针对不同基因靶点的胃黏膜标本幽门螺杆菌PCR检测敏感性分析

目的分析针对3种不同基因靶点的胃黏膜标本幽门螺杆菌PCR检测的敏感性,评价PCR方法从胃黏膜标本中检测幽门螺杆菌用于临床诊断的价值。方法采集320例13C呼气试验阳性患者的胃黏膜标本,用针对ureA、ca-gA和vacA基因的3对引物进行PCR检测,同时进行幽门螺杆菌分离培养。分别对3对引物的PCR结果相互进行Kappa一致性检验,并比较组合PCR与培养结果。结果幽门螺杆菌培养的阳性率为81.88%(262/320);ureA、cagA和vacA PCR扩增阳性率分别为56.25%(180/320)、58.13%(186/320)和81.56%(261/320),组合PCR阳性率为90.94%。ureA、cagA和vacA PCR结果经一致性检验,Kappa值分别为0.209、0.137、0.129,检测结果具有互补性。结论单一基因PCR扩增的敏感性较低且不同基因扩增效果间的一致性较差。3对引物组合使用可提高PCR方法的敏感性,幽门螺杆菌检出率高于培养法,具有一定的实际应用价值。     

胃黏膜组织中恶臭假单胞菌临床意义的探讨

目的探索恶臭假单胞菌在幽门螺杆菌感染相关胃肠疾病中的意义。方法采集14 C尿素呼气试验阳性患者病变胃黏膜354例,进行细菌的分离培养。根据菌落形态、革兰染色、尿素酶试验及幽门螺杆菌特异性16SrRNA基因片段的PCR进行幽门螺杆菌的鉴定,同时提取胃黏膜组织DNA,通过幽门螺杆菌特异性PCR进行快速诊断。将非幽门螺杆菌转种于营养琼脂培养基,进行快速尿素酶试验。尿素酶阳性的非幽门螺杆菌染色体DNA利用细菌16SrRNA基因通用引物进行PCR扩增、测序及序列比对。使用全自动细菌鉴定仪对经测序比对为恶臭假单胞菌的菌株进行鉴定。采用K-B纸片扩散法进行药物敏感性试验。结果从354例样本中分离出革兰阴性、尿素酶阳性的恶臭假单胞菌10株,经16SrRNA基因测序和序列比对,与GenBank中恶臭假单胞菌的相似性≥98%。10株恶臭假单胞菌的胃黏膜标本中,6例标本幽门螺杆菌特异性PCR为阳性,4例为阴性。传代存活的7株恶臭假单胞菌的K-B法药物敏感试验显示对左氧氟沙星均敏感,1株对四环素敏感,5株对阿莫西林耐药,6株对克拉霉素耐药,7株对甲硝唑、氨苄青霉素均耐药。7株菌经全自动细菌生化鉴定仪鉴定结果均为恶臭假单胞菌。结论病变胃黏膜中分离出尿素酶阳性且对治疗幽门螺杆菌感染的多种抗生素耐药;可能造成临床上14 C-尿素呼气试验假阳性,并继发感染影响胃肠疾病的进展。     

原发性肝癌组织中螺杆菌属16S rRNA基因的检测及意义

目的探讨原发性肝癌（HCC）组织中螺杆菌感染情况。方法选取经病理诊断的28例HCC患者的肝癌组织为实验组，22例非肝癌肝病患者肝组织和25例胃癌患者胃癌组织作对照组。采用聚合酶链反应（PCR）扩增螺杆菌属16S rRNA基因、幽门螺杆菌相关功能基因空泡毒素基因（vacA）和细胞毒素相关基因（cagA），16S rRNA的扩增产物经Southern杂交确认，并将PCR产物进行测序及同源性比较。结果28例HCC标本中有17例检出螺杆菌属16S rRNA基因，阳性率为60．7％；25例胃癌标本有18例检出螺杆菌16S rRNA，阳性率为72．0％；其他肝病组未扩增出16S rRNA基因。16Sr RNA PCR产物经Southern杂交证实为幽门螺杆菌。序列测定表明，肝癌和胃癌组织中的螺杆菌16S rRNA序列与幽门螺杆菌序列有97．8％的同源性。肝癌组相关功能基因有3例cagA基因阳性，胃癌组有2例cagA基因阳性，均未扩增出VacA基因。提示，幽门螺杆菌菌株的基因型多为Ⅱ型，而少数为Ⅰ型。结论HCC患者肝组织中存在螺杆菌感染且感染率较高。螺杆菌感染与HCC可能存在相关性。     

聚合酶链反应快速检测胃粘膜幽门螺杆菌

本研究的目的是了解简单的PCR方法诊断幽门螺杆菌感染的价值。选用互补于幽门螵杆菌尿素酶A基因片段的一对引物，建立PCR方法扩增幽门螺杆菌DNA．扩增产物经琼脂糖电泳显示一条411bp区带。用PCR扩增41株HP分离菌均阳性，而空肠弯曲菌等8种肠道细菌均阴性．显示100%特异，系列稀释试验显示PCR能检测0．1pg的HP DNA；126例胃粘膜标本用PCR、尿素酶试验、培养和涂片检查，HP检出率分别为70．6%、56．3%、32．5%和56．3%，这些结果提示简单快速的PCR方法是检测FIP的有价值的方法。     

肝癌患者肝组织中螺杆菌感染的研究

目的　探讨螺杆菌感染是否与人类肝癌的发生相关。方法　选取经病理诊断的肝癌组织及癌旁组织 2 0例为研究对象 ,非肝癌组织 16例作对照 ,采用聚合酶链反应 (PCR)扩增螺杆菌 16SrRNA基因 (16SrDNA)检测螺杆菌 ,扩增产物经Southern杂交证实 ,并对部分标本的PCR产物进行测序及同源比较。阳性者再扩增幽门螺杆菌 (H pylori)的特异基因 (2 6 -kDa蛋白 )和相关功能基因 (cagA、vacA、glmM、rps4 )来验证是否为该菌。结果　 4 0 % (8/ 2 0 )的肝癌组织中发现螺杆菌 16SrD NA存在 ,其对应的癌旁组织大部分亦阳性 (7/ 8) ,而非肝癌组无一例阳性 (P <0 0 1)。所有PCR产物用Southern杂交得到证实。 6例测序及同源比较显示 ,肝癌组织中的螺杆菌 16SrDNA序列与H pylori的 16SrDNA序列有 98 5 %～ 99 0 %的同源性。阳性标本中 2 6 -kDa基因大部分亦阳性 (7/ 8) ,但仅 2例扩增出cagA基因 ,2例扩增出glmM基因 ,一直未扩增出vacA基因和rps4基因。 结论　肝癌患者肝组织中螺杆菌感染率较高 ,它与肝癌的发生可能存在某种联系。     

幽门螺杆菌对喹诺酮类药物体外耐药情况研究

目的分析幽门螺杆菌对喹诺酮类药物体外耐药率及耐药机制。方法采用脑心浸液培养基在微需氧环境下培养幽门螺杆菌,琼脂稀释法测定幽门螺杆菌对左氧氟沙星及莫西沙星的MIC（最低抑菌浓度）值,并对耐药菌株的gyrA基因QRDR（喹诺酮类药物耐药决定区）进行聚合酶链反应（PCR）扩增、测序。结果从67例患者胃黏膜中分离培养出幽门螺杆菌株,4株对左氧氟沙星耐药,耐药率为5．97％,2株对莫西沙星耐药,耐药率为2．99％,其中2株为多重耐药菌株,对左氧氟沙星及莫西沙星均耐药。4株耐药菌株中,有2株的QRDR发生新的点突变,其点突变的位点与国外研究结果不同。结论幽门螺杆菌对喹诺酮类药物的体外耐药率仍较低,幽门螺杆菌对喹诺酮类药物耐药与该菌株gyrA基因的QRDR点突变密切相关。     

慢性乙型肝炎患者肝组织中螺杆菌菌属特异性16SrRNA基因及HP特异性基因分析

目的对慢性乙型肝炎患者肝组织进行螺杆菌菌属特异性16SrRNA基因及幽门螺杆菌（HP）特异性基因检测,探讨螺杆菌在慢性乙型肝炎发生、发展中的作用。方法对56例行肝穿刺活检的慢性乙型肝炎患者的肝组织应用针对螺杆菌菌属特异性16SrRNA基因的通用引物进行基因扩增及微需氧分离培养,并对螺杆菌菌属特异性16SrRNA基因阳性者进一步应用HPcagA、vacA和glmM基因特异引物进行扩增。结果对56例慢性乙型肝炎患者的肝组织DNA应用螺杆菌菌属特异性16SrRNA基因通用引物进行扩增,共有35例患者的肝组织中发现了螺杆菌菌属特异性16SrRNA基因,其中肝硬化组（72.7%）和原发性肝癌组（87.5%）的检出率明显高于慢性肝炎组（42.3%,P〈0.05）,而慢性肝炎组中随着炎症评分的增加,检出率亦增加。对这35例螺杆菌菌属特异性16SrRNA基因阳性的肝组织DNA进一步应用HPcagA、vacA和glmM基因特异性引物进行扩增,结果证实有21例为HPDNA。所有肝组织经微需氧分离培养均未发现可疑菌落生长。结论慢性乙型肝炎患者肝组织中除存在HPDNA外,可能还存在其他螺杆菌DNA。螺杆菌在慢性乙型肝炎向肝硬化和肝癌的发展中可能发挥致病作用。     

聚合酶链反应快速检测胃粘膜幽门螺杆菌

本研究的目的是了解简单的PCR方法诊断幽门螺杆菌感染的价值。选用互补于幽门螺杆菌尿素酶A基因片段的一对引物,建立PCR方法扩增幽门螺杆菌DNA,扩增产物经琼脂糖电泳显示一条411bp区带。用PCR扩增41株HP分离菌均阳性,而空肠弯曲菌等8种肠道细菌均阴性,显示100％特异,系列稀释试验显示PCR能检测0.1pg的HP DNA;126例胃粘膜标本用PCR、尿素酶试验、培养和涂片检查,HP检出率分别为70.6％、56.3％、32.5％和56.3％,这些结果提示简单快速的PCR方法是检测HP的有价值的方法。     

胃内尿素酶阳性细菌对幽门螺杆菌感染诊断的影响

目的探讨胃内可分解尿素酶菌群对基于尿素酶阳性诊断幽门螺杆菌(Helicobacter.pylori,Hp)感染的影响。方法胃镜下取疑为Hp感染患者的胃黏膜,行快速尿素酶检测(Rapid urease test,RUT)及细菌培养,根据培养物的菌落形态、革兰染色、RUT及Hp特异性16SrRNA基因片段PCR进行Hp的鉴定;提取胃黏膜组织DNA,通过Hp特异性PCR进行Hp感染快速诊断。对Hp阴性(Hp培养或特异性PCR阴性)而RUT阳性胃黏膜培养的非Hp(nonHp)进行常规尿素酶生化试验,选取20株尿素酶阳性non-Hp利用细菌16SrRNA通用引物进行PCR扩增并测序,利用NCBI系统进行序列比对,鉴定细菌种类。结果 606例患者胃黏膜RUT阳性率为58.4%(354/606),Hp培养阳性率29.7%(180/606)。Hp培养阴性胃黏膜特异性PCR阳性113例,Hp感染率为48.35%(293/606)。胃黏膜RUT阳性率高于胃黏膜Hp感染(χ2=1,2.337,P0.05)。61例RUT阳性Hp培养或特异性PCR阴性的胃黏膜培养出80株non-Hp,其常规尿素酶生化检查均阳性。对其中20株尿素酶阳性non-Hp进行测序鉴定,均为产尿素酶菌。结论胃内存在除Hp外其他细菌,包括尿素酶阳性non-Hp,可造成RUT阳性,干扰Hp感染的实验诊断。     

Hp鞭毛素A中央区氨基酸序列多态性研究

利用聚合酶联（PCR）技术从6例消化性溃疡患者的胃组织中分离6株幽门螺杆菌菌株扩增鞭毛素A中央区基因序列,另外10株幽门螺杆菌的序列来自Genbank,比较相应氨基酸序列寻找变异性氨基酸。结果显示,东西方菌株间无明显差别。幽门螺杆菌鞭毛素A中央区氨基酸序列存在多态性。     

胃粘膜石蜡切片PCR法检测幽门螺杆菌

目的建立从石蜡包埋的胃粘膜标本中扩增ＨｐＤＮＡ的聚合酶链反应（ＰＣＲ）．方法以一对Ｈｐ特异的寡核苷酸为引物，采用双扩增ＰＣＲ扩增Ｈｐ１６ＳｒＲＮＡ基因，并与常规检测方法进行了比较．结果双扩增ＰＣＲ检出的最小ＨｐＤＮＡ量为００１ｐｇ．用该方法检测十二指肠溃疡患者２０例石蜡包埋的胃粘膜标本，并与尿素酶试验、细菌培养、Ｗａｒｔｈｉｎ＿Ｓｔａｒｒｙ银染色及ＰＣＲ对新鲜胃粘膜标本的检测作比较，结果１８例患者上述五项检测结果一致，２例尿毒酶试验、银染色及ＰＣＲ对新鲜胃粘膜标本的检测呈阳性的患者，采用双扩增ＰＣＲ对石蜡包埋标本的检测未发现ＨｐＤＮＡ．ＰＣＲ对石蜡包埋标本及新鲜胃粘膜标本的检测有显著相关性．结论双扩增ＰＣＲ为分子水平上Ｈｐ感染的回顾性研究提供一有利工具．     

Interleukin-1 and TNF-α polymorphisms and Helicobacter pylori in a Brazilian Amazon population

AIM： To study the association between Interleukin-1 （IL-1） and tumor necrosis factor （TNF）-α polymorphisms, infection by Helicobacter pylori （H pylori） and the development of gastrointestinal diseases.
METHODS： Genomic DNA was extracted from the peripheral blood of 177 patients with various gastrointestinal diseases and from 100 healthy volunteers. The polymorphisms in IL-1β and TNF-α genes were analyzed using the polymerase chain reactionrestriction fragment length polymorphism method （PCRRFLP） and those from IL-1RN with PCR. The presence of infection due to H pylori and the presence of the CagA toxin were detected by serology. The histopathological parameters in the gastric biopsies of the patients were according to the Sydney classification.
RESULTS： A comparison of the frequencies of the different polymorphisms studied among the patients and the control group demonstrated that the allele IL- 1RN＊2 was more frequent among patients with gastric ulcers and adenocarcinoma. Carriers of the allele IL- RN＊2 and those with reactive serology for anti-CagA IgG had a greater risk of developing peptic ulcer and gastric adenocarcinoma, as well as a higher degree of inflammation and neutrophilic activity in the gastric
CONCLUSION： Our results indicate a positive association between IL-1RN gene polymorphism and infection by positive H pylori CagA strains and the development of gastric ulcers and adenocarcinoma.     

Use of the 'Polymerase Chain Reaction' for the diagnosis of Helicobacter pylori infection

PURPOSE: H. pylori infection can be diagnosed by means of non-invasive tests or invasive techniques using endoscopy. The choice of the test depends on available instruments, type of diseases, aim of diagnostic research (therapeutic or epidemiological) and test features. PCR is able to reveal pathogenic germs in biological material with very high sensitivity and specificity. In vitro DNA amplification method consists of hybriding denaturated DNA by means of two oligonucleotide primers that allow to copy DNA fragment. The aim of our study was to determine, using PER, H. pylori colonization in the gastric mucosa of 18 consecutive patients under-went gastroscopy. MATERIALS AND METHODS: Eighteen patients complaining of dyspeptic symptoms and referred to us for upper GI endoscopy participated in the study. The studied population comprised 9 males and 9 females with mean age of 55.4 yrs (range 26-73 years). All patients underwent gastroscopy during which 4 biopsies from the antrum and 4 from the corpus were obtained for Giemsa stain, PCR analysis and histologic examination. A pair of synthetic oligonucleotides for H. pylori urease A gene, designated as HPU1 and HPU2, were used. Urease A gene fragment amplified by PCR was analyzed by 1.5 agarose gel electrophoresis. Positivity for H. pylory corresponded to PCR DNA products migrating at 411 bp after staining with ethidium bromide. RESULTS: The patients were divided into two groups, according to H. pylori infection, determined by means of Giemsa stain: group A, comprising 11 H. pylori-positive patients; and group B, with 7 H. pylori-negative patients. Our PCR assay of gastric mucosa samples proved positive in 7 cases of group A (63.6%), whereas it always proved negative among group B subjects (100%). CONCLUSIONS: Our findings, apparently in contrast with the high sensitivity of PCR, may be attributed to the lower specificity of histology or, alternatively, the absence of H. pylori in the samples tested by PCR due to the patchy distribution of H. pylori colonization in the gastric mucosa. These observations are in agreement with those from other investigations.     

幽门螺杆菌致肝脏病变的动物实验观察

目的观察经口接种的幽门螺杆菌（Hp）能否到达肝脏，并作为独立的致病因素能否导致小鼠肝脏病变。方法Hp悉尼株经口接种C57BL／6小鼠，8个月时处死，观察小鼠肝组织细菌定植与病理变化，提取肝组织DNA，巢式聚合酶链反应（PCR）扩增Hp基因，16SrRNA PCR产物测序与胃黏膜培养Hp、接种Hp SS1 PCR产物同源比较。结果实验组15只小鼠肝组织6只基因阳性。肝组织扩增Hp 16S rRNA PCR产物测序分析结果显示与胃黏膜分离培养细菌、接种细菌同源性100％。4只肝脏观察到Hp，主要分布在中央静脉与肝血窦内，3只小鼠肝脏观察到以淋巴细胞为主的炎症浸润，部分肝细胞出现气球样变。结论经口接种的Hp可到达小鼠肝脏，能作为独立的致病因素引起肝脏炎症反应，其到达肝脏可能有血行和（或）胆道逆行两种途径。     

Is apoptosis in antral mucosa correlated with serum nitrite concentration in Japanese Helicobacter pylori‐infected patients?

BACKGROUND AND AIM: Helicobacter pylori infection in gastric mucosa is a form of chronic active gastritis that leads to expression of inducible nitric oxide synthase in host macrophages and polymorphonuclear leukocytes. Nitric oxide produced by these cells infiltrating the gastric mucosa could damage DNA. We correlated apoptosis in H. pylori-infected antral tissue from peptic ulcer patients with serum nitrate-plus-nitrite. METHODS: Biopsy specimens were obtained endoscopically from antrum and fundus in 17 peptic ulcer patients before and after H. pylori eradication. Tissue samples were subjected to rapid urease testing and histopathological scoring (updated Sydney system), as well as immunohistochemical detection of single-stranded DNA indicating apoptotic cells. Fasting serum samples were analyzed for combined nitrate and nitrite content. RESULTS: In all cases atrophy was absent to mild in antral mucosa and H. pylori was eradicated successfully. A strong positive correlation was present between apoptosis and both inflammation and activity scores in infected antral mucosa. A significant positive correlation also was noted between apoptosis and H. pylori density. Serum nitrite concentrations were decreased significantly by successful eradication of H. pylori, and showed a strong positive correlation with H. pylori density. Serum nitrite concentrations showed a significant positive correlation with numbers of single-stranded DNA-positive cells. CONCLUSIONS: High H. pylori density was associated with elevated serum nitrate-plus-nitrite (a marker of nitric oxide production in gastric mucosa). Increased apoptosis and abnormal gastric cell turnover are likely results.     

Gastric T lymphocyte responses to Helicobacter pylori in patients with H pylori colonisation.

Helicobacter pylori has been identified as a dominant factor in the pathogenesis of duodenal ulcer. The aim of this study was to examine peripheral blood and gastric lymphocyte proliferation and cytokine production in patients with H pylori colonisation. Sixty five dyspeptic patients attending for endoscopy were studied; 35 of these were H pylori positive and 30 H pylori negative as assessed by culture, histology, and rapid urease test. H pylori antigen was capable of stimulating peripheral blood lymphocyte proliferative responses even in H pylori negative patients. Peripheral blood lymphocyte proliferative responses to H pylori (but not to purified protein derivative or phythaemagglutinin) were significantly lower in H pylori positive than H pylori negative patients. Similarly, antigen specific proliferative responses and interferon gamma production by gastric lamina propria lymphocytes were also depressed in H pylori positive patients compared with H pylori negative patients. CD8 and CD22 positive lamina propria lymphocytes were increased in H pylori positive patients. These data show that antigen specific responses to H pylori are significantly lower in H pylori positive patients and could indicate activation of antigen specific suppression.     

Role of Helicobacter pylori CagA + Infection in Determining Oxidative DNA Damage in Gastric Mucosa

Background: Although Helicobacter pylori is a risk factor for gastric cancer, the role of the bacterium in the development of this malignancy is not defined precisely. Reactive oxygen species (ROS) could play an important role in carcinogenesis by inducing DNA damage. The aims of the present study were: 1) to assess the production of ROS and 8-hydroxy-2'-deoxyguanosine (8-OHdG), a sensitive marker of oxidative DNA injury, in gastric mucosa, according to H. pylori status and cytotoxic associated gene product A (CagA); 2) to determine the relationship between ROS generation and amount of 8-OHdG. Methods: Gastric biopsy specimens were obtained from 60 consecutive patients. ROS generation was measured by luminol enhanced chemiluminescence. 8-OHdG detection was performed by an immunoperoxidase method, using a specific anti 8-OHdG monoclonal antibody. Results: 40/60 patients (67%) were H. pylori -positive. ROS generation was significantly higher in patients positive for H. pylori infection as compared to negative. 8-OHdG detection was performed in 30 patients in which CagA presence was also investigated. High expression of 8-OHdG was detected in 14/20 (70%) H. pylori positive patients (13 CagA + and 1 CagA - ) and in 2/10 (20%) H. pylori -negative patients. A significant correlation was found between ROS production and 8-OHdG content. Conclusion: H. pylori infection by a CagA + strain is associated with the highest production of ROS to which a severe oxidative DNA damage corresponds. This sequence of events could support the hypothesis that the oxygen-free radicalsmediated damage due to H. pylori cytotoxic strains could be a driving force that leads from chronic gastritis to gastric carcinoma.     

球形幽门螺杆菌致小鼠感染

目的 证明球形幽门螺杆菌体内致病性。方法 用抗生素和水诱导幽门螺杆菌（Hp）球变,螺旋形和球形Hp分别经胃灌注接种BALB／c小鼠,实验组小鼠（各16只）接种Hp菌液0.4ml/只（10^9/ml）,接种4次,2w完成,对照组（10只）接种生理盐水,距最后一次接种后3和4w分别处死小鼠各半,取胃粘膜组织作细菌学检测（包括胃粘膜快速尿素酶试验,细菌培养鉴定,电镜观察）和组织学检测。结果 螺旋菌、抗生素旅为的球形菌、水中球形Hp这3个实验组的胃粘膜组织快速尿素酶试验阳性率分别为93.8%（15／16）、87.5%(14/16)、50％（8／16）,由此反映在的细菌定居量评分为1.75、1.30、0.56,细菌培养阳性率分别为87.5%(14/16)、75.0%（12／16）、68.8%（11／16）,对照组阴性,Hp感染3w和4w的实验结果无差异。电镜下可见3个实验组均有弯曲形、杆状和球形Hp粘附于胃粘膜上。组织学检验发现感染的小鼠胃粘膜呈正常、轻度或重度糜烂、溃疡等不同的表现,有炎症细胞浸润。水中球形Hp感染引起的胃粘膜损伤较轻。结论 球形Hp可致胃炎或溃疡。     

Eradication therapy of Helicobacter pylori directly induces apoptosis in inflammation-related immunocytes in the gastric mucosa--possible mechanism for cure of peptic ulcer disease and MALT lymphoma with a low-grade malignancy

BACKGROUND/AIMS: A possibility that the eradication therapy not only eliminates Helicobacter pylori (H. pylori) but also influences some factors regulating pathological changes in the gastric mucosa should be taken into consideration from some phenomena. Such as non-recurrent cases of peptic ulcer long-term in spite of unsuccessful anti-H. pylori eradication therapy and the effectiveness of eradication therapy for mucosa-associated lymphoid tissue with a low-grade malignancy except stomach. We hypothesized and investigated that antibiotic treatment for elimination of H. pylori might directly affect inflammatory cells to induce apoptosis in them and protect against pathological changes of gastric mucosa. METHODOLOGY: Subjects consisted of twenty-one patients with chronic gastritis. All were H. pylori positive and we investigated the effects of eradication therapy of H. pylori on inflammation-related immunocytes in the gastric mucosa of patients with chronic gastritis caused by H. pylori isolated mononuclear leukocytes which were taken from the patients and were examined for apoptosis-related morphological changes and DNA fragmentation before and after the therapy. Eradication therapy of H. pylori was performed by lansoprazole 30 mg/day, amoxicillin 1500 mg/day and clarithromycin 400 mg/day for one week. RESULTS: After the H. pylori eradication therapy, regardless of its effect on H. pylori status, marked vacuolation and degeneration were observed in mononuclear leukocytes in the gastric mucosa with a concomitant enhancement of nuclear DNA fragmentation. CONCLUSIONS: This observation suggests that H. pylori eradication therapy itself induces apoptosis in mononuclear leukocytes in the gastric mucosa.