口服幽门螺杆菌疫苗后小鼠粘膜免疫应答研究

为观测幽门螺杆菌 (Hp )全菌抗原和粘膜佐剂LT口服免疫Balb/c小鼠后的粘膜免疫应答 ,采用ELISPOT和ELISA法分析免疫小鼠胃粘膜、派伊尔小结 (PP )抗原特异性抗体分泌细胞和小肠粘液唾液sIgA抗体。结果表明抗原免疫组、抗原 +佐剂组胃粘膜、PP抗原特异性sIgA ASC、IgG ASC数量明显增加 ,尤以sIgA ASC为甚 ,并且抗原 +佐剂组明显高于单纯抗原组和对照组 ;小肠粘液唾液特异sIgA水平两免疫组均明显高于对照组 ,提示口服免疫可有效诱导粘膜免疫应答 ,局部特异sIgA在抗Hp感染中具有重要作用     

以壳聚糖为佐剂的Hp疫苗诱导的体液免疫应答及其免疫保护效应

目的：探讨以壳聚糖为佐剂的Hp疫苗的免疫保护作用及其机制。方法:BALB/c小鼠随机分为9组：①空白对照组：PBS溶液；②壳聚糖酸溶液组；③壳聚糖颗粒组；④Hp抗原组；⑤Hp抗原+壳聚糖酸溶液组；⑥Hp抗原+壳聚糖颗粒组；⑦Hp抗原+CT组；⑧Hp抗原+壳聚糖酸溶液+CT组；⑨Hp抗原+壳聚糖颗粒+CT组，各组于第0、7、14、21 d 灌胃各免疫1次，免疫后4周给予1×1012CFU/L的SS1 Hp菌液每只 0.5 mL进行攻击，隔日1次，共2次。4周后，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法检测血清抗Hp IgG、IgG1、IgG2a及唾液和胃黏膜内抗Hp IgA，用SP免疫组织化学法检测胃黏膜内分泌型IgA（sIgA）。结果:①以壳聚糖为佐剂的Hp疫苗的免疫保护率达60%，与以CT为佐剂的Hp疫苗的免疫保护率（58.33%）相似，显著高于单纯Hp抗原组及其它不含Hp抗原组（P<0.01或P<0.05），同时以CT＋壳聚糖为佐剂的Hp疫苗的保护率为84.62%、85.71%，其Hp的定植评分显著低于无佐剂组及以CT为佐剂组（P<0.01，P<0.05）。②含佐剂的Hp疫苗所诱导产生的Hp IgG水平显著高于对照组及无佐剂组（P<0.01，P<0.05），而以CT＋壳聚糖为佐剂组所产生的抗Hp IgG水平显著高于仅以 CT或壳聚糖为佐剂组（P<0.05）。③胃黏膜内sIgA及特异性抗Hp IgA水平在壳聚糖为佐剂组与以CT为佐剂组无差别（P>0.05），显著高于无佐剂组，而壳聚糖与CT联合应用组显著高于单以CT为佐剂组（P<0.01，P<0.05）。结论:以壳聚糖为佐剂的Hp疫苗对Hp感染具有免疫保护作用，并可成功诱导黏膜局部的特异性体液免疫应答，从而发挥免疫防御作用。     

幽门螺杆菌全菌抗原口服免疫BLAB／c小鼠的免疫应答机理研究

目的 分析幽门螺杆菌全菌抗原的口服免疫应答反应。方法 ELISA分析免疫小鼠血清、唾液、粪便提取物特异抗体水平,ELISPOT分析胃粘膜、派伊尔小结（PP）抗原行异性抗体分泌细胞（ASC）,RT－PCR分析PP T细胞因子mRNA表达水平。结果 ①口服免疫可诱导强烈的血清IgG反应和唾液、粪便提取物特sIgA反应;②胃粘膜、PP结产生大量抗原特异性抗体分泌细胞（ASC）,尤以sIgA-ASC型居多,PP结抗原特异性形成细胞（ASC）数量与特异抗体水平密切相关;③加佐剂免疫组小鼠PP T细胞,体外抗原刺激下,早期高表达IFN－γ晚期高表达IL－4。结论 全菌抗原和粘膜佐剂免疫可诱导H.pylori特异的系统、粘膜免疫应答,局部sIgA可能在抗H.pylori感染中具有重要作用,肠粘膜免疫主要诱导部位PP早期表现为TH1型优势应答,晚期则转为TH2型优势应答。     

人源轮状病毒转基因马铃薯口服免疫小鼠的免疫应答研究

目的分析人源轮状病毒转基因植物抗原的口服免疫应答反应。方法在根癌脓杆菌介导获得系列转基因马铃薯植株的基础上，用ELISA分析转基因马铃薯中目的蛋白表达水平。马铃薯块茎直接口服免疫Balb／c小鼠，ELISA分析免疫小鼠血清、唾液、粪便提取物特异抗体水平。结果获得一株最高表达量的转化株；口服免疫可诱导较强的血清IgG反应和强烈的黏膜sIgA反应，粪便的sIgA最高，唾液次之，尿液中无sIgA；加霍乱毒素B亚单位（CTB）佐剂免疫组小鼠和霍乱毒素（CT）佐剂免疫组小鼠抗体水平无显著差异，无佐剂免疫组小鼠抗体水平略低。结论人源轮状病毒转基因植物疫苗联合黏膜佐剂免疫动物可诱导特异的系统与黏膜免疫应答，且黏膜免疫强度略高于系统免疫。     

口服免疫机制及口服疫苗的研究进展

口服免疫可诱导机体产生有效的免疫应答和免疫耐受。其通过胃肠粘膜进行抗原递呈 ,较经传统注射途径的免疫效果和依从性好 ,且简易便捷 ,是更为理想的免疫途径。口服疫苗有多种载体系统 ,某些经改造的细菌如沙门氏菌、大肠杆菌、特别是乳酸菌属被认为是有前景的口服疫苗载体 ,因口服后可在肠道寄生繁殖 ,故可大大提高免疫的效率。本文围绕口服免疫主要的机制和口服疫苗的研究进展进行综述。     

以壳聚糖为佐剂的幽门螺杆菌疫苗诱导的细胞免疫反应

目的:探讨以壳聚糖为佐剂的幽门螺杆菌(Hp)疫苗诱导的细胞免疫反应及其在免疫保护中的作用。方法:BALB/c小鼠随机分为空白对照组(PBS溶液)、壳聚糖酸溶液组、壳聚糖颗粒组、Hp抗原组、Hp抗原 壳聚糖酸溶液组、Hp抗原 壳聚糖颗粒组、Hp抗原 霍乱霉素(CT)组、Hp抗原 壳聚糖酸溶液 CT组及Hp抗原 壳聚糖颗粒 CT组,各组于第0、7、14、21天灌胃各免疫1次,末次免疫后4周给予1×1012CFU/L的SS1Hp菌液0·5mL/只进行攻击,隔日1次,共2次。在攻击前后分批处死小鼠,采用Hp培养和病理改良Giemsa染色法检测胃黏膜内Hp感染。用定量ELISA法检测胃黏膜内IL-2、IL-4和IL-10含量;HE染色进行胃黏膜病理学检测。结果:①以壳聚糖为佐剂的Hp疫苗的免疫保护率达60%,与以CT为佐剂的Hp疫苗的免疫保护率(58·33%)相似,显著高于单纯Hp抗原组及其他不含Hp抗原组(P<0·05)。②胃黏膜内IL-2的水平攻击后含佐剂组显著高于对照组(P<0·05)。IL-10水平攻击前以壳聚糖为佐剂组高于无佐剂组,攻击后以CT 壳聚糖颗粒为佐剂组高于其他组(P<0·05)。IL-4水平攻击前以壳聚糖为佐剂组高于无佐剂组(P<0·05),攻击后以壳聚糖颗粒为佐剂组高于以CT为佐剂组(P<0·05),以壳聚糖溶液为佐剂组高于对照组、无佐剂组及佐剂中含CT组(P<0·05)。③胃黏膜炎症程度在单纯壳聚糖组和以壳聚糖颗粒为佐剂组显著低于以CT为佐剂组(P<0·05)。结论:①以壳聚糖为佐剂的Hp疫苗对Hp感染具有免疫保护作用。②以壳聚糖为佐剂的Hp疫苗可促进Th1和Th2的混合免疫反应,并逆转Hp感染所致Th2反应的抑制,使Th1和Th2反应达到平衡,从而发挥其免疫保护作用。③以壳聚糖为佐剂的Hp疫苗所致的免疫后胃炎显著低于以CT为佐剂的Hp疫苗。     

Th免疫反应在以壳聚糖为佐剂的幽门螺杆菌疫苗免疫保护中的作用

目的：探讨以壳聚糖为佐剂的脚疫苗的免疫保护作用及其机理。方法：BALB／c小鼠随机分为7组：空白对照组、壳聚糖酸溶液组、壳聚糖颗粒组、却抗原组、脚抗原＋壳聚糖酸溶液组、却抗原＋壳聚糖颗粒组和脚抗原＋CT组，各组于第0、7、14和21天灌胃各免疫1次，末次免疫后4周给予SS1Hp菌攻击，隔日1次，共2次。在攻击前后分批处死小鼠，取胃黏膜检测坳和Th1、Th2细胞因子含量，同时检测血清中抗Hp IgG2a和IgG1含量。结果：①以壳聚糖为佐剂的坳疫苗的免疫保护率达60％，与以CT为佐剂的印疫苗的免疫保护率（58．33％）相似，显著高于单纯脚抗原组及其他不含Hp抗原组（P〈0．001～0．05）。②却攻击后胃黏膜内IFN-γ、IL-2和IL-12含量在含佐剂组显著高于无抗原和无佐剂组（P〈0．001～0．05）；③坳攻击后胃黏膜内IL-4含量在以壳聚糖颗粒为佐剂组显著高于以CT为佐剂组（P〈0．05），以壳聚糖溶液为佐剂组显著高于对照组、无佐剂组及佐剂中含CT组（P〈0．001～0．05）。结论：以壳聚糖为佐剂的坳疫苗对脚感染具有免疫保护作用，同时可促进Th1和Th2的混合免疫反应。     

以壳聚糖为佐剂的幽门螺杆菌蛋白抗原对幽门螺杆菌感染的免疫保护作用

目的探讨以壳聚糖为佐剂的幽门螺杆菌（脚）抗原对脚感染的免疫保护作用。方法BALB／c小鼠随机分为9组：（1）空白对照组：PBS溶液；（2）壳聚糖酸溶液组；（3）壳聚糖颗粒组；（4）印抗原组；（5）np抗原＋壳聚糖酸溶液组；（6）Hp抗原＋壳聚糖颗粒组；（7）Hp抗原＋CT组；（8）脚抗原＋壳聚糖酸溶液＋CT组；（9）Hp抗原＋壳聚糖颗粒＋CT组。各组于第0、7、14、21天灌胃各免疫1次，免疫后4周给予109CFUIml的SSlnp菌液0．5ml／只进行攻击，隔日1次，共2次。4周后，采用定量砌培养和病理改良Giemsa染色法检测胃黏膜内伽感染情况。结果（1）以壳聚糖为佐剂的印抗原的免疫保护率达60％，与以凹为佐剂的伽抗原的免疫保护率（58．33％）相似，显著高于单纯印抗原组及其他不含印抗原组（P〈0．05），同时以凹＋壳聚糖为佐剂的坳疫苗的保护率为84．62％、85．71％，高于CT或壳聚糖单独作佐剂组。（2）病理组织学检测含佐剂组的铷定植计分显著低于无佐剂组和无抗原组（P〈0．05），壳聚糖和CT联合应用组的跏定植计分最低，显著低于单以CT为佐剂组（P〈0．05）。（3）砌定量培养脚定植密度在佐剂中含壳聚糖组均显著低于对照组和单纯脚抗原组（P〈0．05），而单以CT为佐剂组脚定植密度与对照组和单纯坳抗原组差异无统计学意义（P〉0．05）。结论以壳聚糖为佐剂的坳抗原对Hp感染具有免疫保护作用，并且与CT有协同作用。     

免疫途径及侵袭蛋白表达对痢疾疫苗免疫效果影响的实验研究

目的探讨免疫途径及侵袭蛋白表达对2株痢疾疫苗免疫效果的影响.方法FSM-2117或FS-5416以4×107CFU/只分别经滴鼻、灌胃、肠内注射3种途径免疫小鼠,三免后7?d收集血清、小肠、鼻咽、肺、阴道冲洗液,ELISA法检测其中特异性福氏、宋内LPSIgA和IgG抗体(Ab)水平.结果滴鼻和肠内免疫都能够诱生血清中双价IgA、IgGAb显著升高,但仅滴鼻免疫组Ipa+株较Ipa-株升高显著(P＜0.01).滴鼻免疫组同时诱生鼻咽、肺、小肠内特异性抗体升高,尤其是生殖道冲洗液内抗体升高极为明显;而肠内免疫组诱生小肠、肺冲洗液内特异性抗体升高,但鼻咽及生殖道冲洗液内抗体未见明显升高.结论鼻粘膜免疫不仅诱导多个粘膜部位(特别是生殖道)的抗体反应,且能诱导系统免疫反应.是一个安全有效的免疫途径.研究中发现侵袭蛋白表达在鼻粘膜部位能够显著加强系统特异性抗体生成,但在胃肠粘膜却无此作用.     

Balb/c小鼠口服幽门螺杆菌疫苗rLTB-HspA的免疫应答

目的　研究幽门螺杆菌 (Hp)热休克蛋白A (rHspA)与大肠杆菌不耐热肠毒素B亚单位 (LTB)融合蛋白 (rLTB HspA)作为口服疫苗的免疫应答效果。方法　采用rLTB HspA口服免疫Balb c小鼠 ,ELISA分析小鼠血清、胃肠黏液中IgG、IgA抗体水平 ,体外培养脾淋巴细胞在Hp刺激下的增殖情况及IL 4、IFN γ的变化。结果　Balb c小鼠口服rLTB HspA能有效激发机体产生全身和局部特异性的体液免疫应答和细胞免疫应答。结论　Balb crLTB HspA可作为预防和治疗Hp感染的候选疫苗之一     

Detection of intestinal intraepithelial lymphocytes,goblet cells and secretory IgA in the intestinal mucosa during Newcastle disease virus infection

Newcastle disease, which is caused by Newcastle disease virus (NDV), is a highly contagious viral disease of poultry and other bird species. The mucosa is the first line of defence to invading pathogens, including NDV, and it has been confirmed that the mucosa can contribute to host protection. This study was conducted to evaluate the intestinal mucosal immunology in NDV infection. Forty specific-pathogen-free chickens were divided into two groups, 20 birds in each group. Group 1 was inoculated with NDV by the intravenous route. Group 2 was used as the control group and was given sterile phosphate-buffered saline by the same route. At 24, 48, 72, and 96 h post infection (h.p.i.), five chickens from each treatment were killed. Samples of the duodenum, jejunum, and ileum were collected to quantify intestinal intraepithelial lymphocytes (IEL), goblet cells and secretory IgA (sIgA) by cytochemistry and immunohistochemistry analysis. The results indicated that IEL were increased from 24 to 72 h.p.i. in the infected tissues, and were significantly higher than in the control group at 48 h.p.i. (P < 0.01). In contrast to IEL, goblet cell numbers were reduced dramatically from 24 to 96 h.p.i. in the infected birds (P < 0.01) Furthermore, the content of sIgA was significantly higher at 48 and 72 h.p.i. in the infected tissues (P < 0.01). sIgA positivity was observed in the epithelial lining of the intestinal mucosa. These data suggest that IEL, goblet cells, and sIgA were involved in the intestinal mucosal immunity against NDV infection.     

Effect of dietary restriction on total and bacterium-specific mucosal secretory immunoglobulin A in bile-diverted intestinal self-filling blind loops.

The effect of starvation on the mucosal secretory immunoglobulin A (sIgA) response to bacterial antigens was studied in bile-free rat self-filling blind loops constructed at the end of a Roux-en-Y branch of jejunum. Rats were fed a 50% restricted diet for 1 to 4 weeks after surgery. sIgA was measured in the mucosa and lumen by an enzyme-linked immunosorbent assay. Dietary restriction caused a final rise of luminal sIgA which was less than 50% of that of normally fed controls Luminal bacteria counts were not different in the two groups. The percentage of total sIgA precipitated with intestinal bacteria was not significantly affected by dietary restriction, and there was no change in the specific binding of sIgA to several bacterial species. Nonprecipitated sIgA exhibited a low but significant specific binding to bacteria in both diet-restricted and fed rats. Diet restriction therefore reduced the total sIgA response to luminal bacteria, but the specific bacterial binding capacity per microgram of sIgA was not altered. In these short-term experiments diet-restricted animals appeared to be capable of secreting sIgA in excess of requirement, since the nonprecipitable luminal fraction contained free sIgA with binding capacity for bacteria. The ability of sIgA to react with specific antigens may therefore be of more significance as an indicator of bacterial susceptibility than the measurement of total sIgA.     

Immunological functions of the gut--role of the mucosal immune system

This review summarizes recent information about immune responses in the intestinal mucosa with emphasis on the role of orally-administered antigens from the external environment. The intestinal mucosa provides an extensive surface for potential absorption of pathogenic environmental antigens, such as microbes, chemicals, and food. The intestinal mucosa is densely populated by IgA-producing plasma cells. The humoral immune responses to antigens in the intestinal mucosa are largely of the IgA class in secretory form (sIgA). This sIgA provides an immunological barrier to absorption of antigens on the mucosal epithelium and to penetration into the body. The cell-mediated immune mechanism is also equipped in the mucosal sites. In addition, the mucosal immune response induces hyporesponsiveness of nonmucosal (systemic) immune reactions, and the liver is an integral part of the mucosal immune system. Thus we consider that the mucosal immune system plays a central role in the maintenance of the homeostasis of the total immune system.     

Immunohistologic study of the localization of organ-specific antigens of the stomach and intestine and carcinoembryonic antigen in normal and pathologically altered stomach tissues

Localization of organospecific gastric and intestinal antigens, as well as of carcinoembryonic antigen (CEA) was studied by an indirect immune peroxidase method on the sections of fetal stomach, normal definitive stomach, gastric mucosa with features of superficial and deep gastritis, enterolysis and dysplasia, as well as in gastric tumours. Normally, pepsinogen was found to localize in zymogen cells and to disappear in enterolysis and dysplasia of gastric mucosa. Intestinal antigen is absent from the normal mucosa, but is found in all the cases with enterolysis and dysplasia. CEA is most specific for dysplasia of gastric epithelium. In cancers of intestinal type pepsinogen was found in 54%, intestinal (colonic) antigen in 37.5%, CEA in 62.5%. In diffuse type cancers pepsinogen was absent, intestinal antigen was found in 76.9%, CEA in 92% of tumours.     

Increased apoptosis in gastric mucosa adjacent to intestinal metaplasia

BACKGROUND: The biological processes involved in the development of gastric mucosal atrophy and intestinal metaplasia are still incompletely understood. Reports testing the hypothesis that apoptosis leads to atrophy have yielded conflicting results. The availability of new antibodies for the detection of apoptotic cells in tissue sections has facilitated the analysis of the role of apoptosis in the gastritis-atrophy-intestinal metaplasia sequence. METHODS: Archival material from 40 gastric resection specimens with normal mucosa (n = 5), chronic active gastritis (n = 17), or intestinal metaplasia (n = 18) was studied. Immunohistochemistry was performed using antibodies directed against cleaved cytokeratin 18 and active caspase 3. Slides were scored on a 0-3 scale for the presence of apoptotic cells. RESULTS: Normal gastric mucosa contained low numbers of apoptotic cells at the surface epithelium (mean score, 0.20). This number was significantly increased in cases with chronic gastritis (mean score, 1.06) and in those with intestinal metaplasia (mean score, 2.56). Within the intestinal metaplasia cases, 44 different foci of intestinal metaplasia were identified. In 39 of these 44 areas, concentrations of apoptotic cells were seen immediately adjacent to the foci of intestinal metaplasia, but not in the metaplastic epithelium itself. CONCLUSIONS: Apoptosis is uncommon in normal gastric mucosa. Chronic inflammation and intestinal metaplasia are associated with increased apoptosis, but occur mainly at the mucosal surface and not in the deeper layers. These findings do not support the concept that apoptosis underlies the loss of gastric glands and leads to atrophy, but the observed concentration of apoptotic epithelial cells adjacent to foci of intestinal metaplasia could be related to heterogeneity of epithelial damage, causing apoptosis, to which intestinal metaplasia is a response.     

Differential expression of adhesion molecules and chemokines between nasal and small intestinal mucosae: implications for T- and sIgA+ B-lymphocyte recruitment

Nasal and small intestinal mucosae are the first sites of contact with infectious agents and the sites of T-cell-mediated and secreted immunoglobulin A (IgA)-mediated defences against pathogens. We investigated the factors controlling the infiltration of CD3(+) T lymphocytes and surface IgA(+) (sIgA(+)) B lymphocytes into swine epithelium and lamina propria (LP) within and between these two mucosal effector sites. Vascular addressins, vascular cell adhesion molecule 1 and mucosal addressin cell adhesion molecule-1 were reciprocally expressed in both mucosae. Strong expression of alpha(4)beta(1) relative to alpha(4)beta(7) was characteristic of CD3(+) T cells in nasal mucosa LP and epithelium and of sIgA(+) cells in nasal mucosa epithelium. The same profile was observed on corresponding blood cells. Conversely, higher levels of integrins beta(7) and alpha(4)beta(7) than alpha(4)beta(1) were characteristic of CD3(+) T cells and sIgA(+) cells in the small intestine. However, about 40% of the LP-activated sIgA(+) cells displayed sIgA(high), integrin alpha(4) and integrin alpha(4) expression. Whereas CCL19, CXCL12, CCL21 and CCL28 messenger RNAs were similarly expressed in both mucosae, CCL25 messenger RNA was only expressed in the small intestine. Thus, the nasal and small intestine mucosae represent separate compartments for infiltration by CD3(+) T cells and sIgA(+) effector cells, with the exception of a population of small intestine activated sIgA(+) cells, which may gain access to both mucosae.     

Immunohistochemical study of neuroendocrine cells at the gastric cardia mucosa

BACKGROUND/AIMS: The gastric cardia mucosa is a narrow band of tissue between the oesophagus and the stomach. The physiological role of this tissue is unknown. This study examined the presence and characteristics of neuroendocrine cells at this site. METHODS: Biopsy samples were obtained from across normal appearing squamocolumnar junctions. The cardiac mucosa was defined as the presence of special type mucosa composed of mucous secreting glands in the immediate vicinity of oesophageal squamous epithelium. Biopsy specimens were stained with haematoxylin and eosin, alcian blue (pH 2.5) periodic acid Schiff, and modified Giemsa. The chromogranin A and Fontana-Masson stains were used to identify neuroendocrine cells, which were also stained immunohistochemically for gastrin, serotonin, glucagon, pancreatic polypeptide, somatostatin, and vasoactive intestinal peptide. RESULTS: Chromogranin positive cells were seen in 18 cases with adequate biopsy specimens from the gastric cardia mucosa. These cells were all serotonin positive, but stains for other peptide hormones remained negative. Serotonin positive cells were detected only at the base of foveolae at the periphery of mucous secreting cardiac glands, giving a microscopic appearance resembling that of endocrine cells at the gastric antrum. The presence and numbers of serotonin positive cells did not correlate with chronic inflammation or intestinal metaplasia of the cardiac mucosa. These cells were seen both in Helicobacter pylori positive and negative patients. CONCLUSIONS: Serotonin positive cells appear to be the sole neuroendocrine cell type at the gastric cardia mucosa. These cells may have a role in regulating the physiology of the gastric cardia mucosa and the lower oesophageal sphincter.     

人粘蛋白糖链单抗的制备及在胃化生粘膜和胃肿瘤中的应用

制备抗胃肠道粘蛋白糖链单抗,并研究其抗原在小胃粘膜、化生粘膜及肿瘤中的表达,方法：将肠道粘膜冻干粉碎,ＣｓＣｌ平均密度离心法提取人胃肠粘蛋白,免疫ＢＡＬＢ／ｃ小鼠,取鼠脾细胞与ＳＰ２／Ｏ－Ａｇ１４鼠的骨髓瘤细胞融合成杂交瘤,克隆制备单克隆抗体,并应用ＬＳＡＢ法检测其抗原在胃粘膜,化生取粘膜和肿瘤中的表达。结果制备抗人胃粘蛋白单抗（ＨＧＭ７２,７５）和抗人肠粘蛋白单抗（ＨＣＭ１４,２１）均为抗粘蛋白     

Cancerous and non-neoplastic stem cells in the stomach similarly express CD44 and CD133

CD44 and CD133 have been considered as cancer stem cell (CSC) markers. Stem cell markers are rarely described in healthy stomach tissues. However, the clinicopathological and prognostic value of CD44 and CD133 in gastric cancer remains controversial. This study investigated the expression of CD44 and CD133 in gastric cancer and non-neoplastic gastric mucosa. We used samples of primary gastric adenocarcinomas (n = 69), metastatic lymph nodes (n = 30), intestinal metaplasia (n = 17), and histologically normal gastric tissues of surgical margins (n = 54). The expression of CD44 and CD133 were studied in samples by immunohistochemistry. Fisher’s exact test and a logistic regression model were used in this study. CD44 expression was observed in 12% of samples with intestinal metaplasia, 20% with lymph node metastases, 22% with normal mucosa, to 30% of samples with primary tumors. Most of these positive tumors showed immunostaining in less than 4% of cancerous cells, mainly in the diffuse type. CD133 expression was observed in 7% (intestinal metaplasia) to 46% (normal mucosa). In the positive cases of cancer (24%), in most of them, less than 3% of cells were marked. CD44 and CD133 expression in the histologically normal gastric mucosa was restricted to the deeper regions of the gastric crypts at the level where stem cells and progenitor cells are usually found. CD44 and CD133 expression occurs in few gastric cancer cells, mainly in diffuse carcinomas, and are expressed in histologically normal gastric mucosae. None of the markers are specific for cancer and are also present in intestinal metaplasia and the normal mucosa.