Anti-Helicobacter pylori therapy significantly reduces Helicobacter pylori -induced gastric mucosal damage in Mongolian gerbils

AIM: To investigate the effectiveness of 4 d‘anti-Helicobacter pyloritherapy on the H pylori-infected Mongolian gerbils based on physiological and pathological changes. METHODS: We used 6-wk-old male gerbils orally inoculated with H pylori (ATCC43504, 2×10^8 CFU/mL). Seven weeks alter Hpyloriinoculation, the animals of study group received 4 d‘arti-H pyloritriple therapy (Hpylorieradicated group). Seven days later, all animals of the H pylori-eradicated and control groups (H pylori-infected & H pylori-uninfected groups) were sacrificed. We examined gastric mucosal lesions macroscopically, studied gastritis microscopically and determined the stomach weight ratio, myeloperoxidase (MPO) activity and prostaglandin (PG) E2 level. RESULTS: The results showed that both macroscopic and histological gastric damages were significantly less in H pylori-eradicated group than H pylori-infected group. Stomach weight ratio, MPO activity and PGE2 levels were significantly higher in H pylori-infected group than those in the other two groups. CONCLUSION: Four days‘anti-H pylori therapy was effective in the improvement of H pylori-induced gastric lesions in Mongolian gerbils.     

Anti-Helicobacter pylori therapy significantly reduces Helicobacter py/ori-Induced gastric mucosal damage in Mongolian gerbils

AIM: To investigate the effectiveness of 4 d' anti-Helicobacter pylori therapy on the H pylori-infected Mongolian gerbils based on physiological and pathological changes. METHODS: We used 6-wk-old male gerbils orally inoculated with H pylori (ATCC43504, 2×108 CFU/mL). Seven weeks after H pylori inoculation, the animals of study group received 4 d' anti-H pylori triple therapy (H pylori-eradicated group). Seven days later, all animals of the H pylori-eradicated and control groups (H pylori-infected & H pylori-uninfected groups) were sacrificed. We examined gastric mucosal lesions macroscopically, studied gastritis microscopically and determined the stomach weight ratio, myeloperoxidase (MPO) activity and prostaglandin (PG) E2 level. RESULTS: The results showed that both macroscopic and histological gastric damages were significantly less in H pylori-eradicated group than H pylori-infected group. Stomach weight ratio, MPO activity and PGE2 levels were significantly higher in H pylori-infected group than those in the other two groups. CONCLUSION: Four days' anti-H pylori therapy was effective in the improvement of H pylori-induced gastric lesions in Mongolian gerbils.     

幽门螺杆菌长期感染蒙古沙土鼠腺胃模型的建立及评价

目的 建立幽门螺杆菌（Helicobacter pylori,Hp）长期感染蒙古沙土鼠腺胃模型,验证该模型出现的病理改变及腺胃肿瘤的发生情况。方法 采用国际标准菌株NCTC 11637灌喂蒙古沙土鼠,建立HP长期感染蒙古沙土鼠腺胃模型。结果 成功建立了HP长期感染蒙古沙土鼠腺胃模型,其胃黏膜的组织学变化显示,HP感染可致正常胃黏膜→慢性胃炎→萎缩→肠化生→异型增生的发展过程,Hp NCTC 11637定植于蒙古沙土鼠腺胃65财哩,可引起胃黏膜出现严重的萎缩、肠化生及不典型增生等胃癌前状态,暂未发现早期癌。结论 Hp NCTC 11637易长期定植于蒙古沙土鼠腺胃,模型的稳定性及重复性极佳,且与Hp感染人胃黏膜后出现的各种病理变化极为相似。     

Helicobacter pylori strain-specific modulation of gastric inflammation in Mongolian gerbils

AIM: The cag pathogenicity island (PAI) is one of potential virulence determinants of Helicobacter pylori. The Mongolian gerbil is a suitable experimental animal for the screening of virulence factors of H pylori. METHODS: Five-week-old Mongolian gerbils were inoculated with a standard H pylori strain (ATCC 43504) possessing the cag PAI or a clinical isolate lacking the genes' cluster (OHPC-0002). The animals were killed at 2, 4, 8, 24 and 48 wk after inoculation (n=5 each), and macroscopic and histopathological findings in the stomachs were compared. RESULTS: In gerbils infected with ATCC 43504, a more severe degree of infiltration of polynuclear and mononuclear cells and lymphoid follicles was observed from 4 wk after inoculation compared to gerbils infected with OHPC-0002 especially in the antrum and transitional zone from the fundic to pyloric gland area. In addition, glandular atrophy, intestinal metaplasia, gastric ulcer and hyperplastic polyps were noted in gerbils infected with ATCC 43504, whereas only mild gastric erosions occurred in those infected with OHPC-0002. CONCLUSION: Our results indicate that the cag PAI could be directly involved in gastric immune and inflammatory responses in the Mongolian gerbils, leading to a more advanced gastric disease.     

Development of gastric adenocarcinoma in Mongolian gerbils after long-term infection with Helicobacter pylori

BACKGROUND AND AIM: The experimental evidence that long-term colonization of Helicobacter pylori results in the development of gastric cancer in Mongolian gerbils has been reported only by two Japanese groups to date. This study aimed to investigate the carcinogenicity of H. pylori infection in a Mongolian gerbil model. METHODS: Thirty-six Mongolian gerbils (inner Mongolian origin) were divided into two groups (male to female ratio, 1:1) and orally inoculated with a standard H. pylori strain (ATCC43504) or H. pylori161 (isolated from a Chinese patient with gastric adenocarcinoma), respectively, once a week for 5 weeks. Another 10 control gerbils were given phosphate-buffered saline. The animals were killed 8, 20, 28 and 84 weeks after inoculation for bacterial and histological examination. RESULTS: Seven inoculated gerbils died at the week 42. Overall, H. pylori colonization was detected in 24 (83%) of the 29 available inoculated gerbils. The gastric lesions were aggravated gradually over time. At week 84, moderate to severe gastritis, characterized by diffuse infiltration of mononuclear cells and formation of multiple lymphoid follicles in mucosa and submucosa, and even the lymphoepithelial lesions, were observed. Epithelial hyperplasia were dominant in almost all gerbils. Four (24%) of the 17 animals had hyperplastic polyps. Intestinal metaplasia were rarely seen (in three gerbils). Well-differentiated gastric adenocarcinomas developed in three (18%) of the 17 gerbils after 84 weeks. Of the three gerbils, one female gerbil was infected with H. pylori161 and the others (one male and one female) were infected with ATCC43504. CONCLUSIONS: The present study reconfirms that H. pylori infection alone can induce gastric adenocarcinoma in Mongolian gerbils and suggests that different species of gerbil and both standard and clinically isolated H. pylori strains can be used for investigating the carcinogenesis of H. pylori. This is the first report of the development of gastric cancer in female gerbils, which highlights the importance of using both sexes to investigate the pathogenesis of H. pylori and whether host susceptibility is influenced by sex.     

蒙古沙土鼠不同幽门螺杆菌菌株感染相关性胃病的研究进展

幽门螺杆菌(Helicobacter pylori,H.pylori)感染在世界范围内高发,他定植于人胃黏膜,导致慢性胃炎及胃癌的发生.蒙古沙鼠(mongolian gerbil,MG)很少患自发性胃炎,且不是H.pylori 的自然宿主.人工接种H.pylori后,蒙古沙鼠患H.pylori相关性胃病与胃病患者最相似...     

NSAIDs在幽门螺杆菌相关性胃黏膜病变中的作用

目的 了解NSAIDs与Hellicobecter pylori感染在胃黏膜病变中的作用。方法 患者190例，①病例选择：连续服用NSAIDs治疗2周-12周190例。男性121例，女性69例。平均年龄55岁。②均经胃镜检查和病理组织学检查。对糜烂性胃炎的胃镜诊断和病理诊断胃黏膜炎症分级。③进行H．pylori感染的检测。分为H．pylori感染组与H．prlori阴性组。分析两组的病理组织学改变的特点，了解是否有显著性差异。结果 ①胃镜检查，轻度糜烂106例（55．8％，106／190）。中．重度糜烂84例（44．2％，84／190）。糜烂性胃炎的轻重程度与服药的剂量时间无明显的相关性。②H．pylori感染组46例（24．2％）。H．prlori阴性组144例（75．8％）。③两组病人胃镜诊断的糜烂性胃炎程度无显著性差异（P〉0．05）。④病理情况：H．prlori感染组黏膜中．重度胃炎明显多于H．prlori阴性组（P〈0．01）。⑤病理改变中有淋巴组织增生56例。其中H．prlori感染组有淋巴组织增生22例（47．8％），H．prlori阴性组34例（23．6％）。134例未见淋巴组织增生，其中H．pylori感染组24例（52．2％），H．pylori阴性组110例（76．4％）。两组相比，有显著性差异（P〈0．01）。结论 服用NSAIDs2周以上对胃黏膜有不同程度的损伤。服用NSMDs同时合并H．pylori感染的患者的胃黏膜损伤的严重程度远远高于非感染组。NSAIDs与H．pylori感染是导致胃黏膜损伤的独立危险因子，它们对胃黏膜的损伤作用是叠加的。NSAIDs相关性胃病合并H．pylori感染，根除H．prlori治疗是必要的。     

幽门螺杆菌长期感染蒙古沙土鼠建立胃癌模型的研究

目的：幽门螺杆菌（Hp）长期感染蒙古沙土鼠（MGs)发生胃癌鲜见报道。本实验旨在研究Hp长期定植于MGs导致胃黏膜病变及其致癌性。方法：36只交封闭MGs（雌雄各半）分别接种Hp标准株ATCC43504，或从胃癌患者胃内分离的Hp161株，10只MGs作为对照，接种后第8、20、28和84周分别处死，检查细菌定植及胃黏膜病变情况。结果：绝大多数MGs胃内Hp持续定植，胃黏膜炎症随时间逐渐加重，第84周组织学特征是胃黏膜中－重度胃炎，以淋巴细胞为主的单核细胞弥漫性浸润，黏膜，黏膜下，甚至浆膜下有大量淋巴滤泡浸润，偶见淋巴上皮病变，萎缩，肠化较少见，上皮增生明显，24％（4／17）发生增生性息肉，第84周时18％（3／17）发生高分化腺癌（Hp161组1例，ATCC43504组2例；1雄2雌），结论：单独感染Hp能诱导MGs发生胃癌，并提示可利用不同种属的MGs和不同Hp菌株进行相关研究，首次报道了雌性MGs感染也可发生胃癌。     

Non-steroidal anti-inflammatory drugs have bacteriostatic and bactericidal activity against Helicobacter pylori

BACKGROUND: Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) are each associated with gastrointestinal mucosal damage, but the extent and direction of their interactions remain controversial. Therefore, the purpose of the present paper was to examine whether specific NSAIDs inhibit the growth of Helicobacter pylori in vitro. METHODS: Sodium salicylate, ibuprofen, indomethacin, the selective cyclooxygenase-2 inhibitor NS-398 and two derivatives of sulindac sulfoxide were tested against two laboratory strains of H. pylori, the mouse-adapted Sydney strain, and against seven fresh clinical isolates of Helicobacter pylori. Possible effects on Campylobacter jejuni, Staphyloccoccus aureus, Escherichia coli, Salmonella typhimurium, and Shigella boydii were also examined. RESULTS: Certain NSAIDs possess antibacterial activity against Helicobacter pylori at therapeutically achievable doses; an effect that appears to be independent of cyclooxygenase enzymes inhibition. For Helicobacter pylori, >90% growth inhibition and bactericidal activity were observed consistently for sulindac sulfide at < or =70 microg/mL and sulindac sulfone at < or =175 microg/mL. The minimal inhibitory concentration against Helicobacter pylori was 125 microg/mL for ibuprofen, 100 microg/mL for indomethacin and 300 microg/mL for NS-398 but much higher concentration of sodium salicylate (4000 microg/mL) and sulindac sulfoxide (> or =1250 microg/mL) were required to inhibit the growth of Helicobacter pylori. CONCLUSIONS: The decreased prevalence of Helicobacter pylori in specimens from some NSAID users and the chemopreventive effects of NSAIDs in gastric cancer may be related to inhibition of Helicobacter pylori growth.     

Long-term effects of Helicobacter pylori eradication in Mongolian gerbils

Background: In this study, to clarify whether Helicobacter pylori eradication alters the course of the development of gastric mucosal changes in the stomach, we examined the long-term effects of H. pylori eradication on H. pylori-inoculated gerbils. Methods: A total of 40 H. pylori-inoculated gerbils were randomized and subjected, at 22 months after inoculation, to eradication treatment with dual therapy of omeprazole plus clarithromycin, or with therapy with a novel quinolone compound, Y-34867, alone. The animals were killed at the start of administration (control group) or at 8 months after the completion of therapy (vehicle or eradication-treatment groups). Results: Severe histopathological changes in the gastric mucosa were observed in all H. pylori-inoculated gerbils at the start of administration. At 8 months after completion of therapy, the frequency of gastritis, erosion, intestinal metaplasia, and gastric carcinoid in the eradication therapy groups was markedly reduced compared with that in the control and vehicle groups. Values for anti-H. pylori IgG titer, bacterial counts, and gastrin also decreased significantly. Conclusions: These results suggest that H. pylori eradication may have had a therapeutic effect not only on gastritis, erosion, and gastric ulcer but also on glandular atrophy, intestinal metaplasia, and gastric carcinoid. Received: November 8, 2001 / Accepted: May 31, 2002 Reprint requests to: F. Hirayama     

幽门螺杆菌诱导蒙古沙鼠胃上皮细胞凋亡可能涉及线粒体途径

目的建立幽门螺杆菌(Hp)感染蒙古沙鼠模型,探讨线粒体途径在Hp诱导胃上皮细胞凋亡中的作用。方法 48只雄性蒙古沙鼠均分为Hp感染组和对照组,每组分别于1、3和6个月3个时相点各处死8只动物,取胃黏膜行组织学检查:用Warthin-Starry银染、PCR和快速尿素酶法检测 Hp;通过H-E染色,光镜下观察胃黏膜病理变化;流式细胞仪测定细胞凋亡、线粒体膜电位及胞内游离 Ca2+含量。结果 Hp感染蒙古沙鼠后,胃黏膜出现慢性胃炎、肠化生及异型增生改变,而对照组胃黏膜基本正常,Hp感染组肠化生及异型增生发生率明显高于对照组(P<0．05)。Hp感染胃上皮细胞1、3、 6个月后的凋亡率分别为(16．71±3．30)％、(5．90±0．82)％、(5．69±0．70)％,而对照组的凋亡率分别为(4．20±0．94)％、(3．17±0．43)％、(4．70±0．55)％。其中Hp感染1个月后胃上皮细胞的凋亡率高于其他各组(P<0．05)。Hp感染胃上皮细胞1、3、6个月后的线粒体膜电位分别为43．10±17．62、 71．19±38．03、80．56±32．90,而对照组分别为84．70±23．50、84．39±37．51、79．54±30．24,其中Hp 感染1个月后胃上皮细胞的线粒体膜电位低于其他各组(P<0．05);Hp感染1、3、6个月后胃上皮细胞内游离Ca2+含量分别为18．60±9．32、5．18±2．06、4．94±3．25,而对照组分别为4．82±3．70、6．86 ±2．34、5．28±3．13,Hp感染1个月后胃上皮细胞内游离Ca2+含量高于其他各组(P<0．05)。结论 Hp诱导蒙古沙鼠胃上皮细胞凋亡主要发生在Hp感染早期;线粒体膜电位的下降和胞内游离Ca2+含量的升高参与了Hp诱发蒙古沙鼠胃上皮细胞凋亡的过程。     

Effects of Helicobacter pylori infection on gastric acid secretion and serum gastrin levels in Mongolian gerbils

BACKGROUND AND AIMS: Body gastritis caused by Helicobacter pylori infection appears to inhibit gastric acid secretion. The aim of this study was to determine the effects of H pylori infection on gastric acid secretion and clarify its mechanisms with reference to interleukin 1beta (IL-1beta). METHODS: (1) Mongolian gerbils were inoculated orally with H pylori. Before, six, and 12 weeks after inoculation, serum gastrin levels, gastric acid output, and IL-1beta mRNA levels in the gastric mucosa were determined. Pathological changes were also determined according to the updated Sydney system. (2) Effects of recombinant human IL-1 receptor antagonist (rhIL-1ra) on gastric acid output and serum gastrin levels were also determined. RESULTS: (1) Scores for activity and inflammation of gastritis and serum gastrin levels were significantly increased, and gastric acid output was significantly decreased six and 12 weeks after inoculation with H pylori. IL-1beta mRNA levels in the gastric mucosa were also elevated six and 12 weeks after inoculation with H pylori. (2) Acid output and serum gastrin levels in the infected groups returned to control levels after rhIL-1ra injection. CONCLUSIONS: Gastric acid secretion is decreased and serum gastrin levels are increased in Mongolian gerbils infected with H pylori. This change in gastric acid secretion appears to be mediated by IL-1beta induced by H pylori infection.     

幽门螺杆菌相关性胃部疾病的病理变迁

目的：探讨幽门螺杆菌（Hp)清除与否与胃黏膜病理转归的关系。方法：191Hp感染的胃炎或溃疡病患者分别随机给予抗Hp或非抗Hp治疗,1年后复查胃镜,病理分型根据悉系统。结果191例患者中,慢性炎症1年后的炎症程度较1年前减轻（P＜0．05）。其中萎缩和肠化生的程度也较前减轻（P＜0．05）,但活性动性炎症和蔼前后比较差异无显著性（P＜0．05）。根据1年后胃镜复查有无Hp清除分为两个队列,Hp清除列有107例,Hp未肖除列有84例,Hp清除列较未清除列1年后慢性炎症程度轻（P＜0．05）活动性炎症者少（P＜0．05）。对不疾病和不同的治疗分层后发现,Hp清除者的胃黏膜炎症程度总是较Hp未清除者轻（P＜0．05）。结论本研究提示,Hp感染与胃黏膜活动性炎症关系较为密切。Hp清除有利于胃黏膜炎症程度的减轻。     

Long‐term infection with Helicobacter pylori in Mongolian gerbils

Objective: To investigate pathological changes occurring in the stomach of the Mongolian gerbil during long‐term Helicobacter pylori infection. Methods: Four‐week‐old male Mongolian gerbils were used, which were free from specific pathogens. Eighty Mongolian gerbils were inoculated orally with a suspension of H. pylori NCTC 11637 (0.5 mL, 2 × 10¹⁰ CFU/L) in a Brucella broth. To act as controls, a further 30 gerbils were fed with a Brucella broth only. Infected gerbils were killed 10, 25, 45, 55 and 65 weeks after infection. Control gerbils were killed at 10, 45 and 65 weeks. The stomach of each gerbil was removed and opened. Stomach samples for histological examination were fixed in neutral buffered formalin, embedded in paraffin, sectioned and stained with hematoxylin and eosin for analyzing histological changes, Giemsa stain for detecting H. pylori and Alcian blue (AB)/periodic acid?Schiff stain for examining intestinal metaplasia. Results: The Mongolian gerbil model for studying long‐term H. pylori infection was successfully established. Helicobacter pylori induced a progression from normal gastric mucosa to chronic gastritis, glandular atrophy, intestinal metaplasia and dysplasia, although no adenocarcinomas were found in the experimental animals. Conclusions: Helicobacter pylori NCTC 11637 is able to easily colonize the glandular stomach mucosa of the Mongolian gerbil. This model is stable, and the histological changes observed in the stomach are similar to those that occur in humans with H. pylori infection.     

幽门螺杆菌和非甾体抗炎药对胃上皮细胞增殖的影响

目的　从体外研究的角度探讨幽门螺杆菌 (Hp)和非甾体抗炎药 (NSAID)对胃上皮细胞增殖的影响及其相互作用。方法　胃癌细胞株AGS与Hp和 (或 )吲哚美辛、阿司匹林体外共培养 ,通过MTT比色法和WesternBlot法检测增殖细胞核抗原 (PCNA) ,观察Hp和NSAID对胃上皮细胞增殖的影响。结果　MTT比色法显示CagA阳性的标准Hp菌株NCTC116 37能明显促进胃上皮细胞增殖 ,吸光度 (A)值明显升高 (P <0 .0 5 ) ,而CagA阴性的标准Hp菌株NCTC12 90 8则未发现有促增殖作用 ,且Hp对上皮细胞生长的效应取决于Hp作用的密度 ,在低密度 (3.2× 10 4～ 4 .0× 10 6CFU/ml)时NCTC116 37促进胃上皮细胞生长 ,在高密度 (>2× 10 7CFU/ml)时则抑制其生长 (P <0 .0 5 )。吲哚美辛和阿司匹林均能抑制胃上皮细胞生长 (P <0 .0 5 ) ,并呈浓度依赖性。当Hp和NSAID共同作用于AGS细胞时 ,Hp的促生长作用被逆转 ,呈现出抑制细胞生长的效应 ,A值明显降低 (P <0 .0 5 )。PCNA的WesternBlot检测结果发现 ,Hp菌株NCTC116 37可明显促进细胞PCNA的表达 ,而吲哚美辛和阿司匹林则抑制其表达 ,当两者共同作用于AGS细胞时 ,PCNA的表达明显减弱。结论　Hp对胃上皮细胞的增殖效应与Hp的密度及菌株差异有关 ,CagA阳性的Hp易促进胃上皮细胞生长 ,NSAID可抑制其     

胃石及其并发幽门螺杆菌感染相关性胃病的临床诊治分析

对12例胃石在胃镜下用活检钳反复进行钳夹，对合并幽门螺杆菌感染相关性胃病的患者进行抗幽门螺杆菌、抑酸和保护胃黏膜治疗。最后，胃石被夹碎后排出胃腔，幽门螺杆菌被清除，胃溃疡和胃炎得到治愈。     

13C-尿素呼气试验在蒙古沙鼠幽门螺杆菌感染检测中的应用

目的　应用13 C -尿素呼气试验检测蒙古沙鼠幽门螺杆菌感染 ,从而建立一长期监控小型试验动物幽门螺杆菌感染无创检测技术。方法　分别在蒙古沙鼠感染幽门螺杆菌后第 2 0 ,5 0 ,10 0及 2 0 0d用13 C -尿素呼气试验进行检测 ,并对检测后沙鼠以细菌分离培养、ELISA、PCR、快速尿素酶试验、病理切片等五种常规方法检测幽门螺杆菌。结果　在上述不同检测时期 ,用13 C -尿素呼气试验所得蒙古沙鼠幽门螺杆菌感染阳性率分别为 77 78% ,83 33% ,84 2 1%和 80 0 0 % ,而应用常规方法检测结果阳性率为 83 33% ,88 88% ,94 2 1%和 85 0 0 %。比较两组试验结果发现 ,13 C -尿素呼气试验比常规检测方法检出阳性率相对偏低 ,但统计学分析发现其具有一致性。结论　13 C -尿素呼气试验用于幽门螺杆菌感染蒙古沙鼠模型检测是一种可行的无创检测方法 ,可作为评价Hp感染的重要参考指标之一     

胃黏蛋白在抗幽门螺杆菌感染中的作用

黏蛋白(MUCs)是特殊的上皮细胞分泌的大分子量的糖蛋白,是构成胃黏液凝胶的主要组成成分.多项研究显示幽门螺杆菌(H.pylori)通过其表面的黏附素分子或非黏附素分子与胃黏蛋白结合从而定植在胃黏膜上皮上.在H.pylori感染过程中,H.pylori导致了胃黏蛋白的表达发生了改变.反之,胃黏蛋白也因其特有的结构在抗H.pylori感染中也发挥了重要作用.此文就目前有关胃黏蛋白在抗H.pylori感染中的作用的研究现状及进展作一简要概述.     

Eradication of Helicobacter pylori reduced the immunohistochemical detection of p53 and MDM2 in gastric mucosa

BACKGROUND: Although Helicobacter pylori has been regarded as a pathogen of gastric cancer, the mechanism by which H. pylori is involved in gastric carcinogenesis remains unknown. To clarify the role of H. pylori in carcinogenesis, the expression of tumor suppressor p53 and its regulator multiple double minute 2 (MDM2) in gastric mucosa were examined before and after H. pylori eradication. METHODS: Biopsy specimens were obtained from 31 patients with H. pylori-infected gastric mucosa. Endoscopic biopsies were repeated 6 months after successful eradication. In addition, biopsy specimens from 12 patients with non-infected gastric mucosa were obtained. Immunohistochemical analysis was performed on the specimens using primary antibodies specific for p53 and MDM2. RESULTS: Six months after H. pylori eradication, labeling indices for p53 were significantly reduced in the gastric corpus (2.3-fold; P < 0.01), and in the gastric antrum (2.0-fold; P < 0.01). Similarly, labeling indices for MDM2 were significantly reduced in the corpus (1.7-fold; P < 0.01), and in the antrum (3.5-fold; P < 0.01). In the non-infected group, labeling indices for p53 and MDM2 in the gastric mucosa were significantly lower (P < 0.01) than those of the H. pylori-infected group. CONCLUSION: A significant increase is shown in p53 and MDM2 expression in H. pylori-infected gastric mucosa as compared to normal gastric mucosa; but successful eradication of H. pylori dramatically reduced the p53 and MDM2 levels. Therefore, H. pylori infection may be associated with alteration of cell proliferation and apoptosis.