Unger Z, Molnár B, Szaleczky E, Törgyekes E, Müller F, Zágoni T, Tulassay Z, Prónai L
Second Department of Internal Medicine, Clinical Gastroenterology and Endocrinology Unit, Semmelweis University, Budapest, Hungary.
J Physiol Paris. 2001 Jan-Dec;95(1-6):355-60. doi: 10.1016/s0928-4257(01)00048-1.
the effect of Helicobacter pylori infection on gastric epithelial cell proliferation and apoptosis is still controversial. Our aim was to evaluate the effect of H. pylori infection on cell kinetic parameters in normal gastric epithelium, gastritis with/without intestinal metaplasia and gastric cancer.
antral biopsies were taken from 121 patients (61 women, 60 men, mean age 58.5+/-14.3 years of age) who underwent routine gastroscopy for upper gastrointestinal symptoms. Sections were scored for normal epithelia (n=15), gastritis without intestinal metaplasia (n=74), gastritis with intestinal metaplasia (n=24), and gastric adenocarcinoma (n=8). Fifty-two patients had H. pylori positive gastritis, and success of H. pylori eradication therapy was controlled in 12 cases, all with intestinal metaplasia. To characterize cell proliferation and assess apoptosis, immunohistochemistry [Proliferating Cell Nuclear Antigen (PCNA)], histochemistry [Argyrophil Nucleolar Organizer Regions (AgNOR)], and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridinetriphosphate (dUTP) nick end-labeling (TUNEL) were used, respectively.
both cell proliferation and apoptosis is was higher in chronic gastritis when compared with normal epithelia, but neither PCNA LI (54.79+/-19.1 vs. 53.20+/-20.7) nor AgNOR counts (291.43+/-44.3 vs. 277.8+/-57.54) were different in H. pylori positive versus negative chronic gastritis. A significant positive correlation (P<0.05) was found in this group between PCNA and AgNOR techniques. Apoptosis was significantly higher (P<0.05) in H. pylori positive cases only when intestinal metaplasia was not present. Cell proliferation in intestinal metaplasia decreased to the activity of normal epithelium after successful eradication of H. pylori but remained high if eradication therapy failed.
epithelial cell proliferation does not depend on H. pylori status in chronic gastritis. H. pylori increases apoptosis only in the absence of intestinal metaplasia.
幽门螺杆菌感染对胃上皮细胞增殖和凋亡的影响仍存在争议。我们的目的是评估幽门螺杆菌感染对正常胃上皮、伴或不伴肠化生的胃炎以及胃癌细胞动力学参数的影响。
对121例因上消化道症状接受常规胃镜检查的患者（61例女性，60例男性，平均年龄58.5±14.3岁）取胃窦活检组织。对正常上皮（n = 15）、无肠化生的胃炎（n = 74）、有肠化生的胃炎（n = 24）和胃腺癌（n = 8）的切片进行评分。52例患者患有幽门螺杆菌阳性胃炎，其中12例伴肠化生的患者接受了幽门螺杆菌根除治疗并观察疗效。分别采用免疫组织化学[增殖细胞核抗原（PCNA）]、组织化学[嗜银核仁组成区（AgNOR）]和末端脱氧核苷酸转移酶（TdT）介导的脱氧尿苷三磷酸（dUTP）缺口末端标记（TUNEL）来表征细胞增殖和评估凋亡。
与正常上皮相比，慢性胃炎中的细胞增殖和凋亡均较高，但幽门螺杆菌阳性与阴性慢性胃炎之间的PCNA LI（54.79±19.1对53.20±20.7）和AgNOR计数（291.43±44.3对277.8±57.54）均无差异。在该组中，PCNA和AgNOR技术之间存在显著正相关（P<0.05）。仅在无肠化生时，幽门螺杆菌阳性病例的凋亡显著更高（P<0.05）。成功根除幽门螺杆菌后，肠化生中的细胞增殖降至正常上皮的活性水平，但如果根除治疗失败则仍保持较高水平。
慢性胃炎中的上皮细胞增殖不依赖于幽门螺杆菌状态。幽门螺杆菌仅在无肠化生时增加凋亡。
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