EPITHELIAL CYTOTOXICITY, IMMUNE-RESPONSES, AND INFLAMMATORY COMPONENTS OF HELICOBACTER-PYLORI GASTRITIS
EPITHELIAL CYTOTOXICITY, IMMUNE-RESPONSES, AND INFLAMMATORY COMPONENTS OF HELICOBACTER-PYLORI GASTRITIS
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DOI：
10.3109/00365529409091404
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发表时间：
1994-01-01
影响因子：
1.9
通讯作者：
SOLCIA, E
中科院分区：
文献类型：
--
作者：
FIOCCA, R;LUINETTI, O;SOLCIA, E
为了阐明幽门螺杆菌感染引起的胃粘膜免疫炎症反应的机制，对来自无症状未感染、无胃炎个体和来自幽门螺杆菌感染者的手术和活检标本进行了研究。用光镜和电镜观察了幽门螺杆菌阳性溃疡伴慢性胃炎患者。在H.幽门定植的胃上皮。这些发现可能是至关重要的粘膜免疫炎症反应的生产H。幽门感染细胞质肿胀和空泡化、微乳头改变、粘蛋白丢失、胃粘膜细胞质侵蚀和细胞脱落是细菌细胞毒性对胃表面-小凹上皮的主要作用。活化的巨噬细胞和粒细胞（部分与粘膜IgG免疫应答相关）集中在粘膜的小凹颈部区域，在那里它们可能增强上皮的损伤并损害上皮的再生。直接的细菌细胞毒性和炎性细胞对胃上皮的侵袭都可能使患者易患消化性溃疡病。
To clarify the mechanisms of the gastric mucosal immune-inflammatory response to Helicobacter pylori infection, surgical and biopsy specimens from asymptomatic uninfected, gastritis-free individuals and from H. pylori-positive ulcer patients with chronic gastritis were investigated using light and electron microscopy. Activation of the antigen-transporting endocytic-endosomal system, enhanced expression of the antigen-processing enzyme cathepsin E and de novo expression of antigen-presenting human leukocyte antigen (HLA)-DR molecules have been detected in H. pylori-colonized gastric epithelium. These findings may be crucial in the production of a mucosal immune-inflammatory response to H. pylori infection. Cytoplasmic swelling and vacuolation, micropapillary change, mucin loss, erosion of the juxtaluminal cytoplasm and cell desquamation were the main effects of bacterial cytotoxicity on gastric surface-foveolar epithelium. Activated macrophages and granulocytes (partly linked to the mucosal IgG immune response) concentrate in the foveolar-neck region of the mucosa, where they may enhance damage and impair regeneration of the epithelium. Both direct bacterial cytotoxicity and inflammatory cell aggression against gastric epithelium may predispose the patient to peptic ulcer disease.