幽门螺杆菌BALB/c小鼠适应性菌株的驯化及模型建立

目的:通过体内连续传代获得幽门螺杆菌(Hpylori)的BALB/c小鼠适应性定植菌株并建立稳定的感染模型.方法:以H pylori蒙古沙鼠适应株GS_(10)连续传代感染BALB/c小鼠,每次感染20只,感染后4 wk进行微生物学检查(分离培养、直接涂片染色镜检、快速尿素酶试验、PCR鉴定),观察H pylori的定植情况,计算每批动物的感染率,直至感染率稳定在80%以上,然后对已稳定感染的小鼠胃黏膜组织进行H pylori定量培养及病理学检查.结果:随着H pylori菌株GS_(10)在BALB/c小鼠内的连续传代,感染率逐渐升高.GS_(10)株初次感染率仅为11.1%,传代至第6代(BS_6株)以后,感染率稳定在80%以上;BALB/c小鼠适应株BS_8感染小鼠后4 wk在胃窦、胃体和胃底的定植密度(CFU/g组织)的常数对数均值分别为5.32±0.88,4.14±1.05和1.05±2.25,与SS1的定植密度相比,相差不显著(P>0.05).感染鼠病理学检查在胃窦黏膜上皮细胞间及固有层中发现大量炎症细胞浸润;在胃窦及幽门部上皮细胞表层黏液、胃腺窝中见到大量H pylori存在.结论:经过连续传代感染,驯化出一株高定植力和感染率的Hpylori BALB/c小鼠适应株,并成功建立稳定的H pylori小鼠感染模型.     

海尔曼螺杆菌感染小鼠的病理学研究

目的 建立海尔曼螺杆菌(Hh)感染小鼠模型,以了解Hh感染小鼠的病理学特点。方法 50只Ⅱ级Balb／c小鼠随机分为实验组(30只),实验组小鼠采用由Hh感染患者转归的小鼠胃粘膜组织磨碎后直接灌喂方法建立Hh感染小鼠模型,而对照组不作相应处理。于灌喂后第1、2、4、8、及16周分批处死小鼠,每批处死实验组小鼠6只、对照组小鼠4只。取胃粘膜组织分别进行细菌培养、涂片Gram染色、快速尿素酶试验(RUT)、组织切片Warthin-Starry银染、组织病理学检查。结果 Hh容易在Balb／c小鼠胃内定植,成功率达到100％。在感染第4周始,部分Hh感染小鼠胃粘膜可见少量淋巴细胞、中性粒细胞和嗜酸性粒细胞浸润,至感染第16周,全部感染小鼠胃粘膜均可见不同程度的淋巴细胞、浆细胞浸润,部分小鼠伴有中性粒细胞浸润,而对照组小鼠未见有明显的炎细胞浸润。结论 Hh可长期稳定定植于小鼠胃内,并可引起慢性活动性胃炎,可用于Hh的致病性研究。     

建立幽门螺杆菌感染BALB/c小鼠动物模型的实验研究

[目的]建立幽门螺杆菌(Hp)BALB/c小鼠感染动物模型。[方法]用cagA基因和vacA基因同时阳性的Hp小鼠适应株给BALB/c小鼠灌胃。[结果]经Hp小鼠适应株灌胃4周后,病理模型组10只感染的小鼠胃黏膜尿素酶试验、细菌学培养和组织病理学检查均为阳性,感染率为100%;正常对照组未见Hp生长,两者比较差异有统计学意义(P<0.05)。[结论]成功地建立了云南Hp小鼠适应株感染的BALB/c小鼠动物模型。这种ca gA基因和vacA基因同时阳性的Hp小鼠适应株毒力强容易定植;可在普通饲养条件下建立,即有利应用于云南地区Hp的相关研究,又可节约研究经费,易于推广使用。     

经腹腔注射建立免疫抑制BALB/c小鼠系统念珠菌感染模型的研究

目的经腹腔注射建立免疫抑制BALB/c小鼠系统念珠菌感染模型。方法 BALB/c小鼠用环磷酰胺致免疫低下后,腹腔注射不同浓度白色念珠菌SC5314,观察小鼠不同时间血液常规、肾脏真菌载量和组织病理变化。结果白色念珠菌SC5314孢子浓度在2×106～5×107个/ml间的5种0.1ml菌液均造成小鼠系统感染白色念珠菌,病理表现以注射2×107个/ml孢子组小鼠最为典型,在心、肺、肾、脑、横膈、肠系膜等组织内均可见真菌孢子和菌丝。结论经腹腔注射白色念珠菌SC5314可成功建立免疫抑制BALB/c小鼠系统念珠菌感染模型,最适感染剂量为每鼠0.1ml的1×107～2×107个孢子/ml菌液。     

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。     

田鼠巴贝虫实验动物模型的建立

目的建立田鼠巴贝虫(Babesia microti)的实验动物模型。方法自感染田鼠巴贝虫的种鼠取血,腹腔注射接种3~4周龄雌性BALB/c小鼠(7只)、免疫抑制BALB/c小鼠(4只)、雄性SCID小鼠(4只)和NOD-SCID小鼠(4只)。感染后每天采血,涂制薄血片,吉氏染色,油镜下观察田鼠巴贝虫的生长、增殖情况,记录红细胞的感染率。解剖3只不同红细胞感染率的BALB/c小鼠,油镜下观察心、肝、脾、肺、肾、脑和骨髓等组织的感染情况。记录各组织中红细胞的感染率,并分析与外周血红细胞感染率的关系。取红细胞感染率大于40%的BALB/c小鼠血液,冷冻保存2个月后用同样的方法接种小鼠,观察田鼠巴贝虫的增殖情况。结果 BALB/c小鼠、免疫抑制BALB/c小鼠、SCID小鼠和NOD-SCID小鼠接种后,末梢血液中均检测出田鼠巴贝虫。BALB/c小鼠的红细胞感染率在d7达到峰值(82.4%),免疫抑制BALB/c小鼠的红细胞感染率在d5达到峰值(73.2%),SCID小鼠和NOD-SCID小鼠的红细胞感染率均在d8达到峰值(86.4%和72.5%)。红细胞感染率达到峰值后,BALB/c小鼠的红细胞感染率迅速下降,免疫抑制BALB/c小鼠的红细胞感染率缓慢降低,SCID小鼠和NOD-SCID小鼠的红细胞感染率则出现震荡变化。感染的BALB/c小鼠的心、肝、脾、肺、肾、脑和骨髓等组织内均可观察到田鼠巴贝虫,虫体主要位于红细胞内,各组织内的红细胞感染率随外周血红细胞感染率的升高而增高。冷冻保存的虫种复苏后可感染健康BALB/c小鼠,末梢血中出现虫体的时间与新鲜含虫血液感染鼠的比较滞后2 d,达到感染高峰的时间滞后1 d。结论成功建立田鼠巴贝虫的小鼠模型,红细胞的感染情况与机体的免疫状态相关。     

猪链球菌2型BALB/c小鼠动物感染模型的建立

目的研究猪链球菌2型(SS2)中国高致病株05ZYH33株对BALB/c小鼠的致病性,探讨其作为SS2动物感染模型的可行性。方法用猪链球菌活菌经腹腔注射感染小白鼠,并做阴性对照。通过LD50测定、临床症状观察、病理剖检、病原分离鉴定、菌株在各脏器内定植分布检测、细胞因子测定,观察和分析小鼠感染SS2后机体的一系列改变。结果 BALB/c小鼠对05ZYH33株易感,其LD50为4×107 CFU/ml,并可区分强毒株和无毒株毒力差异;病原分离鉴定证实各脏器感染菌株均为SS2;涂板计数表明野生株05ZYH33在小鼠各脏器定植量显著高于无毒株Δcps2B;病死鼠的特征性组织病理学变化表现为典型的弥漫性血管内凝血和微血栓形成;野生株及无毒株均可引起炎症因子IL-6及趋化因子MCP-1的释放,但无毒株△cps2B诱导细胞因子水平显著低于野生株(P0.05)。结论 BALB/c小鼠可被SS2感染并引发炎症反应。适龄SPF BALB/c小鼠是中国SS2强致病株良好的动物感染模型。     

人巨细胞病毒先天性感染胎鼠致肝脏损伤的小鼠模型

目的为探讨人巨细胞病毒(HCMV)先天性感染致肝脏损伤的病理机制,建立 HCMV先天性感染胎鼠致肝脏损伤的小鼠模型。方法将不同剂量的 HCMV 接种至10周龄 Balb/c 雌雄小鼠腹腔后,交配。待雌鼠临产时,剖腹取出胎鼠肝脏,进行病毒分离、病理学检查、HCMV DNA 原位杂交检测。结果在接种1.0ml HCMV 组胎鼠,肝组织匀浆上清液中分离出HCMV;在病毒分离出现典型 CPE 的细胞培养上清中用 PCR 检测出 HCMV DNA;原位杂交证实病毒核酸存在于肝细胞核内和胞浆内;病理学研究证实肝组织有炎性改变,肝细胞水肿变性,核内有特异性 HCMV 包涵体,部分肝细胞坏死。0.5ml 组原位杂交见肝细胞核内和胞浆内有少量病毒核酸存在;病理学研究表明肝组织仅有轻度炎性改变和肝细胞水肿变性,但肝细胞坏死不明显。上述结果在0.25ml 组表现均不明显,与正常对照组相似。结论 HCMV 可以通过胎盘造成胎鼠的先天性感染,并导致肝脏损伤;胎鼠先天性 HCMV 感染与母体感染的病毒量有关。该模型的建立为进一步研究人类先天性 HCMV 感染造成肝脏损伤的病理过程以及对先天性感染的预防、诊断和抗病毒药物的筛选提供了可能。     

隐孢子虫感染小鼠动物模型

目的建立隐孢子虫感染小鼠动物模型,为药物筛选和分子生物学研究奠定基础。方法饮水中添加地塞米松(DEX)抑制鼠免疫功能,5d后经口灌喂隐孢子虫卵囊感染小鼠。比较粪便中排卵囊量和小鼠生存情况,从不同品系小鼠(KM、BALB/c)、不同鼠龄(乳鼠断乳2d、56周、1012周)、不同免疫抑制剂量(0,2.5,5,7.5,10,12.5mg/L)、不同卵囊接种量(75,1.5×102,1.5×103,1.5×104,3.0×104)及不同保存时间(1,2,6,8个月)等影响小鼠感染的因素中,选出最佳条件,建立稳定的隐孢子虫感染小鼠动物模型。结果(1)KM、BALB/c两种小鼠都能感染微小隐孢子虫,BALB/c组小鼠开始死亡的时间比KM组的早,BALB/c组收集的卵囊数比KM组的少;(2)乳鼠组小鼠排卵囊的数量总体大于其他年龄段小鼠,但是其生存时间较短;(3)7.5,10mg/LDEX剂量组排卵囊数量较多,且持续整个实验期,低于此剂量组小鼠排卵囊数量少,多于此剂量组易死亡;(4)接种75个以上微小隐孢子虫卵囊均能使小鼠感染;(5)保存1,2,6,8个月的微小隐孢子虫卵囊均能感染小鼠。结论采用56周龄的KM雌性鼠,在饮水中添加7.5～10mg/LDEX,接种75个以上保存时间在8个月内的微小隐孢子虫卵囊可以建立较稳定的感染模型。     

幽门螺杆菌与胃粘膜的抗原相似性在胃体萎缩性胃炎中的致病机理

大部分幽门螺杆菌(Hp)感染者体内存在与胃粘膜抗原起交叉反应的自身抗体。本文旨在探讨Hp感染与自身抗体、胃体粘膜组织病理学改变之间的关系以及不同Hp菌株在诱导胃自身免疫能力上的差异。 方法:(1)100名患者分别作Hp培养及血清学鉴定、组织病理学检查、自身抗体检测;(2)来自10例萎缩性胃炎(AG)和10例非萎缩性胃炎患者(NAG)的20株Hp分别免疫Balb/C小鼠后检测其血清中胃粘膜自身抗体;(3)利用     

CagA+幽门螺杆菌裸鼠感染模型的建立

目的用携带ｃａｇＡ基因的Ｈｐ成功感染ＢＡＬＢ／ｃ裸鼠。方法分别采用ｃａｇＡ基因阳性和阴性的具有较强动力的新鲜Ｈｐ分离菌株，通过灌胃方式感染ＢＡＬＢ／ｃ裸鼠，感染后４周和８周分两批处死，进行微生物学和病理组织学检查。结果灌喂８周后，ｃａｇＡ＋实验组和ｃａｇＡ－实验组均成功定植Ｈｐ（１６／１６）；ｃａｇＡ＋组胃粘膜表现明显炎症及坏死病变，而ｃａｇＡ－组仅有轻微炎症发生。结论建立典型的Ｈｐ动物感染模型应选择ｃａｇＡ＋菌株。     

幽门螺杆菌疫苗接种小鼠产生免疫后胃炎的影响因素

目的:研究幽门螺杆菌(H pylorl)疫苗接种小鼠产生免疫后胃炎的影响因素．方法:将H pylori疫苗免疫C57BL／6和BALB／c的小鼠,观察攻击后胃黏膜H pylori定植和炎症情况．将H pylori疫苗免疫C57BL／6小鼠,然后予不同菌量的H pylori攻击,观察胃黏膜H Pylori定植和炎症情况．将H pylori疫苗经口和经腹腔免疫C57BL／6小鼠,观察攻击后胃黏膜H pylori定植和炎症情况.对感染H pylori的C57BL／6小鼠予H pylori疫苗治疗,观察治疗免疫后胃黏膜H pylori定植和炎症情况．结果:不同品系的小鼠免疫保护程度无明显差异,但C57BL／6小鼠免疫后胃炎重于BALB／c小鼠．接受不同攻击茵量的小鼠保护程度无明显差异,但大的攻击茵量可诱导更严重的免疫后炎症．不同免疫途径诱导的免疫保护程度及攻击后不同时间点的炎症程度均无显著性差异．治疗性免疫导致H pylori定植明显降低,同时也引发更为严重的胃炎．结论:在不同的免疫宿主、免疫途径和治疗性免疫中均存在免疫后胃炎．免疫后胃炎的强弱程度受免疫宿主和攻击菌量的影响．     

Prevention of Helicobacter pylori infection by lactobacilli in a gnotobiotic murine model.

BACKGROUND: Helicobacter pylori is a bacterium which causes gastric inflammatory diseases. Oral inoculation of H pylori usually results in only a temporary colonisation without a successful infection in the stomach of conventional mice in which lactobacilli are the predominant indigenous bacteria. AIM: To determine whether lactobacilli exert an inhibitory effect on colonisation by H pylori in the stomach. METHODS: The effects of H pylori on attachment to murine and human gastric epithelial cells and the H pylori mediated release of interleukin-8 (IL-8) by these cells were examined in vitro. Lactobacillus salivarius infected gnotobiotic BALB/c mice and control germ free mice were inoculated orally with H pylori to examine whether L salivarius can inhibit colonisation by H pylori. RESULTS: L salivarius inhibited both the attachment and IL-8 release in vitro. H pylori could not colonise the stomach of L salivarius infected gnotobiotic BALB/c mice, but colonised in large numbers and subsequently caused active gastritis in germ free mice. In addition, L salivarius given after H pylori implantation could eliminate colonisation by H pylori. CONCLUSION: These findings suggest the possibility of lactobacilli being used as probiotic agents against H pylori.     

幽门螺杆菌感染Balb/c 小鼠模型的建立及对N-甲基-N-亚硝基脲诱发胃癌的影响

目的建立一种稳定的造模周期短的幽门螺杆菌(Hp)感染模型,观察Hp对小鼠胃黏膜的损害程度,同时研究Hp感染是否促进亚硝基类化合物的致癌作用.方法 94只Balb/c小鼠分为4组.第1组单用N-甲基-N-亚硝基脲(MNU);第2、3组小鼠用灌胃法定植Hp,第3组小鼠加用MNU灌胃;第4组为正常对照.36周后处死全部小鼠,分别用尿素酶、Giemsa染色和微需氧细菌培养检测Hp定植;H-E染色进行鼠胃黏膜病理诊断.结果 Balb/c小鼠Hp定植率达93.9%.Hp单一处理组中度以上炎症占100.0%,其中萎缩性胃炎占20.0%;而Hp和MNU联合处理组中度以上炎症占100.0%,其中萎缩性胃炎占23.1%,不典型增生占42.3%和57.7%(胃体和胃窦),并发现2只小鼠有低分化腺癌,占7.1%.Hp处理组和Hp MNU联合处理组在炎症程度上与正常对照组相比,差异有统计学意义(P＜0.01).结论本实验成功建立了Hp感染小鼠模型,验证了Hp和胃癌的发生有高度相关性,证实Hp在协同MNU致癌性中的作用,提示胃癌的发生并非Hp感染单一因素的结果,而和多因素共同作用有关.     

The therapeutic effect of bovine lactoferrin in the host infected with Helicobacter pylori

BACKGROUND: It remains unclarified whether bovine lactoferrin (bLF) can exert a therapeutic effect on the host infected with Helicobacter pylori. METHODS: Germfree BALB/c mice were orally inoculated with H. pylori to induce infection. Three weeks after infection the mice were given bLF orally once daily for 2 or 4 weeks and were then killed to examine the bacterial number in the stomach and the serum antibody titer to H. pylori. To count the number of epithelium-bound H. pylori, the resected stomach was agitated in phosphate-buffered saline to remove non-bound H. pylori before bacterial enumeration. RESULTS: The administration of 10 mg bLF for 3 to 4 weeks decreased the number of H. pylori in the stomach to one-tenth and also exerted a significant inhibitory effect on the attachment of H. pylori to the stomach. As a result, the serum antibody titer to H. pylori, whose level is presumed to represent the size of the immune response by the host, thereby reflecting the degree of bacterial attack, decreased to an undetectable level. CONCLUSIONS: These findings suggest that bLF exerts an inhibitory effect on colonizing H. pylori by detaching the bacterium from the gastric epithelium and by exerting a direct anti-bacterial effect.     

蒙古沙鼠感染幽门螺杆菌后的胃部病理学变化研究

目的　建立幽门螺杆菌 (Helicobacterpylori,Hp)的蒙古沙鼠长期感染模型并观察其胃内的病理学改变。 方法　蒙古沙鼠 (8周龄 ) 80只 ,随机分为实验组 (40只 )和对照组 (40只 ) ,所有沙鼠禁食水 1d ,第 2天灌喂 5 0 %的乙醇 0 3ml,试验组第 3天及第 4天分 3次灌喂cagA Hp菌液 (10 9cfu/ml) ,0 5ml/只·次 ,对照组灌喂相同量无菌肉汤。最后一次灌喂后 2h进食水。距最后一次灌菌后 4、8、12、2 0、2 4周分别剖杀动物 ,每次实验组、对照组各 8只 ,进行微生物学检查 (粘膜涂片染色镜检、分离培养、快速尿素酶试验 )、血清学检查 (ELISA测抗Hp抗体 )和病理学检查。结果　实验组沙鼠在不同时间Hp感染率均达到 10 0 %。从第 4周开始 ,可见所有实验组沙鼠胃组织中有大量炎性细胞浸润 ,随着时间推移形成淋巴滤泡。部分沙鼠在第 12周后至 2 4周可见明显出血、慢性活动性胃炎及溃疡 ,有的溃疡可深达肌层。对照组沙鼠均无Hp定植及组织学病变。结论　蒙古沙鼠感染Hp后 ,可出现与人极相似的病理组织学改变 ,对于研究Hp的致病机制及疫苗具有重要价值     

A noninvasive H. pylori stool antigen assay to detect H. pylori infection of in vivo BALB/c mice models.

BACKGROUND/AIMS: Previous tests for H. pylori infection status of mice have required sacrificing the small host for histological evaluation. We thus aim to determine whether a noninvasive HpSA (H. pylori-specific stool antigen assay) could be applied to detect H. pylori infection in living mice. METHODOLOGY: A total of 60 BALB/c specific pathogen-free mice were used, 20 per control group and 40 per exposed group, the exposed group being challenged with H. pylori isolates. In both groups, the stool samples of each mouse were collected before, 7 days, and 4 weeks after the challenge with H. pylori isolates in the exposed group. All the stool samples were processed with HpSA to detect the presence of H. pylori infection. Four weeks after the inoculation of the exposed group and no inoculation in the control group, each mouse received gastrectomy for histology to judge the presence of H. pylori. RESULTS: None of the mice had a positive histology in the control group. Five BALB/c mice expired due to H. pylori inoculation in the exposed group. Four weeks after inoculation, 85.7% (30/35) of the BALB/c mice achieved the H. pylori infection. Applying the stool samples collected on the 7th day and selecting cutoff point as 0.2, the sensitivity and specificity of HpSA to detect the H. pylori colonization achieved as 100% and 88%, respectively. The 4th week stool samples for HpSA achieved a high sensitivity as 96.6% and specificity as 96% to detect H. pylori infection rate, while choosing cutoff point as 0.20. CONCLUSIONS: HpSA can be an effective tool without subject lethality to detect H. pylori infection in BALB/c mice model.     

Transmission of Helicobacter pylori in an Animal Model

An experimental murine model was studied to evaluate the orogastrointestinal colonization of Helicobacter pylori and the animal-to-animal transmission. Balb/C mice were infected with H. pylori and housed with uninoculated mice in cages with and without a grate on the floor. Mice were killed after 7, 14, 30, and 45 days, and samples from the esophagus, stomach, small intestine, colon, and rectum were analyzed for H. pylori by PCR and immunohistochemistry and for histological changes. Bacterial colonization was assessed also by culture from stomach samples. H. pylori was cultured by stomach samples of infected mice at 7, 14, and 30 days. Using PCR and immunohistochemistry, H. pylori was detected in inoculated and uninoculated mice in all areas examined, with an high percentage of positive samples in the esophagus and stomach. Moreover transmission was detected, without differences, regardless of whether mice were housed with or without a grate on the floor, supporting an orooral animal transmission.     

Development of Helicobacter pylori Infection Model in BALB/c Mice with Domestic cagA-Positive and-Negative Strains in Taiwan

We aimed to develop an H. pylori-infected mousemodel using clinically stored strains in Taiwan and totest whether development of H. pylori infection in an invivo animal model is related to the status of the cagA gene. A total of 100 male BALB/cmice, 6-8 weeks old, including 80 in the experimentalgroup and 20 in the control group, were used. Twoclinically stored H. pylori isolates, a cagA-positive and a cagA-negative strain, were selected toinduce the H. pylori infection in half (N = 40) of themice in the experimental group. Bacterial isolates of0.8 × 10⁹ CFU/ml were orally inoculatedin each mouse of the experimental group for threeconsecutive days. Ten mice in the control group weresacrificed to confirm the initial absence of H. pylori.Eight weeks after inoculation of the experimental group and no inoculation of the remaining 10mice of the control group, each mouse was killed.Gastrectomy was then performed for rapid urease test(CLOtest) and histology. In the control group, none of 20 mice had positive results from the CLOtestor histology. In contrast, excluding eight of 80 micethat died before the eighth week, 90.3% (65/72) of themice challenged with H. pylori showed persistent presence of H. pylori by histology. Theseverity of gastritis at the eighth week was moreevident in H. pylori-infected mice than in control andnoninfected mice (P < 0.05). Although gastritis wasmore severe in mice inoculated with thecagA-positive strain than with the cagA-negative strain,the rates of H. pylori infection in mice were notdifferent between cagA-positive and -negative strains(91.4% vs 89.2%, P > 0.05). In summary, storedstrains of H. pylori can be applied to induce aninfection model in BALB/c mice. The less virulentcagA-negative strain can induce H. pylori infection inmice as effectively as the cagA-positive strain. Thehigh prevalence of cagA-positive strains in Taiwanesepatients may be related to factors other than only thecagA gene of the bacteria.