crypt cell destruction, inflammatory distension of villi and villus fusions.

摘要

对4例马肉芽肿性肠炎病例和2匹对照马的空肠黏膜进行了光学显微镜检查以及扫描和透射电子显微镜检查。重点关注炎症黏膜中黏膜形态和肠上皮细胞形态的变化。结构变化的严重程度不一,从绒毛仅轻微增厚和缩短到几乎呈扁平状的黏膜出现,在这种扁平黏膜上,隐窝直接开口或通过由上皮细胞环包围的浅腔开口。在这些极端情况之间,黏膜呈现出多种模式,其特征均为明显异常的绒毛突起。这些突起常通过上皮桥相连,通常明显短、宽且不规则。轻度改变的黏膜中的肠上皮细胞显示出正常的组织学和精细结构,而改变更严重的标本则显示表面上皮扁平且有超微结构异常,最一致的是微绒毛明显缩短。特别是,高度扁平的细胞显示出细胞损伤的迹象,如溶酶体突出和粗面内质网的退行性变化,而其他细胞主要表现为大量无膜结合核糖体和其他表明不成熟状态的特征。表面上皮的细胞膜紧密连接似乎完好无损。未检测到细胞内微生物。提示该疾病中异常黏膜形态的形成涉及多种因素,包括肠上皮细胞过度丢失、隐窝细胞破坏、绒毛的炎症性扩张和绒毛融合。

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