摘要
AIM： To investigate the expression of different cytokeratins （CKs） in gastric epithelium of adult patients with chronic gastritis infected with Helicobacter pylori （H pylon） cagA ＋ strains. METHODS： The expression of CK 7, 8, 18, 19 and 20 was studied immunohistochemically in antral gastric biopsies of 84 patients. All the CKs were immunostained in cagA＋Hpylori gastritis （57 cases）, non-Hpylori gastritis （17 cases） and normal gastric mucosa （10 cases）. RESULTS： In cagA＋ H pylori gastritis, CK8 was expressed comparably to the normal antral mucosa from surface epithelium to deep glands. Distribution of CK18 and CK 19 was unchanged, i.e. transmucosal, but intensity of the expression was different in foveolar region in comparison to normal gastric mucosa. Cytokeratin 18 immunoreactivity was significantly higher in the foveolar epithelium of H pylori-positive gastritis compared to both Hpylori-negative gastritis and controls. On the contrary, decrease in CK19 immunoreactivity occurred in foveolar epithelium of H pylori-positive gastritis. In both normal and inflamed antral mucosa without Hpyloriinfection, CK20 was expressed stronglyl moderately and homogenously in surface epithelium and upper foveolar region, but in H pylod -induced gastritis significant decrease of expression in foveolar region was noted. Generally, in both normal antral mucosa and H pylori-negative gastritis, expression of CK7 was not observed, while in about half cagA＋ H pylori-infected patients, moderate focal CK7 immunoreactivity of the neck and coiled gland areas was registered, especially in areas with more severe inflammatory infiltrate. CONCLUSION： Alterations in expression of CK 7, 18, 19 and 20 together with normal expression of CK8 occur in antral mucosa of H pylori-associated chronic gastritis in adult patients infected with cagA＋ strains. Alterations in different cytokeratins expression might contribute to weakening of epithelial tight junctions observed in H pylori-infected gastric mucosa.
瞄准：为了与长期的胃炎在成年病人的胃的上皮调查不同 cytokeratins (CK ) 的表示，与 Helicobacter pylori (H pylori ) 感染了 cagA+ 紧张。方法：CK 7 的表示， 8， 18， 19 和 20 在 84 个病人的窦的胃的活体检视组织化学地是学习免疫。所有 CK 是在 cagA+H pylori 胃炎(57 个案例) 染色的免疫， non-H pylori 胃炎(17 个案例) 和正常胃粘膜(10 个案例) 。结果：在 cagA+ H pylori 胃炎， CK8 从表面上皮可比较地被表示到正常的窦粘膜到深腺。CK18 和 CK 19 的分发是未改变的，即表示的 transmucosal，而是紧张在与正常相比的小凹的区域是不同的胃粘膜。Cytokeratin 18 免疫反应在与 H pylori 否定的胃炎和控制相比的 H pylori 积极的胃炎的小凹的上皮是显著地更高的。相反，在 CK19 免疫反应的减少发生在 H pylori 积极的胃炎的小凹的上皮。在没有 H pylori 感染的正常、煽动的窦粘膜， CK20 在表面上皮和上面的小凹的区域强烈 / 中等并且同类地被表示，但是在 H， pylori 导致了胃炎在小凹的区域的表示的重要减少被注意。通常，在正常窦的粘膜和 H pylori 否定的胃炎，， CK7 的表示没被观察在关于半 cagA+ ， H 感染 pylori 的病人，节制颈的焦点的 CK7 免疫反应，卷的腺区域被登记，特别在区域与更严重煽动性渗入。结论：在 CK 7 的表示的改变， 18， 19 和 20 在感染 cagA+ 紧张的成年病人和 CK8 的正常表示发生在 H 联系 pylori 的长期的胃炎的窦粘膜。在不同 cytokeratins 表示力量的改变贡献在 H 感染 pylori 的胃粘膜观察的上皮的紧密的连接变弱。
基金
Supported by a grant from Serbian Ministry for Science and Environmental Protection,No.1752
