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.     

慢性萎缩性胃炎患者Hp 感染与TGF-β、IL-6 和TNF-αRII 的表达研究

目的:探讨慢性萎缩性胃炎患者幽门螺旋杆菌感染与胃黏膜中转化生长因子茁受体域、白介素6 和肿瘤坏死因子琢的表达情况。方法:选取76例慢性萎缩性胃炎(CAG)患者胃黏膜病变组织的胃镜活检标本,采取PCR 荧光法检测Hp 感染情况,免疫组化法检测TGF-βRⅡ、IL-6 和TNF-α在胃小凹上皮和间质炎细胞中的表达。结果:慢性炎症程度在Hp感染阳性组和阴性组中差异有统计学意义(P<0.05);间质炎细胞中IL-6的表达在Hp感染阳性组和阴性组中差异有统计学意义(P<0.05);TGF-βRⅡ、TNF-α的表达在Hp感染阳性组和阴性组中无显著性差异(P>0.05);间质炎细胞中IL-6与慢性炎症程度呈正相关关系(r=0.249,P=0.03);萎缩程度与肠上皮化生严重程度、上皮内瘤变程度呈正相关关系(r=0.697,0.366)。结论:IL-6在间质炎性细胞中的表达与Hp相关性CAG患者的慢性炎症程度有关,慢性萎缩程度促进肠上皮化生和上皮内瘤变的发生。     

慢性萎缩性胃炎患者Hp感染与TGF-βRⅡ、IL-6和TNF-α的表达研究

目的:探讨慢性萎缩性胃炎患者幽门螺旋杆菌感染与胃黏膜中转化生长因子β受体Ⅱ、白介素6和肿瘤坏死因子α的表达情况。方法:选取76例慢性萎缩性胃炎(CAG)患者胃黏膜病变组织的胃镜活检标本,采取PCR荧光法检测Hp感染情况,免疫组化法检测TGF-βRⅡ、IL-6和TNF-α在胃小凹上皮和间质炎细胞中的表达。结果:慢性炎症程度在Hp感染阳性组和阴性组中差异有统计学意义(P0.05);间质炎细胞中IL-6的表达在Hp感染阳性组和阴性组中差异有统计学意义(P0.05);TGF-βRⅡ、TNF-α的表达在Hp感染阳性组和阴性组中无显著性差异(P0.05);间质炎细胞中IL-6与慢性炎症程度呈正相关关系(r=0.249,P=0.03);萎缩程度与肠上皮化生严重程度、上皮内瘤变程度呈正相关关系(r=0.697,0.366)。结论:IL-6在间质炎性细胞中的表达与Hp相关性CAG患者的慢性炎症程度有关,慢性萎缩程度促进肠上皮化生和上皮内瘤变的发生。     

主要组织相容性复合体在人乳腺癌组织的表达

目的通过观察主要组织相容性复合体(MHC)在乳腺癌组织的表达,探讨MHC与乳腺癌发生发展的关系,为临床进行乳腺癌的生物治疗提供实验依据。方法收集手术切除的人乳腺癌组织和癌旁相对正常乳腺组织,用免疫组织化学方法和图像分析技术,观察人白细胞抗原(HLA-DR)阳性细胞、CD4+T细胞和TCD8+T细胞在不同乳腺组织中的表达。结果在乳腺癌组织中HLA-DR阳性细胞平均光密度值和面数密度明显高于正常乳腺组织(P<0.05);CD4+T和TCD8+T细胞阳性细胞面数密度与正常乳腺组织相比明显减少(P<0.05),且CD4+T细胞多分布在HLA-DR阳性细胞附近。结论人乳腺癌局部微环境中HLA-DR阳性细胞数多于正常乳腺组织,CD4+T和TCD8+T在人乳腺癌组织低于乳腺正常组织。     

HIV感染者胃黏膜炎症及细胞凋亡研究

目的 研究人类免疫缺陷病毒(HIV)感染者胃黏膜炎症及上皮细胞凋亡特点,并分析可能的相关因素.方法 对有消化道症状的30名HIV-1阳性患者和20名HIV-1阴性的普通患者进行胃镜检查,对于活检标本进行常规病理诊断、幽门螺杆菌(Hp)检测和原位细胞凋亡检测.结果 HIV感染者慢性萎缩性胃炎发病率[33.3%(10/30)]高于对照组[5%(1/20,P＜0.05)];HIV感染患者Hp检出率[23.3%(7/30)]低于对照组[55.0%(11/20,P＜0.05)];HIV感染组胃黏膜上皮细胞凋亡指数AI,[(24.83±10.296)%]高于对照组[(16.50±7.626)%,P＜0.01];HIV感染组Hp阳性患者(7例)胃黏膜上皮细胞AI[(35.71±12.724)%]高于Hp阴性患者(23例)[(21.52±6.815)%,P＜0.05)].结论 细胞凋亡可能在HIV感染者消化道疾病的发病机制中占有重要的地位,胃黏膜凋亡指数可能与局部炎症及Hp感染无关,而与HIV本身及黏膜免疫环境改变有关.     

过表达SIRT1通过上调幽门螺杆菌感染的胃癌细胞自噬通量以促进其凋亡并抑制炎症因子释放北大核心CSCD

目的:探究沉默信息调节因子1(SIRT1)在幽门螺杆菌(Hp)阳性胃癌(GC)中的表达及其对Hp感染的胃癌细胞自噬、炎症因子分泌和凋亡的影响。方法:选取37例Hp阴性GC患者[GC(Hp-)组]、31例Hp阳性GC患者[GC(Hp+)组]和32例癌旁正常胃黏膜组织样本(Normal组),应用免疫组化(IHC)和Western blot检测3组样本中SIRT1表达;体外培养并筛选SIRT1表达水平最高的胃癌细胞系AGS进行探究,Western blot检测Hp感染对AGS细胞中SIRT1表达的影响;慢病毒感染以过表达AGS中的SIRT1水平,RT-PCR检测感染效率;将AGS分为4组:LV-NC组、LV-SIRT1组、Hp+LV-NC组和Hp+LV-SIRT1组,Western blot检测各组胃癌细胞中SIRT1和自噬标志蛋白LC3Ⅱ/LC3Ⅰ及SQSTM1/p62蛋白水平;转染mRFP-EGFP-LC3B串联质粒,免疫荧光观察各组胃癌细胞中自噬通量变化;ELISA检测各组胃癌细胞上清液中炎症因子TNF-α、IL-1β和IL-8表达水平;Annexin V-FITC/PI染色结合流式细胞术检测各组胃癌细胞凋亡情况;Western blot检测各组胃癌细胞中凋亡相关蛋白Bcl-2、Bad及cleaved caspase-9与cleaved-caspase-3表达。结果:与Normal组或GC(Hp-)组相比,SIRT1在GC(Hp+)组中表达显著降低(P<0.05);Hp感染AGS细胞后,能以时间依赖性下调细胞中SIRT1表达;感染慢病毒LV-SIRT1可显著促进AGS细胞中SIRT1 mRNA水平(P<0.05);Western blot结果显示,与LV-NC组相比,LV-SIRT1组中SIRT1蛋白和LC3Ⅱ/LC3Ⅰ均明显升高、而SQSTM1/p62蛋白水平显著降低(P<0.05),Hp+LV-NC组与Hp+LV-SIRT1组中SIRT1表达显著降低,LC3Ⅱ/LC3Ⅰ及SQSTM1/p62蛋白均显著升高(P<0.05或P<0.01),而与Hp+LV-NC组相比,Hp+LV-SIRT1组除LC3Ⅱ/LC3Ⅰ无明显改变外,其他蛋白表达趋势均明显降低(P<0.05);荧光显微镜观察结果表明,Hp感染促进了胃癌细胞中自噬通量的抑制,与Hp+LV-NC组相比,Hp+LV-SIRT1组中自噬通量受损现象显著改善(P<0.05);与LV-NC组或LV-SIRT1组相比,Hp+LV-NC组和Hp+LVSIRT1组中炎症因子TNF-α、IL-1β和IL-8表达均显著增加(P<0.05);而Hp+LV-SIRT1组较Hp+LV-NC组均明显降低(P<0.05);凋亡检测结果显示与LV-NC组相比,LV-SIRT1组和Hp+LV-SIRT1组胃癌细胞凋亡率和细胞中促凋亡蛋白Bad及cleaved caspase-9与cleaved-caspase-3表达均显著升高(P<0.05),而凋亡抑制蛋白Bcl-2明显降低(P<0.05);Hp+LV-NC组凋亡率及上述蛋白表达均无明显变化(P>0.05);与Hp+LV-NC组相比,Hp+LV-SIRT1组细胞凋亡率及凋亡相关蛋白变化趋势均明显升高(P<0.05)。结论:Hp感染可显著降低胃癌组织及细胞中SIRT1表达,过表达胃癌细胞中SIRT1可通过削弱Hp诱导的自噬通量受损现象,上调细胞自噬水平,从而促进胃癌细胞凋亡,并降低炎症因子表达。     

肝癌细胞冻融抗原负载树突状细胞瘤苗的制备与活化

目的: 探讨制备肝癌树突状细胞(DCs)瘤苗和体外诱导DCs活化的优化方法。方法: 取健康人新鲜血50mL, Ficoll密度梯度离心分离外周血单个核细胞(PBMC), 制备肝癌细胞冻融抗原, 采用不同因子组合培养PBMC, 诱导和激活DCs, A组: rhGM-CSF+IL-4; B组: rhGM-CSF+IL-4+冻融抗原负载;C组:rhGM-CSF+IL-4+TNF-α; D组: rhGM-CSF+IL-4+TNF-α+冻融抗原负载。结果: 各组均诱导出DCs, 并高表达CD11c和CD54, 冻融抗原可明显上调CD86、CD80、HLA-DR表达和IL-12 p40分泌(P<0.01), TNF-α促进CD86表达的作用更显著, 但对IL-12分泌无影响, 依次用TNF-α诱导和冻融抗原负载可进一步促进CD86表达和IL12 p40分泌(P<0.05)。CD54和HLA-DR双标记免疫细胞化学染色显示, 各组DCs大多为CD54⁺。表达HLA-DR的DCs均为CD54⁺HLA-DR⁺, 其中, A组CD54⁺HLA-DR⁺细胞数量最少, D组最多, 平均每个细胞HLA-DR的表达水平也与此对应。结论: 采用rhGM-CSF、IL-4诱导的未成熟DCs, 依次使用TNF-α刺激与肝癌细胞冻融抗原修饰可有效促进DCs的活化与成熟。     

冬虫夏草对慢性阻塞性肺疾病大鼠树突状细胞功能的影响

目的: 研究冬虫夏草对慢性阻塞性肺疾病(COPD)大鼠树突状细胞(DCs)功能的影响及其分子机制。方法: 将大鼠随机分为COPD模型组、冬虫夏草治疗组和正常对照组,观察各组大鼠气道病理改变,分离培养鼠DCs,ELISA法检测DCs培养上清液和DCs-T细胞共培养上清液中细胞因子含量。结果: 与正常对照组相比,COPD模型组和冬虫夏草治疗组的平均肺泡计数减少(P＜0.05),冬虫夏草治疗组高于COPD模型组,但差异无统计学意义(P>0.05)。冬虫夏草治疗组DCs-T细胞共培养后上清液中IFN-γ水平高于COPD模型组和正常对照组(P<0.05),IL-5水平各组无显著差异(P>0.05)。冬虫夏草治疗组DCs上清液中TNF-α和IL-12 p70水平高于COPD模型组和正常对照组(P<0.05)。结论: 冬虫夏草可促使COPD大鼠DCs产生Th1型细胞因子,机制可能与DCs产生的IL-12 p70促进T细胞产生IFN-γ有关。     

肾癌细胞冻融抗原负载树突状细胞瘤苗的活化

目的: 探索体外诱导DCs活化的方法和制备肾癌树突状细胞(DCs)瘤苗。方法: 制备肾癌细胞冻融抗原；取健康人新鲜血分离外周血单个核细胞(PBMC),应用GM-CSF+IL-4刺激，诱导PBMC为iDCs,然后进行分组，采用不同因子刺激iDCs转化为mDCs,其中Ａ组:冻融抗原负载；Ｂ组: TNF-α+冻融抗原负载；Ｃ组: IL-1β+冻融抗原负载；Ｄ组: TNF-α+IL-1β+冻融抗原负载。 结果:各组均可诱导iDCs的成熟,并高表达CD86、CD80和HLA-DR；相对于其它组，D组DCs 更显著上调CD83和CD54表达(P<0.05)和IL-12分泌(P<0.01)，且D组mDCs更有效地刺激淋巴细胞增殖(P<0.05)。 结论: TNF-α+IL-1β与肾癌细胞冻融抗原协同可有效促进DCs成熟、增强诱导淋巴细胞活化的能力。     

固相MHCI类相关抗原A刺激的NK细胞对树突状细胞活性的影响

目的:观察固相MHCI类相关抗原A(iMICA)刺激的NK细胞对树突状细胞(DCs)活性的影响.方法:首先取新鲜分离及受固相MICA刺激的异体NK细胞,或IL-2、及IL-2联合iMICA刺激的自体NK细胞与未成熟DCs(iDCs)按5:1比例孵育24 h后,用流式细胞术(FCM)分析HLA-DR+或CD86+频率的DCs.然后取自体NK细胞以iMICA刺激后,按1:5的比例与iDCs孵育24 h后,FCM检测DCs上HLA-DR、CD86的表达.最后在NK细胞与DCs的共培养体系中加人抗IFN-γ抗体,观察DCs上HLA-DR、CD86表达的变化.结果:当NK细胞与iDCs孵育比例为5:1时,异体新鲜分离的与自体活化的NK细胞均能杀伤iDCs;而MICA无协同作用.当NK细胞与iDCs孵育的比例为1:5时,iMICA刺激的NK细胞可促进DCs表达HLA-DR和CD86;而加人抗IFN-γ抗体可抑制 NK细胞诱导DCs表面HLA-DR和CD86表达的上调.结论:异体新鲜分离的或自体活化的NK细胞杀伤iDCs时,无需iMICA的刺激;但当NK细胞的数目明显低于iDCs时,iMICA可刺激NK细胞分泌IFN-γ促进DCs成熟.     

Association of Helicobacter pylori with HLA-DR antigen expression in gastritis.

AIMS: To assess the association between Helicobacter pylori-associated gastritis and HLA-DR antigen (class II antigen) expression. METHODS: Fifty endoscopic gastric biopsy specimens were studied for the presence of H pylori, degree and type of inflammation, and for HLA-DR antigen expression in the epithelium. The cases were chosen to represent different categories: inflamed gastric mucosa with (n = 13) and without (n = 20) H pylori, and non-inflamed mucosa (n = 17). RESULTS: The antigen was aberrantly expressed in the antral mucosal epithelium in 11 of 12 cases (92%) with acute-on-chronic gastritis when H pylori was also present. It was present in the antrum in only seven of 18 H pylori negative cases (39%) with acute-on-chronic/chronic gastritis. One of three cases of acute gastritis and three of seven cases of chronic gastric erosions (non-inflamed category) showed positive staining. Generally, there was more staining in the antral than body mucosa and in the surface/foveolar epithelium than in the glands. No aberrant HLA-DR antigen expression was found in the 10 cases of normal gastric mucosa examined. CONCLUSIONS: These findings suggest that H pylori may have a role in the induction of class II HLA antigen expression in chronic gastritis and lend support to the view that these organisms may be responsible for part of the inflammatory response.     

IgE-containing cells in gastric mucosa with and without Helicobacter pylori infection

Gastric mucosa responds with inflammation to Helicobacter pylori (H. pylori) infection. While numerous reports have shown that the immune system produces specific IgG, IgA, and IgM isotype anti H. pylori antibodies, IgE-mediated pathways of H. pylori-associated gastritis are mostly unknown. Our aim was to evaluate whether an increased presence of IgE in the antral gastric mucosa is responsible for the severity of the H. pylori-associated gastritis. The number of IgE-containing cells was estimated in formalin-fixed, paraffin-embedded antral gastric biopsy specimens using immunohistochemistry in three groups of patients: (i) 20 H. pylori-positive cases with moderate inflammation, (ii) 19 H. pylori-negative cases with moderate inflammation, and (iii) 19 H. pylori-negative cases with normal mucosa. In chronic gastritis, the number of IgE-positive cells increased significantly as compared to normal mucosa. In gastritic patients, H. pylori positivity was accompanied by a significant accumulation of IgE-positive cells, mainly plasma cells. These data suggest that IgE-mediated immune response probably plays an important role in the development of H. pylori-associated gastritis.     

Role of activated protein C in Helicobacter pylori-associated gastritis

The protein C (PC) pathway has recently been suggested to play a role in the regulation of the inflammatory response. To further extend the anti-inflammatory effect of activated PC (APC) in vivo, particularly its biological relevance to human disease, the activity of APC in the mucosa of patients with Helicobacter pylori-associated gastritis and the effect of vacuolating cytotoxin (VacA), cytotoxin-associated antigen (CagA), and H. pylori lipopolysaccharide (LPS) on PC activation were evaluated. This study comprised 35 patients with chronic gastritis. There were 20 patients with and 15 without H. pylori infection. The levels of PC and APC-PC inhibitor (PCI) complex were measured by immunoassays. The level of PC was significantly decreased and the level of APC-PCI complex was significantly increased in biopsy specimens from gastric corpus and antrum in patients with H. pylori-associated gastritis as compared to H. pylori-negative subjects. The concentrations of VacA, CagA, and LPS were significantly correlated with those of the APC-PCI complex in biopsy mucosal specimens from the gastric corpus and antrum. H. pylori LPS, VacA, and CagA induced a dose-dependent activation of PC on the surface of monocytic cells. APC inhibited the secretion of tumor necrosis factor alpha (TNF-alpha) induced by H. pylori LPS. Overall, these results suggest that H. pylori infection is associated with increased APC generation in the gastric mucosa. The inhibitory activity of APC on TNF-alpha secretion may serve to protect H. pylori-induced gastric mucosal damage.     

Mast cells in Helicobacter pylori associated antral gastritis

Mast cells are known to be effector cells in various inflammatory reactions, but their role in gastritis is unclear. The present study was undertaken to investigate the extent of mast cell involvement in antral gastritis with and without Helicobacter pylori (H. pylori) infection and thus evaluate the possible role of mast cells in the pathogenesis of H. pylori-associated gastritis. Antral mucosal biopsies were taken from 212 subjects with symptoms suggestive of acid peptic disease. Sections were assessed for inflammation. Modified Giemsa stain was used to detect H. pylori infection and 1% toluidine blue to count mast cells. Mast cell counts were significantly higher in the antral mucosa even in H. pylori-negative gastritis (68.4 +/- 6.7/mm2), as compared to normal non-inflamed mucosa (45.7 +/- 5.8/mm2) (P < 0.05). However, with H. pylori infection, the mucosal mast cell count were markedly increased (123.8 +/- 4.7/mm2) as compared to normal mucosa (P < 0.01). and H. pylori-negative gastritis (P < 0.01) this increase was noticed uniformly in patients with H. pylori-positivity, irrespective of the presence or absence of a peptic ulcer. After cure of H. pylori infection, the mast cell density decreased significantly (44.9 +/- 4.6/mm2) to reach levels that were similar to those in normal mucosa. There was a positive correlation between the antral mucosal mast cell density and polymorphonuclear and mononuclear cell infiltration (rs = 0.61). H. pylori infection, and 0.73 respy. It was concluded that could be responsible for increasing the mast cell density in the gastric antrum. Probably by inducing castain mucosal cytokine.     

The role of apoptosis and proliferation of epitheliocytes in morphogenesis of Helicobacter pylori-associated gastritis

77 patients with chronic Helicobacter gastritis verified endoscopically and exacerbation of duodenal ulcer were examined. H. pylori infection was identified by the rapid ureasa test (CLO-test) and Giemza staining. The patients received 7-day three-component therapy for eradication of H. pylori. Apoptosis and proliferation were studied in 16 patients in serial sections with the use of monoclonal antibodies. Eradication of H. pylori resulted in relief of inflammation and transformation of active gastritis in inactive one. H. pylori-associated gastritis is associated with activation of apoptosis of gastric mucosa epithelial cells and epitheliocytes proliferation. H. pylori eradication alters correlation between apoptosis of epitheliocytes and their proliferation: successful eradication of the infection decreases apoptosis, high proliferative activity of epitheliocytes persists reflecting enhancement of regeneration in gastric mucosa.     

Gastric Epithelial Cells in Helicobacter pylori-Associated Gastritis Express HLA-DR but not ICAM-1

Induced expression of the intercellular adhesion molecule 1 (ICAM-1) and of the major histocompatibility complex (MHC) class II antigens has been simultaneously observed on keratinocytes and epithelial cells in the thyroid and kidney, suggesting that ICAM-1 and HLA-DR expression might be under common regulation. We have previously found an association between the presence of Helicobacter pylori and an induced expression of class II antigens on gastric epithelial cells in gastric biopsy specimens from patients with gastritis. In this study we investigated whether ICAM-1 could also be expressed on the gastric epithelium. Thirty-one patients with clinical indications for upper gastrointestinal endoscopy were examined. In 23 patients gastritis was diagnosed endoscopically and histologically and H. pylori was cultured from biopsy specimens. In eight patients neither histological gastritis nor growth of the bacteria was observed. Immunoperoxidase staining demonstrated expression of HLA-DR but not ICAM-1 on the gastric epithelial cells in all patients with H. pylori-associated gastritis, indicating regulatory mechanisms different from those of other epithelial cells.     

Absence of CD4+CD25+ regulatory T cells is associated with a loss of regulation leading to increased pathology in Helicobacter pylori-infected mice

Helicobacter pylori induces symptomatic chronic gastritis in a subpopulation of infected individuals. The mechanism(s) determining the development and severity of pathology leading to symptoms are not fully understood. In a mouse model of H. pylori infection we analysed the influence of immunoregulatory CD4+CD25+ T cells on H. pylori colonization and gastritis. Athymic C57BL/6 nu/nu mice were reconstituted with (a) lymph node (LN) cells (b) LN cells depleted of CD25+ T cells (CD25(-) LN) or (c) not reconstituted at all. Mice were then infected orally with 3 x 10(8)H. pylori SS1 bacteria. At 2 and 6 weeks after the inoculation there was a significant (P < 0.001) reduction in H. pylori colonization in athymic mice transferred with CD25(-) LN cells compared to mice transferred with LN cells. Colonization was still reduced at 12 weeks after inoculation. Mice transferred with CD25(-) LN cells showed an earlier onset and increased severity of gastritis as compared to mice receiving LN cells. Splenic cells isolated from mice receiving CD25(-) LN cells produced the highest level of IFN-gamma on stimulation with H. pylori antigens in vitro, had a higher H. pylori-specific DTH response and increased infiltration of CD4+ T cells and macrophages in the gastric mucosa. Athymic mice not transferred with T cells had persistent high H. pylori colonization and displayed a normal gastric epithelium without inflammatory cells. In conclusion, CD4+CD25+ cells reduce immunopathology in H. pylori infection, possibly by reducing the activation of IFN-gamma producing CD4+ T cells, even at the expense of a higher H. pylori load in the gastric mucosa.     

Interleukin-6 polymorphism and Helicobacter pylori infection in Brazilian adult patients with chronic gastritis

Helicobacter pylori is recognised as the most common cause of chronic active gastritis and this bacterium is also an important pathogenic factor in peptic ulcer disease. The biological factors that influence clinical outcome in H. pylori infection have been extensively studied. In addition to immunological factors in the host, bacterial virulence determinants in H. pylori strains are likely to play a crucial role in gastric cancer development. Singlenucleotide polymorphisms at the 5' flanking region of the interleukin (IL)-6 gene promoter (G or C at -174 base) have been identified and individuals with the G allele at position -174 have been shown to produce higher levels of IL-6 than those with the C/C genotype. The mucosal levels of IL-6 were reported to be increased in H. pylori-associated gastritis. The present study was conducted to examine any relationship between inflammatory cytokine polymorphisms and the inflammatory process in mucosa infected by H. pylori. In our study we did not find any association between the C and G alleles in adult patients with chronic gastritis and inflammatory process in gastric mucosa.     

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.     

Simultaneous EBV-positive lymphoepithelioma-like carcinoma and EBV-negative intestinal-type adenocarcinoma in a patient with Helicobacter pylori-associated chronic gastritis

We report the case of a 72-year-old man with 2 simultaneous gastric carcinomas. The larger, ulcerated mass in the antrum was a conventional infiltrating intestinal-type adenocarcinoma. The associated antral-type mucosa showed moderate chronic gastritis, foci with complete and incomplete intestinal metaplasia, and mild to moderate Helicobacter pylori infection. The second, smaller tumor was found within fundic-type mucosa and was a lymphoepithelioma-like carcinoma associated with Epstein-Barr virus (EBV) infection shown by the EBV-encoded small RNA (EBER) test. The EBER test result was negative in the intestinal type adenocarcinoma. To our knowledge, this is the first report of simultaneous gastric carcinomas with 2 different morphologic phenotypes, in which only one tumor was associated with EBV infection, while the second tumor was related to H pylori-associated chronic gastritis. Our report demonstrates 2 different but simultaneous etiologic pathways of gastric carcinogenesis in the same patient.