幽门螺杆菌下调人胃黏膜分泌性白细胞蛋白酶抑制因子的表达

目的通过低剂量阿斯匹林的处理作为炎性模型,研究分析人胃和十二指肠黏膜分泌性白细胞蛋白酶抑制因子(SLPI)表达下调是否与幽门螺杆菌(Helicobacter pylori,Hp)定居或感染有关。方法选择20例健康志愿者分成Hp+和Hp-组,其中Hp+组成功进行了根除治疗。每组10人,每人口服阿司匹林100 mg/d。通过活检提取受试者不同部位胃黏膜的总RNA和蛋白,采用RT/real-time PCR检测SLPI的mRNA表达水平和单抗ELISA定量测定SLPI蛋白,统计分析SLPI基因表达的相关数据。结果与Hp-组比较,Hp+组胃窦黏膜SLPI表达水平显著降低,但Hp+组经抗生素根除治疗后其SLPI水平恢复至与Hp-组相当的水平。在低剂量阿司匹林处理下,所有受试者表现组织学观察到的活动性或慢性炎性征。各组在药物处理的不同时间虽有一定的差异,但与药物处理对照组(第0天)比较,SLPI的表达差异没有统计学意义[第1天:(77±880)pg/10μg蛋白;第3天:(941±149)pg/10μg蛋白;第7天:(763±363)pg/10μg蛋白]。阿司匹林处理的1周内以胃窦为主的胃炎持续存在(活动性:1.5~1.7;慢性:1.2~2.1),但与Hp-和Hpe(根除组)比较,Hp+组的胃窦黏膜SLPI蛋白表达仍显著降低。结论低剂量阿司匹林处理所致炎性反应对人胃黏膜SLPI的表达没有影响,胃窦黏膜SLPI基因表达的下调与Hp感染有关。     

免疫佐剂联合中药治疗Hp感染BALB/c小鼠免疫状态的研究

本文研究用SS1HP株以约10^9／ml的菌液，每次0．4ml／只连续灌喂SPF级BABL／c小鼠4次，10d完成，灌喂后8周经组织学等检查证实全部感染Hp后，随机分成5组，并灌喂：A组尿素酶＋霍乱毒素B亚单位（CTB）＋羟磷灰石（HAP），B组中药胃泰＋尿素酶＋CTB＋HAP，C组单纯中药胃泰，D组尿素酶，E组为空白对照。治疗剂量：尿素酶250mg、CTB4μg、HAP1mg，中药为胃泰胶囊（主要由黄莲、     

慢性萎缩性胃炎合并Hp与未合并Hp患者胃镜病理表现差异分析

目的:分析慢性萎缩性胃炎合并幽门螺旋杆菌(helicobacter pylori,Hp)感染与胃镜病理变化之间的相关性.方法:收集2018年5月至2020年5月在本院收治的慢性萎缩性胃炎合并Hp感染者80例(Hp阳性组),另选取院同期治疗单纯慢性萎缩性胃炎患者80例(Hp阴性组).对比单纯慢性萎缩性胃炎患者与慢性萎缩性胃炎合并Hp感染者病理改变分布情况,分析患者病理特征与Hp感染之间的关系,及不同病理特征Hp感染程度.结果:Hp阳性组患者胃部炎症、中性粒细胞浸润、肠上皮分化、胃粘膜萎缩发生情况均明显高于Hp阴性组(P<0.05);Hp阳性组患者炎症、中性粒细胞浸润、肠上皮分化、胃粘膜萎缩情况为中-重度者明显高于Hp阴性组(P<0.05);不同病理特征之间患者Hp感染程度不一,胃粘膜萎缩患者其Hp感染程度以强阳性为主,炎症患者则以弱阳性为主(P<0.05).结论:Hp感染与慢性萎缩性胃炎患者胃镜下病理特征存在密切联系,在临床治疗中需要注意Hp诊断、根除有助于改善患者临床症状.     

探讨三联疗法对不同类型的Hp相关性胃炎的疗效

目的探讨三联疗法对不同类型的Hp相关性胃炎的疗效。方法选取我院74例诊断为幽门螺旋杆菌（HP）感染引起胃炎的患者,进行兰索拉唑、克拉霉素、阿莫西林的三联疗法治疗14d,在治疗完成后4~6w采用C-尿素呼气试验进行HP检查。结果经检测得到 ITT患者HP根除率为68.9％,PP分析的幽门螺旋杆菌感染根除率为83．6％。全胃型胃炎的根除率TPP分析66．2％,PP分析80．3％,胃窦型胃炎的根除率TPP分析74．6％,PP分析87．1％。多因素分析未能确定与治愈相关的因素。结论相比胃窦型胃炎,全胃型胃炎14d三联疗法的根除率低,14d三联疗法没有达到可接受的幽门螺旋杆菌的治愈率。     

美洲大蠊多肽对MFC荷瘤小鼠免疫影响的初步探究

目的初步探究美洲大蠊多肽对MFC荷瘤小鼠免疫的影响,以了解其抗肿瘤机制。方法建立MFC荷瘤Balb/c小鼠模型,随机分为模型组(生理盐水20 ml/kg灌胃,1次/d)、CTX组(45 mg/kg,10 ml/kg隔日腹腔注射1次)、CⅡ-3高剂量组(400 mg/kg,20 ml/kg灌胃,1次/d)、CⅡ-3低剂量组(200 mg/kg,20 ml/kg灌胃,1次/d)、短肽HFDT1组(7.8 mg/kg,10 ml/kg腹腔注射,1次/d)及正常对照组(生理盐水20 ml/kg灌胃,1次/d)。处理结束后测小鼠抑瘤率、脾及胸腺指数、外周血细胞变化,流式细胞术检测脾淋巴细胞变化。结果 CⅡ-3高、低剂量、HFDT1及CTX均能抑制肿瘤生长。与CTX比较,CⅡ-3高、低剂量、HFDT1能够增加荷瘤小鼠的体质量,升高白细胞总数、淋巴细胞、单核细胞及粒细胞(P0.05),能升高脾指数及胸腺指数(P0.05),增加脾淋巴细胞总数及NK细胞比例(P0.05)。与模型组比较,CⅡ-3高、低剂量、HFDT1能增加脾T细胞比例。结论美洲大蠊多肽及人工合成短肽HFDT1能够抑制肿瘤的生长,其抗肿瘤作用可能是通过提高机体的免疫力且无毒副作用来实现的,详细的免疫调节机制有待进一步研究,其有望成为抗肿瘤及毒副作用低的候选药物。     

壳聚糖体内抗幽门螺杆菌作用及其对机体体液免疫反应的调节

目的研究壳聚糖体内抗幽门螺杆菌（Hp）作用，及其对机体体液免疫反应的调节作用。方法建立BALB／c小鼠Hp感染的动物模型后，随机分为8组：（1）对照组；（2）PPI组；（3）AM组；（4）AM＋PPI组；（5）壳聚糖组；（6）壳聚糖＋PPI组；（7）壳聚糖＋AM组；（8）壳聚糖＋AM＋PPI组。分别给予上述药物每日2次灌胃，共2周。停药后4周，处死小鼠，无菌条件下取胃黏膜、唾液和血清。采用定量Hp培养和病理改良Giemsa染色法检测胃黏膜内Hp感染。用ELISA法检测血清、唾液和胃黏膜内Hp抗体，用SP免疫组织化学法检测胃黏膜内分泌型IgA（sIgA）。结果以上8组的却根除率分别为0、0、41．7％、58．3％、58．3％、66．7％、83．3％、91．7％，其中（3）～（8）组的肋根除率与（1）和（2）组比较差异有统计学意义（P〈0．05）。Hp定植密度研究发现各组之间Hp定植密度差异有统计学意义（P〈0．001），坳定植密度在（3）～（8）组显著低于（1）和（2）组（P〈0．05），（7）组显著低于（3）组（P〈0．05），（8）组显著低于（4）组（P〈0．05）。血清中抗Hp　IgG、IgG1、IgG2a及唾液中抗Hp　IgA含量，各组差异无统计学意义（P〉0．05）。胃黏膜中抗Hp　IgA含量，在壳聚糖组和壳聚糖＋AM组显著高于无壳聚糖组（P〈0．05）。胃黏膜sIgA阳性腺体百分率，含壳聚糖组显著高于不含壳聚糖组（P〈0．05）。结论壳聚糖在体内有抗Hp作用，并与AM有协同作用，它与PPI和AM三者联用的Hp根除率高达91．7％，有望成为一抗Hp新药。壳聚糖可促进胃黏膜局部抗Hp　IgA和sIgA的产生，因此它在体内的抗Hp作用除了直接杀灭Hp外，其对机体免疫调节效应可能参与了抗菌机制。     

大黄、黄连、黄芩联合三联序贯治疗Hp感染的疗效分析

目的 对比大黄、黄连、黄芩三味药联合三联序贯治疗Hp感染与三联治疗Hp的临床疗效。方法 把解放军武汉总医院门诊行14C呼气试验检测Hp为阳性的患者67例,随机分为两组,A组:标准三联组（耐信+克拉霉素+阿莫西林）,疗程10 d;B组:先用大黄、黄连、黄芩治疗1周再用标准三联治疗10 d。抗Hp治疗停药4周后复查14C呼气试验。比较各组Hp根除率。结果 A组Hp根除率为51.56%,B组Hp根除率为85.29%,两组差异有统计学意义（P＜0.05）。结论 中药大黄、黄连、黄芩联合标准三联序贯治疗Hp感染的根除率高于三联治疗Hp感染。     

酸枣仁黄酮减轻全氟辛烷磺酸诱导小鼠肝脏氧化损伤

目的 通过全氟辛烷磺酸(PFOS)诱导小鼠肝脏氧化损伤模型来研究酸枣仁黄酮(ZSSF)对其的保护作用.方法 将小鼠随机分为空白组、造模组、维生素C组和ZSSF高、中、低剂量组,每组10只.灌胃给药同时用PFOS(10 mg/kg)造模,连续给药30 d.末次给药6 h后,取小鼠眼球血,取肝脏加入9倍体积的0.9％ 氯化...     

亲和软胶囊调节血脂作用的实验研究

目的:建立蛋黄乳液小鼠急性高脂血症模型和脂肪乳大鼠高脂血症模型,观察亲和软胶囊对血脂的调节作用。方法:昆明种小鼠和SD大鼠各50只,随机分成空白对照组、高脂模型组、亲和软胶囊高/中/低剂量组(2.791、1.396、0.698g.kg-1(小鼠),1.861、0.931、0.465g.kg-1(大鼠)和辛伐他汀对照组(5mg.kg-1(小鼠),3.33mg.kg-1(大鼠))。各组小鼠连续给药12天,末次给药2h后,除空白对照组外,其余各组小鼠腹腔注射75%蛋黄乳液0.5ml/只,于复制模型后20h眼眶取血,分离血清,测定TC和TG。各组大鼠每天上午灌胃给药,下午除空白对照组外,其于各组大鼠灌胃脂肪乳(…     

IL-22对Hp感染的UC模型小鼠的影响

目的探究白细胞介素-22(IL-22)对幽门螺旋菌(Hp)感染的溃疡性结肠炎(UC)模型小鼠的影响。方法无特定病原级雌性Balb/c小鼠80只,依次分为空白对照组(自由饮用蒸馏水7 d,于第1、3、5天注射0.9%氯化钠溶液)、Hp感染组(灌服Hp菌液,自由饮用蒸馏水7 d,于第1、3、5天注射0.9%氯化钠溶液)、Hp+DSS组[灌服Hp菌液,自由饮用3%葡聚糖硫酸钠(DSS)溶液7 d,于第1、3、5天注射0.9%氯化钠溶液]、IL-22干预组(灌服Hp菌液,自由饮用3%DSS溶液7 d,于第1、3、5天注射重组小鼠IL-22),每组20只,分别重复上述1～3个周期。每日观察小鼠一般情况、收集粪便做大便隐血实验、采用疾病活动指数(DAI)评分判断疾病活动指数;均于建模成功7 d后采用断头法处死小鼠,免疫组化染色/Western blot法检测肠黏膜中紧密连接蛋白occludin、STAT3表达,透射镜下观察结肠上皮细胞间连接程度,苏木素-伊红(HE)染色检测评估UC炎症程度,提取结肠蛋白检测肠道屏障功能指标二胺氧化酶(DAO)、血浆D-乳酸(D-Lacc)。结果空白对照组第3、7、21天DAI评分低于Hp感染组低于Hp+DSS组低于IL-22干预组(P0.05),空白对照组第7、21天体质量百分比高于Hp感染组高于Hp+DSS组,高于IL-22干预组(P0.05)。IL-22干预组小鼠较Hp+DSS组小鼠结肠黏膜上皮完整、管壁增厚,腺体和隐窝结构基本正常、排列完整,炎性细胞浸润更少;空白对照组组织病理学评分低于IL-22干预组,低于Hp+DSS组,低于Hp感染组(P0.05)。空白对照组occludin蛋白表达量高于Hp感染组,高于Hp+DSS组,高于IL-22干预组(P0.05),空白对照组和Hp感染组STAT3蛋白表达量低于Hp+DSS组,低于IL-22干预组(P0.05)。透射电镜结果显示,IL-22干预组小鼠较Hp+DSS组和Hp感染组小鼠有更完整屏障功能。空白对照组D-Lac含量低于IL-22干预组,低于Hp+DSS组,低于Hp感染组(P0.05),空白对照组和Hp感染组DAO含量低于Hp+DSS组,低于IL-22干预组(P0.05)。结论 IL-22干预后Hp感染的UC模型小鼠受损的肠道黏膜上皮细胞得到改善,肠道杯状细胞及紧密连接蛋白增加,考虑IL-22可作为一种新的治疗靶点。     

Suppurative gastritis in BALB/c mice infected with Listeria monocytogenes via the intragastric route

Suppurative gastritis was demonstrated in BALB/c mice 3 days after intragastric inoculation with 10(9) organisms of Listeria monocytogenes strain ATCC19113 (serotype 3). Also tested were four other strains of mice (C3H, C57BL/6, FVB and ICR) and three other strains of L. monocytogenes (HPB 3 [serotype 4b], HPB 410 [serotype 1/2a] and HPB 503 [serotype 1/2b]). After inoculation with ATCC19113 the numbers of bacteria found in the stomach wall were greater in C57BL/6 and ICR mice than in C3H and FVB mice; moreover, the gastritis produced in BALB/c and C57BL/6 mice was more severe than that produced in the other mouse strains. The gastritis produced in BALB/c mice with L. monocytogenes HPB 3, HPB 410 and HPB 503 was much more severe than that produced by ATCC19113. The inflammatory response occurred in the lamina muscularis and mucosa of the fundus. Massive necrosis of the gastric epithelium was observed, and there was oedema in a large part of the mucosal layer of the fundus. In addition, the submucosal layer was apparently expanded due to oedema, and in the cardia, the mucosal layer had become thin and flattened. Immunohistochemically, a polyclonal antibody against Listeria spp. produced labelling in areas of the gastric mucosa in which there was an inflammatory response and gastric epithelial necrosis.     

PGⅠ、PGⅡ、G 17和Hp IgG抗体筛查慢性萎缩性胃炎和胃癌的价值

分析胃蛋白酶Ⅰ（PGⅠ）、胃蛋白酶Ⅱ（PGⅡ）、胃泌素 17（G 17）和幽门螺杆菌（Hp IgG）抗体筛查对慢性萎缩性胃炎和胃癌的诊断价值。方法：以2014年5月至2015年5月胃部不适来我院就诊的90例患者为研究对象,根据病理诊断结果分为正常对照组（包括慢性非萎缩性胃炎）、慢性萎缩性胃炎组和胃癌组,每组各30例,比较三组患者PGⅠ、PGⅡ、G 17水平及Hp IgG抗体阳性检出率。结果：胃癌组患者的PGⅠ、PGⅡ水平低于对照组和慢性萎缩性胃炎组,且慢性萎缩性胃炎组患者上述指标低于对照组;胃癌组G 17水平高于慢性萎缩性胃炎组和对照组,而慢性萎缩性胃炎组和对照组无明显差异;三组间Hp IgG抗体阳性率有明显差别,胃癌组显著高于对照组和慢性萎缩性胃炎组;Hp感染患者的PGⅠ和PGⅡ水平低于未感染Hp者,而G 17水平高于未感染Hp者;胃癌患者的PGⅠ、PGⅡ水平与年龄、病理分期和转移显著负相关,与分化程度显著正相关,而G 17水平及Hp IgG抗体阳性率与年龄、病理分期和转移显著正相关,而与分化程度显著负相关。结论： PGⅠ、PGⅡ和Hp IgG抗体筛查对慢性萎缩性胃炎和胃癌均有很好的诊断价值,而对胃癌的诊断价值更好,G17对胃癌的诊断价值远远好于慢性萎缩性胃炎;且PGⅠ、PGⅡ、G17水平及Hp IgG抗体阳性检出率与胃癌患者的临床病理特征密切相关。     

口服幽门螺杆菌苗免疫小鼠后胃粘膜的免疫应答

目的 观测Hp全菌抗原和粘膜佐剂LT口服免疫Balb/c小鼠后的胃肠粘膜免疫反应。方法 采用ELISPOT法检测了胃粘膜、肠粘膜相关淋巴组织PP结抗原特异性形成细胞（AFC）。结果 抗原免疫组、抗原 佐剂组胃肠粘膜抗原特异性sIgA-AFC、IgG-AFC数量明显增加,尤以sIgA-AFC为甚。并且抗原 佐剂组明显高于单纯抗原组和对照组。结论 口服菌苗可有效诱导胃肠道粘膜免疫应答。局部sIgA可能在抗Hp感染中具有重要作用。     

慢性乙型肝炎患者胃粘膜HBV-DNA检测及临床意义

目的:检测慢性乙型肝炎(乙肝)患者乙肝病毒脱氧核糖核酸(HBV-DNA),探讨HBV与胃粘膜病变的关系。方法:选择慢性乙肝并伴有慢性胃炎的患者58例(H组)及慢性胃炎但其血清HBV标志物(HBVM)和HBV-DNA均阴性对照组52名(C组),两组均进行胃镜检查,同时取胃粘膜,H组取空腹静脉血液,采用荧光定量聚合酶链反应(FQ-PCR)方法进行血清、胃粘膜HBV-DNA含量和血清HBVM检测。结果:H组血清和胃粘膜HBV-DNA阳性例数分别为38例(65.52%)和46例(79.31%),两者相比有显著性差异(χ2=6.125,P<0.05);两者HBV-DNA含量显著正相关。H组32例血清HBeAg阳性患者的血清和胃粘膜HBV-DNA均为阳性,而26例血清HBeAg阴性患者的血清和胃粘膜HBV-DNA阳性只有6例(23.1%)和14例(53.8%)。C组胃粘膜HBV-DNA全部阴性。胃镜下观察H组患者广泛存在胃窦炎,C组以慢性浅表性胃炎为主。结论:HBV存在于胃粘膜中,可能引起胃部的炎性损伤。     

Gastric lesions and immune responses caused by long-term infection with Helicobacter heilmannii in C57BL/6 mice

Helicobacter heilmannii is a gastric micro-organism that can induce gastritis and B-cell MALT (mucosa-associated lymphoid tissue) lymphoma in mice, in a host-dependent manner. The present study was designed to examine gastric lesions and immune responses caused by intragastric H. heilmannii infection of an inbred mouse strain, C57BL/6. Long-term infection led to the formation of gastric nodules and increased mucosal thickness of the stomach, due to gastric epithelial proliferation. Infection also induced the formation of lymphoid follicles in the corpus mucosa and submucosa. The follicular cells were mainly CD45R+ cells that did not produce immunoglobulin. However, scattered in the lamina propria and corpus submucosa, numerous IgA+ cells were found in infected mice, but not in control mice. RT-PCR results showed that H. heilmannii infection led to increased mRNA expression for IFN-gamma (a Th1 cytokine) and IL-10 (a Th2 cytokine) in the mouse stomach, suggesting that both Th1 and Th2 responses are associated with H. heilmannii infection. The mRNA of other cytokines and chemokines (IL-1beta, IL-12p40, TNF-alpha, MCP-1, KC and MIP-2) was also increased by infection.     

Why is the hyperplastic polyp a marker for the precancerous condition of the gastric mucosa?

It is well known from the older literature that gastric carcinomas are more likely to develop in a stomach containing hyperplastic polyps. The reason why such a stomach should represent a precancerous condition is, however, largely unexplained. The aim of this study was to determine the disorders of the gastric mucosa in which hyperplastic polyps occur. In 244 patients with hyperplastic polyp, in whom at least two additional biopsies each from the antrum and corpus were available, gastritis was classified on the basis of the updated Sydney System. In none of the 244 patients was the gastric mucosa found to be normal. The most common disorder, at 51.3%, was autoimmune gastritis of the corpus mucosa, while chronic active Helicobacter pylori (Hp) gastritis was seen in 37.3% of the patients. Of the patients with Hp gastritis, 56.1% had corpus-dominant Hp gastritis. Other forms were relatively rare: when A-gastritis, corpus-dominant Hp gastritis and any other form of Hp gastritis were lumped together as a precancerous condition, these changes were found in 88.6% of the patients with hyperplastic polyps of the stomach. In the presence of hyperplastic polyps of the gastric mucosa, additional biopsies obtained from the antrum and corpus should always be performed to obtain a basis for deciding whether to apply Hp eradication treatment as potential carcinoma prophylaxis.     

Effects of Helicobacter pylori infection on gastric inflammation and local cytokine production in histamine-deficient (histidine decarboxylase knock-out) mice

Helicobacter pylori infection in humans causes gastritis. The infection elicits a complex immune response in which the activation of mast cells and histamine release is of particular importance. Histamine further promotes the immune response and stimulates gastric acid secretion. The inflammatory effects of H. pylori can be studied in intragastrically infected mice. The aim of this study was to compare the local cytokine responses of histamine-deficient, histidine decarboxylase knock-out (HDC KO) and wild-type (WT) mice following H. pylori infection. Methods: H. pylori was administered intragastrically to HDC KO and WT mice. The animals were infected three times in a 1-week-period and were sacrificed 8 weeks after the first intervention. The local TNF-alpha, IL-6 and IL-10 cytokine levels in gastric mucosal specimens were determined by ELISA. Gastric mucosa sections were also analysed for histological signs of inflammation. To investigate the antibody response following H. pylori infection, the total anti-H. pylori IgG and the ratio of IgG1/IgG2a isotypes were determined in the serum by ELISA. Results: H. pylori induced considerable cytokine production in the infected groups. The TNF-alpha and IL-6 levels were significantly higher in the WT mice than in the HDC KO mice, whereas the IL-10 levels did not differ between the groups. Anti-H. pylori IgG was detected only in the infected groups and the titre was higher in the WT mice. A higher IgG1/IgG2a ratio was observed in the H. pylori infected HDC KO group. Histological analysis revealed that the grades of inflammation were less severe in the infected HDC KO animals. Conclusions: The results suggest that H. pylori induces lower TNF-alpha and IL-6 secretion in the gastric mucosa in the HDC KO mice than in the WT animals, while the levels of induction of IL-10 were similar. The imbalance between Th1/Th2 is less pronounced in the HDC KO mice, which might explain the milder inflammation in the gastric mucosa. These results provide further information on the role of histamine in the pathomechanism of H. pylori-induced gastritis.     

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis

BACKGROUND: Gastrin G cells and somatostatin D cells are important regulators of gastric acid secretion and alterations in their relative numbers may play a key role in gastroduodenal disease. AIM: To investigate the effect of Helicobacter pylori infection on the density of immunoreactive G and D cells in gastric antral and corpus biopsies from patients with dyspeptic complaints. METHODS: One hundred and twenty two patients with dyspeptic complaints had two antrum and two corpus biopsies taken during upper endoscopy. The severity of inflammation and the density of H pylori were evaluated semiquantitatively. In addition, the density and distribution of neuroendocrine cells, especially G and D cells, were examined using immunohistochemistry. Patients were divided into three groups, those with H pylori positive gastritis, H pylori negative gastritis, and histologically normal gastric mucosa. RESULTS: The number of immunoreactive G cells was significantly higher and the number of immunoreactive D cells lower in patients with H pylori positive gastritis compared with H pylori negative gastritis or histological normal gastric mucosa. The percentage of G cells as a percentage of mucosal endocrine cells was also raised and that of D cells was decreased. CONCLUSIONS: Helicobacter pylori infection produces alterations in the number of endocrine cells responsible for regulating acid secretion in relation to intragastric pH and feeding. The alterations correlate best with the severity of inflammation and not with H pylori density.     

Local and systemic immune responses in murine Helicobacter felis active chronic gastritis.

Helicobacter felis inoculated per os into germfree mice and their conventional non-germfree counterparts caused a persistent chronic gastritis of approximately 1 year in duration. Mononuclear leukocytes were the predominant inflammatory cell throughout the study, although polymorphonuclear cell infiltrates were detected as well. Immunohistochemical analyses of gastric mucosa from H. felis-infected mice revealed the presence of mucosal B220+ cells coalescing into lymphoid follicles surrounded by aggregates of Thy-1.2+ T cells; CD4+, CD5+, and alpha beta T cells predominated in organized gastric mucosal and submucosal lymphoid tissue, and CD11b+ cells occurred frequently in the mucosa. Follicular B cells comprised immunoglobulin M+ (IgM+) and IgA+ cells. Numerous IgA-producing B cells were present in the gastric glands, the lamina propria, and gastric epithelium. Infected animals developed anti-H. felis serum IgM antibody responses up to 8 weeks postinfection and significant levels of IgG anti-H. felis antibody in serum, which remained elevated throughout the 50-week course of the study.     

Oral Immunization with Recombinant Lactobacillus acidophilus Expressing the Adhesin Hp0410 of Helicobacter pylori Induces Mucosal and Systemic Immune Responses

Helicobacter pylori infection is relatively common worldwide and is closely related to gastric mucosa-associated lymphoid tissue (MALT) lymphoma, chronic gastritis, and stomach ulcers. Therefore, a safe and effective method for preventing H. pylori infection is urgently needed. Given that developing an effective vaccine against H. pylori is one of the best alternatives, H. pylori adhesin Hp0410 was expressed in the food-grade bacterium Lactobacillus acidophilus. The recombinant live bacterial vaccine was then used to orally vaccinate mice, and the immunoprotective effects of Hp0410-producing strains were investigated. H. pylori colonization in the stomach of mice immunized with the recombinant L. acidophilus was significantly reduced, in comparison with that in control groups. Furthermore, mucosal secretory IgA antibodies were elicited in the mucosal tissue of mice immunized with the recombinant bacteria, and specific anti-Hp0410 IgG responses were also detected in mouse serum. There was a significant increase in the level of protection against gastric Helicobacter infection following a challenge with H. pylori Sydney strain 1 (SS1). Our results collectively indicate that adhesin Hp0410 is a promising candidate vaccine antigen, and recombinant L. acidophilus expressing Hp0410 is likely to constitute an effective, low-cost, live bacterial vaccine against H. pylori.