幽门螺杆菌菌株类型与儿童胃粘膜炎症程度的关系探讨

目的探讨幽门螺杆菌菌株类型与儿童胃粘膜炎症程度之间的关系。方法采用免疫印迹法测定134例幽门螺杆菌感染患儿血清细胞毒素相关蛋白(CagA)、空泡毒素(VacA)抗体,对幽门螺杆菌进行分型,并观察胃粘膜病理变化。结果CagA、VacA抗体总检出率分别为85.07%(114/134例)、91.04%(122/134例),检出幽门螺杆菌I型菌株113例,Ⅱ型菌株11例,中间型菌株10例,各型菌株感染引起胃粘膜中重度炎症分别为100例(88.50%)、5例(45.45%)、5例(50.00%),I型菌株与II型菌株、中间型菌株比较,差异有显著性(Hc=20.05,P<0.01)。结论幽门螺杆菌菌株类型与儿童胃粘膜炎症程度有关,I型菌株能引起较重的胃粘膜炎症。     

Helicobacter pylori duodenal colonization in children

To investigate the prevalence and the significance of Helicobacter pylori duodenal colonization, endoscopic duodenal biopsies were performed in 168 children with chronic abdominal pain, gastroesophageal reflux, gastrointestinal bleeding, and malabsorption syndrome. Helicobacter pylori infection was detected in 68 children (40.4%): in 31 of them H. pylori was present in the gastric antrum, and in 37 in the duodenum also. Duodenitis was observed in 25 children with duodenal H. pylori ; gastric metaplasia in 3. Scanning electron microscopy revealed the presence of the micro-organism in 3/13 cases; the bacteria were located in the intercellular spaces and alterations of the epithelial surface were found. In conclusion, H. pylori gastritis in children is often associated with duodenal colonization which can cause duodenitis, and also without gastric metaplasia, which indicates a possible role of the micro-organism in the pathogenesis of the lesions.     

Antibiotic-resistant Helicobacter pylori strains in Portuguese children

BACKGROUND: Data concerning the effectiveness of Helicobacter pylori eradication regimens based in antibiotic susceptibility testing are scanty in children. AIMS: To identify the prevalence of antibiotic resistance in H. pylori strains isolated from Portuguese children in 1999-2003; to evaluate eradication rate after antibiotic susceptibility testing-based treatment; and to identify factors associated with resistance and eradication outcome. METHODS: Included were 109 children with a gastric biopsy culture positive for H. pylori. First treatment (amoxicillin, omeprazole and clarithromycin or metronidazole) was guided by susceptibility testing (E test), and eradication was assessed by [C]urea breath test. RESULTS: Strains were susceptible to amoxicillin and tetracycline; 39.4% were resistant to clarithromycin, 16.5% to metronidazole and 4.5% to ciprofloxacin. No significant association was found between resistance and sex, age, clinical status, gastritis scores, H. pylori density scores and genotype. Clarithromycin resistance was significantly associated with European origin [odds ratio (OR), 3.9], previous H. pylori empiric therapy (OR 2.8) and amoxicillin minimal inhibitory concentration, > or =0.016 (OR 6.0). Eradication rate after susceptibility-based treatment was 74.7% (59 of 79; 95% confidence interval, 65.9-82.9), and a significant association was found between eradication failure and presence of resistance to 1 or more antibiotics (P < 0.05). CONCLUSIONS: The prevalence of H. pylori antibiotic resistance was high in the studied population. The modest therapeutic success of clarithromycin and metronidazole susceptibility-based regimens suggests that in addition to resistance, other factors may be involved. The need of susceptibility-based treatment studies in children and of antimicrobial resistance surveillance in high prevalence areas for H. pylori are emphasized.     

Hp感染儿童胃十二指肠粘膜IL-8及IL-8 mRNA的研究

目的　检测Hp感染儿童胃、十二指肠粘膜中IL 8及IL 8mRNA的变化 ,从蛋白和分子水平探讨Hp对细胞因子IL 8的影响 ,以及IL 8在Hp相关性胃十二指肠疾病中的作用。方法　胃镜下取胃窦及十二指肠粘膜活检标本 ,用ELISA法和RT PCR半定量法测定胃及十二指肠粘膜中IL 8的含量和IL 8mRNA的表达量。结果　Hp阳性者胃粘膜IL 8为 2 4 66～ 177 77pg/mg ,IL 8mRNA为2 3 7～ 4 99;Hp阴性者胃粘膜IL 8为 2 94～ 12 98pg/mg,IL 8mRNA为 0 0 5～ 0 44 ;差异有显著意义(t分别为 12 3 4和 2 9 2 9,P <0 0 1)。Hp阳性者十二指肠粘膜IL 8为 12 98～ 177 77pg/mg ,IL 8mRNA为 1 2 2～ 1 80 ;Hp阴性者十二指肠粘膜IL 8为 2 0 4～ 10 43pg/mg ,IL 8mRNA为 0 0 1～ 0 2 3 ;差异有显著意义 (t分别为 7 18和 3 7 2 0 ,P <0 0 1)。活动性胃炎胃粘膜IL 8为 12 98～ 177 77pg/mg,IL 8mRNA为 0 5 1～ 4 99;非活动性胃炎胃粘膜IL 8为 2 0 4～ 10 43pg/mg,IL 8mRNA为 0 0 1～ 0 44 ;差异有显著意义 (t分别为 10 66和 18 62 ,P <0 0 1)。活动性胃炎十二指肠粘膜IL 8为 5 2 8～ 47 76pg/mg ,IL 8mRNA为 0 2 3～ 1 87;非活动性胃炎十二指肠粘膜IL 8为 3 19～ 8 14pg/mg,IL 8mRNA为0 0 1～ 0 2 0 ;差异有显著意义 (     

IL1RN polymorphism and cagA-positive Helicobacter pylori strains increase the risk of duodenal ulcer in children

Duodenal ulcers in children are associated with Helicobacter pylori gastric infection with cagA-positive strains, but factors linked to the host are poorly known. The authors evaluated the role of proinflammatory interleukin-1 gene cluster polymorphisms in the pathogenesis of duodenal ulcer. They studied prospectively 437 children 1 to years old, 209 of whom were H. pylori positive and 228 of whom were H. pylori negative. IL1B-511-C/T, -31T/C, and IL1RN Variable number of tandem repeats were genotyped by polymerase chain reaction (PCR) restriction fragment length polymorphism, PCR with confronting two-pair primers, and PCR, respectively. cagA status was evaluated by PCR. The role of the proinflammatory cytokine genotypes in the genesis of duodenal ulcer was evaluated before and after stratification of H. pylori status on logistic regression models. In the group of children without duodenal ulcer, no association was observed between H. pylori status and proinflammatory polymorphisms. Furthermore, no association between IL1 cluster genotypes and cagA status was seen in the H. pylori-positive children. However, increasing age, male sex, and IL1RN*2 were independently associated with duodenal ulcer. After stratification, in the H. pylori-positive children, increasing age, male sex, the presence of ILRN*2 allele, and cagA-positive status were independently associated with duodenal ulcer. The risk for the development of duodenal ulcer increased when a combined association of the presence of IL1RN*2 allele and infection by a cagA-positive H. pylori strain was the variable. This study provides evidence supporting independent roles of IL1RN*2 allele and cagA-positive status in the genesis of duodenal ulcer in children.     

Increased mucosal inflammatory cytokines in children with Helicobacter pylori-associated gastritis

The concentrations of tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and IL-1-β in tissue homogenates of gastric mucosal biopsy specimens, and in gastric juice samples from Helicobacter pylori-positive and -negative children, were determined. The study population comprised 30 children with recurrent abdominal pain attending upper gastrointestinal endoscopy. Of these patients 18 were infected with H. pylori. Cytokine concentrations in gastric biopsy homogenate supernatants and in gastric juice were measured by enzyme-linked immunosorbent assay (ELISA). TNF-α levels in gastric juice and in gastric biopsy homogenate supernatants in patients with H. pylori-positive gastritis were found to be significantly higher than those in children without H. pylori infection. IL-6 levels were also higher in H. pylori -infected subjects, but the difference in IL-6 concentrations measured in gastric juice and biopsy homogenate supernatants did not reach statistical significance. IL-1-β concentrations in both specimens showed no significant difference between the two groups of children. It was suggested that increased levels of inflammatory cytokines, especially TNF-α and IL-6 generated locally within the gastric mucosa might be implicated in the pathogenesis of H. pylori-associated gastritis in childhood.     

Cytokines in the gastric mucosa of children with Helicobacter pylori infection

AIM: Few studies have looked at the cytokine profile in gastric mucosa in children with Helicobacter pylori infection. This study investigated cytokines and their effects on histological abnormalities in the gastric mucosa of children with H. pylori infection. METHODS: The levels of interferon-gamma (IFN-gamma), interleukin-4 (IL-4) and IL-8 proteins were measured in biopsy specimens from the gastric antrum and corpus of children with H. pylori infection, and related to inflammatory cell infiltrations. RESULTS: The antral and corporal mucosal levels of IFN-gamma and IL-8 proteins were significantly higher in children with H. pylori infection than in uninfected children, but there was no such difference in the levels of IL-4 protein. The antral mucosal level of IL-8 protein was significantly higher than the corporal mucosal level of IL-8 protein in the infected children. Inflammatory cell infiltration was significantly higher in the infected children than in the uninfected children, but there were no significant correlations between mucosal cytokine levels and inflammatory cell infiltrations. CONCLUSION: The results suggest that the predominant Th1 cytokine response and enhanced IL-8 production in the mucosa may be involved in the gastric inflammation seen in children infected with H. pylori, as well as in adult patients.     

Microarray analysis of gastric mucosa among children with Helicobacter pylori infection

Background: Although initial infection with Helicobacter pylori may occur before 5 years of age, the pediatric mucosal immune response against H. pylori is not clear. The aim of the present study was to evaluate immune responses in the H. pylori‐infected gastric mucosa of children using microarray and real‐time polymerase chain reaction (PCR) analysis of pediatric gastric samples. Methods: Gastric samples were obtained from 12 patients undergoing routine endoscopy of chronic abdominal complaints. Six patients (three boys, three girls) aged 10.1–14.6 years had evidence of H. pylori infection, and the remaining six (three boys, three girls) aged 10.3–15.5 years had no evidence of infection and presented no histological changes associated with gastritis. Microarray and real‐time PCR analyses were performed, and the changes in gene expression‐related immune response were also analyzed. Results: Using microarray analysis, the total number of significantly upregulated and downregulated genes (fold change >5, P < 0.01) was 21 in the antrum and 16 in the corpus when comparing patients with or without infection. Using real‐time PCR, the expression of lipocalin‐2 (Lcn2), C‐C motif chemokine ligand (CCL) 18, C‐X‐C motif chemokine ligand (CXCL) 9 and CXCL11 was upregulated, while the expression of pepsinogen (PG) I and PGII was downregulated when comparing patients with or without infection. Conclusions: Lcn2, CCL18, CXCL9, CXCL11, PGI and PGII play important roles in childhood H. pylori infection.     

幽门螺杆菌感染儿童胃黏膜细胞凋亡相关蛋白的研究

目的：旨在研究儿童胃黏膜细胞凋亡相关蛋白p53和Bax的表达水平与幽门螺杆菌（Hp）感染的关系。方法：采用免疫组化法检测了33例胃黏膜病变儿童胃黏膜上皮细胞中p53和Bax表达水平,并采用快速尿素酶试验和组织病理学检测两种方法检查这些病例的Hp感染情况。结果：在17例Hp阳性组织标本中,15例（88%）p53表达阳性,而在16例Hp阴性组织标本中,9例（56%）呈阳性。分析Bax的表达水平发现,在17例Hp阳性组织标本中,13例（76%）标本Bax表达呈阳性,而在16例Hp阴性组织标本中,6例 （38%）呈阳性。统计学分析显示,Hp阳性标本的p53和Bax表达水平要明显高于Hp阴性标本（P<0.05）。结论：儿童期Hp感染与胃黏膜上皮细胞p53蛋白和Bax蛋白过度表达密切相关。［中国当代儿科杂志,2010,12（2）：110-112］     

Differences in distribution and severity of Helicobacter pylori gastritis in children and adults with duodenal ulcer disease

The presence of Helicobacter pylori and the gastric mucosa histology were investigated in 15 children and 15 adults with duodenal ulcer. The microorganism was isolated from antral and oxyntic mucosa in 100% of patients, both adults and children. The results of Gram stain and preformed urease test were compared with those of culture and there was no difference in sensitivity among the tests. Antral chronic gastritis was observed in all patients. However, children presented oxyntic gastritis more frequently than adults. It was also observed that the endoscopic aspects were different in the two groups of patients. The results here observed strongly support the idea that, as well as in adults, H. pylori is the causative agent of the gastritis seen in children with duodenal ulceration. On the other hand, the histological findings of oxyntic mucosa of children with duodenal ulcer were different from those of adults.     

Helicobacter pylori and associated duodenal ulcer.

Twenty three children with coexistent duodenal ulcer and Helicobacter pylori infection were treated with either two weeks of amoxycillin (25 mg/kg/day) in addition to six weeks of cimetidine, or cimetidine alone. Endoscopy with antral and duodenal biopsies for urease test, microaerophilic culture, and histological studies were performed at entry, six weeks, 12 weeks, and at six months. Children with persistent H pylori infection at six weeks were given a further two weeks'' course of amoxycillin. H pylori persisted in all children not receiving amoxycillin treatment but cleared in six of the 13 children (46%) treated with amoxycillin. With failure of H pylori clearance at six months, only two out of six (33%) ulcers had healed and 50% of patients had experienced ulcer recurrence. In contrast, when H pylori remained cleared all ulcers healed and no ulcer recurred. Persistent H pylori infection was associated with persistent gastritis and duodenitis despite endoscopic evidence of ulcer healing. Detection and eradication of H pylori deserves particular attention in the routine management of duodenal ulceration in children.     

人类白细胞抗原-DQB1与儿童十二指肠溃疡和幽门螺杆菌感染的相关性研究

目的探讨人类白细胞抗原(HLA)-DQB1等位基因与儿童十二指肠溃疡(DU)和幽门螺杆菌(H.pylori)感染的遗传关联性。方法采用非同位素标记的聚合酶链反应-序列特异性寡核苷酸探针(PCR-SSO)杂交的方法,对上海地区汉族健康儿童80例、DU患儿58例的HLA-DQB1等位基因进行分型;并同时检测DU患儿H.pylori感染情况。结果在DU患儿中,HLA-DQB1×05031等位基因频率明显高于正常健康儿童(分别为:6.02%、0.63%,P<0.05,RR=9),而在H.pylori阳性和H.pylori阴性DU组之间差异无显著性。结论HLA-DQB1×05031与DU呈正相关,DU患儿与正常对照组儿童之间存在着遗传学的差异;虽然H.pylori感染是DU的重要致病因素,但HLA-DQB1×05031并不是通过H.pylori感染而影响DU的遗传易感性。     

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目的研究儿童幽门螺杆菌(H.pylori)感染时的T淋巴细胞亚群变化。方法流式细胞仪直接免疫荧光法测定38例[H.pylori+慢性浅表性胃炎(CSG)12例;H.pylori+十二指肠溃疡(DU)5例;H.pylori-CSG21例]儿童胃窦黏膜及外周血T淋巴细胞亚群。各组患儿均在内镜检查下取胃窦黏膜作快速尿素酶试验、组织学检查及淋巴细胞提取,同时抽取外周肝素抗凝静脉血2mL。提取的淋巴细胞经CD3FITC、CD4PE、CD8PerCP染色后行流式测定。其中,胃黏膜T淋巴细胞亚群的检测以CD3设门。结果(1)胃黏膜CD+3(%)细胞的检出率分别为:H.pylori-CSG组3.14±2.03,H.pylori+CSG组4.58±2.30,H.pylori+DU组为6.49±4.49;(2)胃黏膜CD+3细胞中CD+4(%),CD+8(%)的相对比例及CD+4/CD+8值分别为:H.pylori-CSG组为19.81±9.25,47.30±12.83,0.43±0.19,H.pylori+CSG组为40.66±12.52,29.25±8.58,1.42±0.31,H.pylori+DU组为31.98±14.02,49.52±19.00,0.72±0.43。H.pylori+CSG组局部胃窦黏膜CD+4细胞、CD+4/CD+8比值明显高于H.pylori-CSG组,CD+8细胞则低于H.pylori-CSG组(P<0.01)。H.pylori+DU组CD+4、CD+4/CD+8比值也高于H.pylori-CSG组(P<0.05),但CD+8细胞无统计学差异。H.pylori+DU组CD+8细胞高于H.pylori+CSG组而CD+4细胞无统计学差异,CD+4/CD+8比值则低于H.pylori+CSG组(P<0.01)。(3)外周血T淋巴细胞亚群的变化在三组之间并无明显的差异。结论H.pylori+DU与H.pylori+CSG的宿主的T淋巴细胞反应并不相同,而局部胃窦黏膜的T淋巴细胞亚群的异常可能在儿童H.pylori感染的免疫致病机制中起一定的作用。     

儿童幽门螺杆菌感染的菌株类型及治疗

目的评估幽门螺杆菌(H.pylori)不同菌株对儿童胃粘膜炎症程度和治疗效果。方法对94例经胃镜和活检确诊H.pylori相关性胃炎的5～14岁儿童,用免疫印迹试验测血清细胞毒相关蛋白(CagA)、细胞空胞毒素(VacA)、尿素酶(urase)亚型抗体;抗H.pylori三联疗法10d,67例分A组(LAC组,用奥美拉唑 克拉霉素 阿莫仙治疗)和B组(BCF组,用果胶铋 克拉霉素 呋喃唑酮治疗),停药4周后用13C-UBT测定H.pylori根除率。结果①94例中检出CagA和/或VacA阳性86.2%,CagA和/或VacA阴性13.8%;慢性胃炎(CSG)27%,CSG 十二指肠球炎(DG)48%,CSG DG 十二指肠溃疡(DU)21%,胃溃疡(CU) DU4%,滤泡样改变56%,各种疾病检出菌株差异无显著性(χ2=2.551,P>0.05)。②94例H.pylori根除率76%,其中A组90.32%(28/31例),消化性溃疡(PU)根除率100%(12/12例)、CSG根除率84.21%(16/19例);B组H.pylori根除率为88.89%(32/36例),PU76.00%(6/8例),CSG92.86%(26/28例),两组差异无显著性(P>0.05)。各菌株根除率差异无显著性(P>0.05)。症状消退慢、难治及未能根除者大多为阳性菌。结论H.pylori蛋白印迹法简单、可靠,是流行病学筛选H.pylori细胞毒素的指标;阳性患儿必须予以根治。以下各组患儿推荐根治:①慢性活动性胃炎H.pylori阳性者;②胃十二指肠溃疡病患者;③产细胞毒素CagA阳性者。LAC三联根治H.pylori相关性胃炎疗程短、副作用小和根除率高,值得推广。     

Lewis antigen expression in gastric mucosa of children: relationship with Helicobacter pylori infection

OBJECTIVE: Lewis epithelial antigen expression has a role in Helicobacter pylori adherence, presumably mainly in cagA-positive strains. The authors investigated whether Lewis antigen expression in children's gastric mucosa was associated with H. pylori infection, cagA status, patient age, or presence of duodenal ulcer (DU). METHODS: The expression of Lewis A (Le(a)), B (Le(b)), X (Le(x)), and Y (Le(y)) was detected by immunohistochemistry in the antral and oxyntic mucosae of 70 children. Children were divided in four age groups (<4 years; 4-8 years; 9-12 years; and 13-18 years). RESULTS: Forty-seven of the 70 children had H. pylori and 17 had DU. The cagA status was determined by polymerase chain reaction in 34 patients. Le(a) and Le(b) were expressed in 64% and 44% of the patients, respectively; Le(x) and Le(y) were expressed in the glands in all of the patients and in the superficial epithelium. Le(b) expression was more common among patients without H. pylori (15/23, 65%) than in those with H. pylori (16/47, 34%) (P = 0.03). In noninfected patients, Le(b) and superficial Le(y) expression were associated with increased age. Le(b) expression was more common in patients with chronic gastritis than in those with DU. Le(x) superficial expression was significantly associated with DU in patients with H. pylori. CONCLUSION: In children, the expression of Le(b) and Le(y) in the superficial gastric epithelium depends on age. Other receptors, such as Le(x), may have a role in H. pylori colonization, especially in patients with DU. Studies assessing the expression of Lewis antigens in children may contribute to an understanding of the mechanisms of acquisition of H. pylori infection.     

广州地区儿童十二指肠黏膜双糖酶活性检测

目的 探讨儿童十二指肠降段黏膜乳糖酶、蔗糖酶和麦芽糖酶活性与降段黏膜绒毛形态的关系,初步探讨广州地区儿童十二指肠黏膜双糖酶活性水平.方法 收集140名儿童的十二指肠降段黏膜,采用改良的Dahlqvist法检测乳糖酶、蔗糖酶、麦芽糖酶活性,并行十二指肠黏膜绒毛组织学检查.结果 ①140例中110例绒毛形态正常,30例绒毛形态呈部分萎缩,无绒毛完全萎缩病例.②绒毛部分萎缩组乳糖酶、蔗糖酶、麦芽糖酶活性低于绒毛正常组(P＜0.001).③110例绒毛形态正常儿童十二指肠黏膜的双糖酶活性水平为乳糖酶几何均数、95%可信区间、最小值分别为19.91、16.76～23.56、3.22(U/g),蔗糖酶为72.96、62.99-91.70、15.48(U/g);麦芽糖酶为331.13、282.49～388.15、61.62(U/g).结论 十二指肠降段黏膜的双糖酶活性与黏膜绒毛的组织学形态有关,绒毛萎缩可引起双糖酶活性的降低.     

幽门螺杆菌菌株类型与儿童上消化道疾病的关系

目的：幽门螺杆菌（Helicobacter pylori,Hp）感染已被确立为是引起慢性浅表性胃炎和消化性溃疡的重要病因，是胃癌和胃黏膜相关性淋巴样组织（MALT）淋巴瘤的重要危险因素。Hp的致病性与毒力有关，而细胞毒素相关蛋白（CagA）和空泡毒素（VcaA）是Hp的主要毒力因子之一。该研究通过了解Hp菌株类型与儿童胃十二指肠疾病类型及胃窦黏膜病理组织学变化的关系，探讨Hp感染的分型诊断是否有助于判断儿童胃十二指肠疾病的严重程度。方法：采用免疫印迹法对115例有上消化道症状的患儿进行Hp的血清学分型，并行胃镜检查，观察胃十二指肠疾病类型。取胃窦黏膜经Harris配方苏木精染色观察胃窦黏膜病理组织学变化、亚甲基蓝染色观察Hp感染情况。结果：115例患儿中检出Hp Ⅰ型菌株84例（73.0%），中间型菌株21例（18.3%），Ⅱ型菌株10例（8.7%）；Ⅰ型菌株引起胃窦黏膜中、重度炎症分别为83例、1例；中间型菌株引起胃窦黏膜中度炎症21例；Ⅱ型菌株引起胃窦黏膜轻度炎症2例，中度炎症8例，经统计学处理，各型菌株在引起胃窦黏膜炎症程度上差异有显著性（χ2=15.444，P<0.01），Ⅰ型菌株感染引起胃窦黏膜炎症程度最重，Ⅱ型菌株感染引起胃窦黏膜炎症程度最轻；而在活动性、萎缩的发生率上，各型差异无显著性（P＞0.05）；在淋巴滤泡形成的发生率上，各型差异有显著性（χ2=10.171，P<0.01）。各型菌株引起胃镜下胃、十二指肠疾病类型的构成比无明显差异（P＞0.05）。结论：该地区儿童Hp感染以Ⅰ型菌株最为多见。各型菌株100%存在胃窦黏膜组织学改变。Ⅰ型菌株感染所致胃窦黏膜炎症程度最重，且引起淋巴滤泡形成的发生率最高。Hp感染的分型诊断无助于对儿童胃、十二指肠疾病类型的判断，但有助于对儿童胃、十二指肠疾病病情的判断，Ⅰ型菌株感染者需要更为积极的治疗，对于Hp感染的儿童无论其血清分型如何，均应引起重视，并长期随访。［中国当代儿科杂志，2007，9（3）：201-204］     

Helicobacter pylori infection in children

Helicobacter pylori colonizes the human stomach, especially during childhood. However, a variety of H. pylori strains exists, with major differences in virulence characteristics which probably account for different clinical symptoms, and the majority of infected subjects remains asymptomatic. Helicobacter pylori infection is correlated with socioeconomic conditions and hygienic circumstances, resulting in an extremely high prevalence in children in developing countries. Commercial screening tests are not capable of separating the more virulent strains (type I with vacuolating toxin VacA and CagA protein) from the less virulent strains (type II, VacA and CagA negative). Type I strains, but not type II, are associated with an increased risk for duodenal ulcer and gastric cancer. Therefore, future screening tests and vaccinations should focus on the type I strains.