Sakakibara M, Morise K, Takashi H, Ohta M
First Department of Internal Medicine, Nagoya University School of Medicine.
Nihon Shokakibyo Gakkai Zasshi. 1994 May;91(5):956-68.
The distribution and localization of Helicobacter pylori (HP) and mononuclear cells (MNC) in the gastric mucosa were investigated immunohistochemically in 120 patients with gastritis or peptic ulcer. HP was detected in the gastric mucosa of 58% of 40 gastritis patients, 82% of 56 gastric ulcer (GU) patients, and 88% of 24 duodenal ulcer (DU) patients. In the HP-positive mucosa, cells positive for IgG or IgA were increased significantly when compared to the HP-negative mucosa. Neutrophils and eosinophils were also increased under the HP-infected surface and therefore these cells were likely involved in the mucosal damage. Enhancement of the expression of HLA-DR antigen was observed in the gastric epithelium with HP infection and it was associated with a significant increase of lymphoid follicles and B cells in the mucosa. In comparison with the HP-infected mucosa of gastritis patients, the number of MNC were increased significantly in the mucosa of both DU and GU patients. The number of HP in the gastric mucosa of DU patients was significantly higher than those of both gastritis and GU patients. In addition, the grade of the infiltration of MNC and IgA positive cells were always greater in DU than in gastritis, regardless of the number of HP. These findings suggested that activation of the local immunity in the gastric mucosa of gastritis and peptic ulcer patients by HP infection may participate in the pathogenesis of gastroduodenal mucosa damage.
采用免疫组织化学方法,对120例胃炎或消化性溃疡患者胃黏膜中幽门螺杆菌(HP)和单核细胞(MNC)的分布及定位进行了研究。在40例胃炎患者中,58%的患者胃黏膜检测到HP;56例胃溃疡(GU)患者中,82%检测到HP;24例十二指肠溃疡(DU)患者中,88%检测到HP。与HP阴性的胃黏膜相比,HP阳性胃黏膜中IgG或IgA阳性细胞显著增多。在HP感染的黏膜表面下,中性粒细胞和嗜酸性粒细胞也增多,因此这些细胞可能参与了黏膜损伤。HP感染的胃上皮细胞中观察到HLA - DR抗原表达增强,且与黏膜中淋巴滤泡和B细胞显著增多有关。与胃炎患者的HP感染黏膜相比,DU和GU患者黏膜中的MNC数量显著增加。DU患者胃黏膜中的HP数量显著高于胃炎和GU患者。此外,无论HP数量多少,DU患者MNC和IgA阳性细胞的浸润程度总是高于胃炎患者。这些结果提示,HP感染激活胃炎和消化性溃疡患者胃黏膜局部免疫,可能参与了胃十二指肠黏膜损伤的发病机制。