BACTERIAL ADHESION AND DISEASE-ACTIVITY IN HELICOBACTER ASSOCIATED CHRONIC GASTRITIS
BACTERIAL ADHESION AND DISEASE-ACTIVITY IN HELICOBACTER ASSOCIATED CHRONIC GASTRITIS
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DOI：
10.1136/gut.31.2.134
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发表时间：
1990-02-01
期刊：
影响因子：
24.5
通讯作者：
DIXON, MF
中科院分区：
文献类型：
--
作者：
HESSEY, SJ;SPENCER, J;DIXON, MF
幽门螺杆菌相关性慢性胃炎活检的超微结构检查显示胃表面上皮细胞与机体之间的紧密附着。“粘附细胞”的发现代表了细胞对生物体存在的反应，类似于肠细胞对肠致病性大肠杆菌的反应。因此，幽门螺杆菌相关性胃炎中细菌附着位点的发展可能是致病性的指示。因此，我们探索了形成附着位点的生物体的比例与疾病“活动性”的组织学指标之间的关系。对40例幽门螺杆菌阳性胃炎患者胃窦活检组织进行了组织学和超微结构检查，并与上皮变性、粘蛋白耗竭、多形性和慢性炎性细胞浸润的主观评估进行了比较。我们发现在组织学上皮变性的病例中附着细菌的比例显著增加，而在上皮内多形物浸润的病例中附着细菌的比例显著减少。细菌附着和细胞变性之间的直接关系进一步支持了致病作用。在面对多形物浸润的附着减少可能间接反映了免疫反应的方面-即，通过伊加阻断粘附，伴随补体激活和白细胞趋化因子的产生。
Ultrastructural examination of biopsies showing Helicobacter pylori associated chronic gastritis reveals close attachment between gastric surface epithelial cells and the organism. The finding of 'adhesion pedestals', which represents a cellular response to the presence of the organism, is analogous to the response of intestinal cells to enteropathogenic E coli. Thus the development of bacterial attachment sites in H pylori associated gastritis might be an indication of pathogenicity. We have therefore explored the relationship between the proportion of organisms forming attachment sites and histological indices of disease 'activity'. Antral biopsies from 40 patients with H pylori positive gastritis were examined histologically and ultrastructurally, and the percentage of attached organisms compared with subjective assessments of epithelial degeneration, mucin depletion, polymorphonuclear and chronic inflammatory cell infiltration. We found a significant increase in the proportion of attached bacteria in cases showing histological epithelial degeneration, and a significant decrease in cases showing intraepithelial polymorph infiltration. The direct relationship between bacterial attachment and cellular degeneration lends further support to a pathogenic effect. Reduced attachment in the face of polymorph infiltration might indirectly reflect aspects of the immune response--namely, blocking of adhesion by IgA, with complement activation and generation of leucotactic factors.