Helicobacter pylori CagA protein polymorphisms and their lack of association with pathogenesis

AIM: To investigate Helicobacter pylori (H. pylori) CagA diversity and to evaluate the association between protein polymorphisms and the occurrence of gastric pathologies. METHODS: One hundred and twenty-two clinical isolates of H. pylori cultured from gastric biopsies obtained from Colombian patients with dyspepsia were included as study material. DNA extracted from isolates was used to determine cagA status, amplifying the C-terminal cagA gene region by polymerase chain reaction. One hundred and six strains with a single amplicon were sequenced and results were used to characterize the 3' variable region of the cagA gene. To establish the number and type of tyrosine phosphorylation motifs Glutamine acid-Proline-Isoleucine-Tyrosine-Alanine (EPI-YA) bioinformatic analysis using Amino Acid Sequence Analyzer-Amino Acid Sequence Analyzer software was conducted. Analysis of the association between the number of EPIYA motifs and the gastric pathology was performed using χ2 test and analysis of the presence of EPIYA-C motifs in relation to the pathology was made by logistic regression odds ratios. Comparisons among EPIYA types found and those reported in GenBank were performed using a proportion test in Statistix Analytical Software version 8.0. RESULTS: After amplification of the 3' of the cagA gene, 106 from 122 isolates presented a single amplicon and 16 showed multiple amplicons. As expected, diversity in the size of the cagA unique fragments among isolates was observed. The 106 strains that presented a single amplicon after 3' cagA amplification came from patients with gastritis (19 patients), atrophic gastritis (21), intestinal metaplasia (26), duodenal ulcer (22) and gastric cancer. DNA sequence analysis showed that the differences in size of 3' cagA unique fragments was attributable to the number of EPIYA motifs: 1.9% had two EPIYA motifs, 62.3% had three, 33.0% had four and 2.8% had five motifs. The majority of tested clinical strains (62.3%) were found to harbor the ABC combination of EPIYA motifs and a significant statistical difference was observed between the frequencies of ABCC tyrosine phosphorylation motifs and Western strains sequences deposited in GenBank. CONCLUSION: The present report describes a lack of association between H. pylori CagA-protein polymorphisms and pathogenesis. ABCC high frequency variations compared with Western-strains sequences deposited in GenBank require more investigation.

H pylori infection and systemic antibodies to CagA and heat shock protein 60 in patients with coronary heart disease

AIM: To determine the overall prevalence of H pylori and CagA positive H pylori infection and the prevalence of other bacterial and viral causes of chronic infection in patients with coronary heart disease (CHD), and the potential role of anti-heat-shock protein 60 (Hsp60) anti- body response to these proteins in increasing the risk of CHD development. METHODS: Eighty patients with CHD and 160 controls were employed. We also compared the levels of anti- heat-shock protein 60 (Hsp60) antibodies in the two groups. The H pylori infection and the CagA status were determined serologically, using commercially available enzyme-linked immunosorbent assays (ELISA), and a Western blotting method developed in our laboratory. Systemic antibodies to Hsp60 were determined by a sandwich ELISA, using a polyclonal antibody to Hsp60 to sensitise polystyrene plates and a commercially available human Hsp60 as an antigen. RESULTS: The overall prevalence of H pylori infec- tion was 78.7% (n = 63) in patients and 76.2% (n = 122) in controls (P = 0.07). Patients infected by CagA- positive (CagA+) H pylori strains were 71.4% (n = 45) vs 52.4% of infected controls (P = 0.030, OR = 2.27). Sys-temic levels of IgG to Hsp60 were increased in H pylori- negative patients compared with uninfected controls (P < 0.001) and CagA-positive infected patients compared with CagA-positive infected controls (P = 0.007). CONCLUSION: CagA positive H pylori infection may concur to the development of CHD; high levels of anti- Hsp60 antibodies may constitute a marker and/or a con- comitant pathogenic factor of the disease.

镇江地区H pylori的cagA基因及其3′可变区结构的变化

目的:评估镇江地区H pylori临床株的cagA基因阳性率、了解菌株CagA蛋白的可能分型、其羧端可变区EPIYA的数目以及与临床结果之间有无关联.方法:培养分离来自临床胃十二指肠疾病患者的H pvlori,提取基因组DNA,通过PCR方法检测H pylori cagA基因的状况.随机选择不同病种的cagA基因阳性(cagA^+)的PCR产物.通过转化质粒,进行cagA^+PCR产物测序,通过ExPASY-Tranlation软件获得cagA基因相应的CagA蛋白的氨基酸序列.国际标准株NCTC11637的cagA基因以及CagA蛋白序列通过搜索NCBI(www.ncbi.nlm.nih.gov)数据库获得.结果:60株H pylori临床株中,56例为cagA^+,阳性率达93.3%.20例测序的结果表明,CagA蛋白结构可分为2种类型,19株东亚型和1株西方型.所有19株东亚型均为Yamaoka分型的A型,所有20例菌株的EPIYA的数目均为3个,与临床结果无关联.结论:cagA基因阳性率在不同病种之间无差异.镇江地区H pylori临床株的CagA蛋白的一级结构,与日本、韩国菌株一样,主要为东亚型,其CagA蛋白羧端可变区EPIYA数目均为3个,与临床结果无关联.

血清幽门螺杆菌CagA蛋白抗体滴度与消化性溃疡的关系

目的 通过比较消化性溃疡和慢性胃炎病人血清中CagA抗体阳性的流行情况 ,探讨消化性溃疡和血清幽门螺杆菌CagA蛋白抗体滴度之间的关系。方法 采用病例对照研究设计方案。研究对象来源于中山医院门诊因中上腹痛或腹胀进行胃镜检查的人群。自 1998年 10月 -1998年 12月共收集胃溃疡病例 2 6例 ,十二指肠球部溃疡 2 7例 ,对照组为同期胃镜和病理证实慢性浅表性胃炎的病例 6 5例。Hp感染的判断采用快速尿素酶和病理Giemsa相结合的方法 ,二者均阳性定为阳性。采用ELISA方法检测HpCagA抗体。结果 总的HpCagA抗体的阳性率为 6 2 5 % ,在胃溃疡组为 76 9% ( 2 0 / 2 6 ) ,在十二指肠球部溃疡组为 88 9% ( 2 4/ 2 7) ,在慢性胃炎组为 49 3 % ( 3 2 / 6 5 ) ,胃溃疡组和十二指肠球部溃疡组均明显高于慢性胃炎组 ,差异有显著性。结论 本研究提示CagA蛋白阳性的幽门螺杆菌菌株在消化性溃疡的发病中起一定作用。

成人特发性血小板减少性紫癜与幽门螺杆菌CagA蛋白的关系

目的了解成人特发性血小板减少性紫癜(idiopathic thrombocytopenic purpura,ITP)与幽门螺杆菌(helicobacter pylori,Hp)CagA蛋白的关系。方法采用14C尿素呼吸试验对正常成人和ITP患者进行Hp检测后,对Hp阳性的ITP患者进行CagA蛋白抗体检测。依据急性ITP,慢性ITP,难治性ITP对ITP患者进行分类。结果 223例正常患者中123例Hp阳性,感染率为55.2%,而CagA蛋白抗体阳性为42例,占34.1%。278例ITP患者中Hp阳性176例,感染率63.3%,其中CagA蛋白抗体阳性83例,占47.2%,ITP患者的Hp感染率与正常人相似,但CagA蛋白抗体阳性率显著高于正常人(P<0.05)。Hp感染率及CagA蛋白抗体阳性率在急性ITP患者中分别为62.2%和46.4%,慢性ITP为63.2%和47.0%,难治性ITP为64.7%和48.5%,比较显示不同类型的ITP患者Hp感染率及CagA抗体阳性率差异无统计学意义(P>0.05)。结论纳入研究的ITP患者的Hp感染率与正常人相似,但CagA蛋白抗体阳性率明显高于正常人,提示CagA蛋白在成人ITP的发生发展中具有一定作用。进一步分析也显示不同类型的ITP患者Hp感染率及CagA蛋白阳性率差异无统计学意义。

浙江地区小儿幽门螺杆菌cagA基因变异性研究

目的 研究浙江地区儿童感染的幽门螺杆菌 (Hp)cagA基因的变异性。方法 应用3对不同引物对66例Hp感染患儿胃粘膜Hp菌株通过聚合酶链反应 (PCR)技术 ,分别扩增cagA基因不同DNA片段 ,检测cagA基因阳性 (cagA +)检出率 ;用免疫印迹法检测患儿血清CagA抗体。结果 Hp 菌株cagA基因DNA404bp、349bp、298bp 片段分别经3对引物扩增后 ,cagA +检出率分别为56.1%、39.4%、72.7% ,三者之间差别有显著性意义(χ2=14.63,P<0.01) ,总阳性检出率为90.9%。66例患儿血清CagA抗体阳性率为97.0%。结论 浙江地区儿童感染的Hp菌株cagA基因存在变异性和多态性 ,增加引物对数量进行检测可以提高Hp菌株cagA +检出率。

过表达CagA对胃癌细胞中GLUT1表达的影响

目的探究幽门螺杆菌(H.pylori)的细胞毒素相关基因A蛋白(CagA)过表达对胃癌细胞葡萄糖转运蛋白1(GLUT1)表达的影响。方法用过表达cagA腺病毒感染人胃癌细胞株AGS和人原代胃癌细胞,免疫荧光检测GLUT1的表达;用过表达glut1慢病毒及其空载体慢病毒感染胃癌细胞株AGS和BGC-823、0.002 mg/L嘌呤霉素筛选,用Western blot、免疫荧光验证稳转细胞株;最后用过表达cagA腺病毒感染过表达GLUT1的稳转细胞株,免疫荧光检测GLUT1与CagA的细胞定位。结果成功建立过表达glut1的稳转细胞株AGS/glut1和BGC-823/glut1,免疫荧光结果显示CagA和GLUT1蛋白主要在细胞膜上表达,且过表达CagA能引起细胞膜上GLUT1蛋白达降低并出现碎片化,且CagA与Glut1在细胞膜上共定位。结论CagA与GLUT1共定位于细胞膜上,破坏细胞膜,抑制GLUT1蛋白的表达。

CagA EPIYA polymorphisms in Colombian Helicobacter pylori strains and their influence on disease-associated cellular responses

AIM: To investigate the influence of the CagA diversity in Helicobacter pylori (H. pylori ) strains from Colombia on the host cell biology. METHODS: Eighty-four H. pylori-cagA positive strains with different Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs patterns, isolated from patients with gastritis (n=17), atrophic gastritis (n=17), duodenal ulcer (n=16), intestinal metaplasia (n=16) and gastric cancer (n=18), were included. To determine the integrity of the cag pathogenicity island (cag PAI) we evaluated the presence of cagA, cagT, cagE, and cag10 genes by polymerase chain reaction. AGS gastric epithelial cellswere infected with each strain and assayed for translo-cation and tyrosine phosphorylation of CagA by western blot, secretion of interleukin-8 (IL-8) by enzyme-linked immuno sorbent assay after taking supernatants from cocultures and cell elongation induction. For cell elongation quantification, coculture photographs were taken and the proportion of "hummingbird" cells (>15 μm) was determined. RESULTS: Overall 72% (60/84) of the strains were found to harbor a functional cag PAI. Levels of phos-phorylated CagA were significantly higher for isolates from duodenal ulcer than the ones in strains from gas-tritis, atrophic gastritis, intestinal metaplasia and gastric cancer (49.1% ± 23.1% vs 21.1% ± 19.5%, P < 0.02; 49.1% ± 23.1% vs 26.2%±14.8%, P<0.045; 49.1% ± 23.1% vs 21.5% ± 19.5%, P<0.043 and 49.1% ± 23.1% vs 29.5% ± 27.1%, P < 0.047 respectively). We observed variable IL-8 expression levels ranging from 0 to 810 pg/mL and from 8.8 to 1442 pg/mL at 6 h and 30 h post-infection, respectively. cagPAI-defective strains did not induce detectable levels of IL-8 at 6 h post-infection. At 30 h post-infection all strains induced IL-8 expression in AGS cells, although cagPAI-defective strains induced significantly lower levels of IL-8 than strains with a functional cagPAI (57.1 ± 56.6 pg/mL vs 513.6 ± 338.6 pg/mL,P < 0.0001). We did not observe differences in the extent of cell elongation induction between strains with a functional or a defective cagPAI in 6 h cocultures. At 24 h post infection strains with functionalcagPAI showed high diversity in the extent of hummingbird phenotype induction ranging from 7% to 34%. cag PAI defective strains induced significantly lower levels of elongation than strains with functional cag-PAI with one or more than one EPIYA-C motif (15.1% ± 5.2%vs 18.9% ± 4.7%,P < 0.03; and 15.1% ± 5.2% vs 20.0% ± 5.1%, P < 0.003 respectively). No differences were observed in cellular elongation inductionor IL-8 expression among H. pylori strains bearing one and more than one EPIYA-C motifs, neither at 6 h nor at 24 h of coculture. There were no associations between the levels of induction of cell elongation or IL-8 expression and number of EPIYA motifs or pathology. CONCLUSION: The present work describes a lack of association between H. pylori CagA protein EPIYA motifs variations from Colombian isolates and disease-associated cellular responses.

胃黏膜不同病变中表达凋亡蛋白与幽门螺杆菌CagA+东亚型感染的关系研究

目的研究胃黏膜不同病变中表达凋亡蛋白与幽门螺杆菌细胞毒素相关蛋白A(CagA)+东亚型感染的关系。方法将医院收治的120例胃黏膜病变患者作为研究对象,比较不同病变患者感染幽门螺杆菌CagA+东亚型的情况以及感染该菌型患者体内凋亡蛋白表达与未感染者的区别。结果慢性萎缩性胃炎患者幽门螺杆菌CagA+东亚型感染为30.61%,胃癌患者78.26%,胃溃疡患者52.08%,胃癌患者的感染率最高,三组间感染率比较差异显著(F=14.6815,P=0.0000);感染幽门螺杆菌CagA+东亚型的患者体内caspase-3、肿瘤蛋白P53、P73表达阳性率远高于未感染者,差异显著(χ2=37.1537,43.1159,40.9869;P=0.0000),表达水平亦远高于未感染者,两者上述指标差异显著(t=35.8544,30.8209,30.2270;P=0.0000)。结论感染幽门螺杆菌CagA+东亚型的患者体内凋亡蛋白表达水平高于未感染患者,且胃癌患者该菌的感染率高于其他病变患者。

细胞毒力因子CagA上调人胃黏膜上皮GES-1细胞TET2蛋白的表达

目的:探讨幽门螺旋杆菌细胞毒素相关基因A(cytotoxin associated gene A,CagA)与胃黏膜中TET2(ten-eleventranslocation 2)蛋白表达的关系,以及TET2在CagA致癌过程中可能的作用。方法:Real-time PCR检测人胃黏膜上皮细胞株GES-1和胃癌细胞株MGC-803中TET2 mRNA的表达水平,细胞免疫染色法检测TET2蛋白的细胞定位及表达。将pEGFP-CagA通过脂质体介导转染GES-1细胞,用200μmol/L H2O2处理GES-1细胞建立氧化应激模型,流式细胞仪检测细胞中活性氧(reactive oxygen species,ROS)和细胞周期的变化。结果:TET2 mRNA在GES-1细胞的表达水平低于胃癌MGC-803细胞(1.00±0.08 vs 1.68±0.07,P<0.05),TET2蛋白在GES-1细胞表达水平低于胃癌MGC-803细胞(8.09±3.57 vs14.60±2.31,P<0.05)。与阴性对照组pEGFP-N1相比,pEGFP-CagA转染组GES-1细胞中TET2 mRNA表达水平升高(1.00±0.04 vs 0.06±0.00,P<0.05),TET2蛋白表达水平也升高(16.45±4.40 vs 10.82±3.39,P<0.05),ROS积累水平升高(18.39±4.52 vs 15.31±4.40,P<0.05),细胞周期检测出现明显的凋亡峰。氧化应激(H2O2处理)模型中GES-1细胞与空白对照GES-1细胞相比,TET2 mRNA水平升高(1.44±0.02 vs 1.00±0.04,P<0.05),TET2蛋白表达水平增高(15.72±4.52vs 11.74±4.34,P<0.05)。结论:幽门螺旋杆菌毒力因子CagA可诱导GES-1细胞ROS增高和细胞周期的失衡,氧化应激可以诱导TET2表达上调,TET2可能参与CagA的致癌过程。

幽门螺杆菌参与胃癌侵袭转移的研究进展

胃癌(gastric cancer,GC)是一种常见的消化道癌症,在东亚和东南亚人群中高发。全球大约有50%以上的人口感染幽门螺杆菌(Helicobacter pylori,HP),HP感染已被证实是GC的致病因素之一,与GC的发生有着密切的关联,与GC侵袭转移的关系虽尚无定论但也有了一定的研究进展。一方面,HP定植胃黏膜后,通过其关键毒力因子空泡细胞毒素A(vacuolating cytotoxin A,VacA)和细胞毒素相关抗原A(cytotoxin-associated antigen A,CagA)的作用使其得以长期存活于胃内,并参与GC细胞的增殖、上皮‒间质转化来促进侵袭转移;另一方面,肿瘤微环境作为宿主免疫系统与肿瘤相互作用的场所,HP通过干扰肿瘤微环境内肿瘤细胞与免疫细胞的相互作用、促进肿瘤微环境酸性缺氧环境的形成以及改变微环境内细胞分化等方式,促使GC免疫逃逸从而促进GC的侵袭转移。HP感染如今已成为一个全球性的公共卫生问题,对于GC发生发展的作用更是不容忽视。该文主要围绕上述2个方面,即关键毒力因子和肿瘤微环境来阐述HP感染与GC侵袭转移的相关性,期望能为GC的临床和基础研究提供新思路。

急性冠脉综合征患者幽门螺杆菌感染状况调查及其致病危险性分析

目的探讨幽门螺杆菌（Helicobacter pylori，Hp）感染及其产生的毒力因子与急性冠脉综合征（ACS）的关系，并分析Hp感染对炎症反应以及吡脂的影响。方法采用ELISA方法检测358例ACS患者和327例健康对照者血清中的Hp—IgG，用Western—blot方法检测血清抗CagA抗体以及抗VacA抗体。分析血中炎症反应标志物及血脂水平，比较合并Hp感染的ACS患者与非Hp感染者之间的差异。结果①ACS组Hp—IgG阳性率明显高于健康对照组（57．8％和44．3％，P〈0．05），去除年龄、性别、吸烟、高血压、高脂血症以及糖尿病等危险因素后，Hp感染仍增加患ACS的危险性（OR=1．48，95％CI 1．09—2．00）。②Ⅰ型Hp感染增加患ACS的危险性（OR=2．02，95％CI 1．43—2．87），而中间型和Ⅱ型Hp感染并未明显增加患ACS的危险性。③合并Hp感染的ACS患者和健康对照者血清炎症反应物CRP、纤维蛋白原、白细胞以及血小板计数水平明显高于非Hp感染者（P〈0．05）。④合并Hp感染的ACS患者和健康对照者TC、TG、LDL和Lp（a）水平均高于非Hp感染者，HDL低于非Hp感染者（P〈0．05）。结论Hp感染是导致ACS的独立危险因素，Ⅰ型Hp感染可能更增加患ACS的危险性。Hp感染可能通过诱导全身炎症反应并影响脂质代谢而促进动脉粥样硬化的进展。

用噬菌体展示技术筛选幽门螺杆菌细胞毒素相关蛋白基因结合蛋白的研究

目的筛选幽门螺杆菌细胞毒素相关蛋白(CagA)基因结合蛋白,探索CagA致病机理。方法应用噬菌体展示技术,以幽门螺杆菌CagA基因片段作为固相筛选分子,对噬菌体人胃细胞cDNA文库进行4轮"吸附-洗脱-扩增"富集,噬斑裂解液PCR扩增后,进行DNA序列分析和同源性生物信息学搜索,确定编码结合蛋白的种类。结果噬菌体经富集后,筛选出36个阳性克隆,构建了克隆载体。序列测定后经过同源性搜索,确定幽门螺杆菌CagA基因共编码核纤层蛋白B1和胰岛素样生长因子结合蛋白2两种已知蛋白。结论用噬菌体人胃cDNA文库筛选得到幽门螺杆菌CagA基因DNA结合蛋白,为研究CagA致病机理,幽门螺杆菌疫苗的研制和治疗等提供依据。

慢性萎缩性胃炎与幽门螺杆菌感染的关系

幽门螺杆菌(Helicobacter pylori,Hp)是引起慢性胃炎、消化性溃疡及胃癌的重要病因,几乎所有胃部 Hp 感染者均可引起不同程度胃部炎症改变,少数发展为慢性萎缩性胃炎(chronic atrophic gastritis,CAG),甚至胃癌.关于 Hp 感染导致 CAG 的确切发病机制,目前仍不十分清楚.现就 CAG与 Hp 感染关系的研究现状作一综述.

老年脑梗死患者血清细胞毒素相关蛋白阳性幽门螺杆菌抗体、内皮素以及超敏C-反应蛋白的表达及其相关性分析

目的研究老年脑梗死患者细胞毒素相关蛋白阳性幽门螺杆菌抗体（CagA-Hp.lgG）,内皮素（ET）以及超敏C-反应蛋白（hs-CRP）的表达情况,并对三者的相关性进行分析。方法选择2006年7月~2010年5月到河北联合大学附属医院就诊的发病1周内的老年脑梗死患者40例,均为CagA阳性Hp感染者。另选取相同时间区间内到该院进行健康查体的老年者40例。将脑梗死患者与健康查体者分别归于病例组和健康组。采用ELISA法分别检测两组受试者CagA-Hp.lgG浓度、血清ET浓度以及hs-CRP浓度。对病例组中CagA-Hp.lgG浓度与ET和hs-CRP浓度的关系分析采用相关性检验,计算相关系数r值和P值。结果病例组中CagA-Hp.lgG值为（100.3±11.9）U/mL,血清ET为（86.4±14.2）ng/L,hs-CRP值为（74.8±11.5）mg/L;健康组中CagA-Hp.lgG值为（46.2±7.1）U/mL,血清ET为（39.8±7.1）ng/L,hs-CRP值为（17.4±3.5）mg/L;病例组中三种指标值均明显高于健康组,差异有统计学意义（P〈0.05）。相关性分析显示,CagA-Hp.lgG与ET及hs-CRP均呈正相关（r=0.413,P=0.015;r=0.420,P=0.014）。结论 CagA-Hp.lgG、ET以及hs-CRP在老年脑梗死患者中表达比健康查体者明显增多;CagA-Hp.lgG与ET和hs-CRP均呈正相关性。

幽门螺杆菌与肝脏疾病的相关性研究进展

幽门螺杆菌（helicobacter pylori，Hp）是世界各地最常见的感染性病原之一，世界卫生组织将其归为一类致癌因子。Hp感染与人类胃肠疾病的关系中免疫机制最为关键，并可能参与多种胃肠外疾病的发生发展，本文简介Hp与肝脏疾病的相关性研究进展，为Hp致病机制的研究及相关疾病的防治提供新的思路。

不同基因型幽门螺杆菌与冠心病的相关性研究

目的:探讨不同基因型幽门螺杆菌(Hp)与冠心病的相关性。方法:将研究对象分为冠心病组(60例)和非冠心病组(对照组,60例),检测血浆中同型半胱氨酸(HCY)、C反应蛋白(CRP)水平,胃镜下取胃组织检测Hp,对Hp阳性者检测cagA基因。结果:冠心病组的Hp感染率(55%vs 30%,χ2=0.67,P<0.01)及Hp阳性患者的细胞毒性相关基因(cagA)基因检出率(60.6%vs 27.8%,χ2=5.01,P<0.05)显著高于对照组。冠心病组Hp阳性患者血浆HCY水平[(19.60±3.11)μmol/L]显著高于Hp阴性患者[(14.80±4.60)μmol/L](t=4.82,P<0.001);cagA基因型患者血浆HCY水平[(22.61±4.98)μmol/L]显著高于非cagA基因型患者[(17.10±3.41)μmol/L](t=3.48,P<0.001)。cagA基因型患者血浆CRP水平[(4.98±2.02)mg/L]显著高于非cagA基因型患者[(2.06±1.00)mg/L](t=2.355,P<0.05)。结论:cagA基因型Hp感染,可增高血浆HCY和CRP水平,与冠心病的发生、发展相关。

幽门螺旋杆菌空泡/细胞毒素的研究现状

幽门螺旋杆菌感染呈全球性分布，多数地区感染率约为５０％，但并非所有人发生慢性胃炎和消化性溃疡，这与该菌产生细胞毒素的能力有关。本文综述了幽门螺旋杆菌产生的空泡／细胞毒素（ＶａｃＡ）和细胞毒素相关蛋白（ＣａｇＡ）的性质及与临床的关系、ＣａｇＡ阳性菌株在中国人中的流行情况。根据ＶａｃＡ和ＣａｇＡ基因，及它们表达活性产物与否，可将该菌分为两大类型：Ⅰ型具有编码ＣａｇＡ的基因，表达ＣａｇＡ蛋白和空泡毒素，Ⅱ型没有编码ＣａｇＡ的基因，不表达ＣａｇＡ蛋白和空泡毒素，其中Ⅰ型菌株毒力和致病力强。

幽门螺杆菌与肝脏疾病的相关性研究进展

幽门螺杆菌（helicobacter pylori，Hp）是世界各地最常见的感染性病原之一，世界卫生组织将其归为一类致癌因子。Hp感染与人类胃肠疾病的关系中免疫机制最为关键，并可能参与多种胃肠外疾病的发生发展，本文简介Hp与肝脏疾病的相关性研究进展，为Hp致病机制的研究及相关疾病的防治提供新的思路。

幽门螺杆菌根除疗法治疗慢性特发性血小板减少性紫癜的疗效预测

目的:观察抗幽门螺杆菌三联疗法治疗Hp阳性的慢性特发性血小板减少性紫癜的疗效,并分析抗Hp治疗后,血小板应答的预测因子。方法:59例Hp阳性的慢性特发性血小板减少性紫癜患者,随机分组为抗Hp组和安慰剂对照组,对照组在随访3个月后给予三联抗Hp治疗。每例患者治疗前检测血清CagA蛋白浓度。结果:抗Hp组有效率明显高于对照组(63.3%vs 27.6%,P<0.01),抗Hp组血小板计数升高值明显高于对照组(33.5±21.6vs 12.6±19.5,P<0.05)。全部59例患者有效率59.3%(35/59),有效组血清CagA蛋白浓度明显高于无效组,病程<1年者有效率明显高于1年以上者(75.0%vs 45.0%,P<0.05),初治患者有效率明显高于曾经多种治疗者(71.05%vs 33.33%,P<0.01)。结论:抗HP疗法可升高轻中度Hp阳性慢性ITP患者的血小板计数。血清CagA蛋白浓度高、病程1年以内以及初治患者有较好的疗效。