The effect of gender on Helicobacter felis-mediated gastritis, epithelial cell proliferation, and apoptosis in the mouse model

The murine Helicobacter felis model has been extensively used to investigate the importance of host factors in the development of chronic gastritis. The effect of gender in this murine model is unknown. Male and female C57BL/6J mice were infected with H felis for up to 1 year. At 4, 8, 19, 36, and 52 weeks post-infection, gastric histopathology, epithelial cell proliferation, and apoptosis were examined and compared with age- and gender-matched controls. In female mice, infection with H felis resulted in an earlier onset of chronic gastric inflammation, epithelial hyperplasia, and oxyntic cell loss than males. In females, there was a trend towards increased gastric pathology compared with males, with long-term-infected female mice having significantly greater (p < 0.05) chronic inflammation than male mice. The histopathological differences in male and female mice did not relate to the density of H felis infection. Female mice infected with H felis had significantly increased gastric epithelial cell proliferation in the cardia and corpus at both 8 and 52 weeks post-infection (p < 0.05). Epithelial cell apoptosis in the glandular mucosa of the corpus at 36 and 52 weeks post-infection was significantly increased (p < 0.05) in female mice compared with uninfected gender controls. In contrast, there was no significant increase in epithelial cell proliferation or apoptosis in any area of the stomach at any time point after H felis infection in male mice. These results demonstrate that there are gender differences in the gastric inflammatory and epithelial response to H felis in the murine model. The functional importance of gender should be considered in future murine studies on H felis- and H pylori-induced chronic gastritis.     

幽门螺杆菌诱导蒙古沙鼠胃类癌发生的实验研究

目的 探讨幽门螺杆菌(Hp)感染在蒙古沙鼠胃类癌发生中的作用及Hp去除后对胃类癌发生的影响.方法 100只蒙古沙鼠分成7组,A、B为空白对照组,C、D、E、F、G为Hp感染组,其中F、G组Hp感染后再去除.结果 空白对照组(A、B组)未见ECL细胞增生/异型增生及类癌形成,Hp感染后(C、D、E组),血清抗Hp IgG抗体、胃泌素水平均明显增高(P<0.01),ECL细胞增生/异型增生及类癌发生率分别为27.8%(5/18)、31.2%(5/16)、58.3%(14/24)和16.7%(3/18)、31.2%(5/16)、62.5%(15/24),均明显高于对照组(P<0.01),随着Hp感染时间的延长,ECL病变面积明显增加(P<0.01);Hp去除后,血清抗Hp ISG抗体、胃泌素水平明显降低,ECL细胞增生/异型增生及类癌的发生率降低,分别为25.0%(4/16)、15.4%(2/13)和37.5%(6/16)、23.1%(3/13).早期阶段去除Hp(G组),ECL病变发生率及类癌的面积明显低于非去除组(E组)(P<0.001).血清抗Hp ISG抗体与胃泌素水平及胃泌素水平与胃类癌的发生呈正相关(P<0.001).结论 Hp感染在蒙古沙鼠胃类癌发生中起重要作用,去除Hp可有效预防蒙古沙鼠胃类癌的发生.     

Comparative analysis of gastric bacterial microbiota in Mongolian gerbils after long-term infection with Helicobacter pylori

Quantitative (qt) real time PCR using 16SrDNA primers is useful for determination of the bacterial composition of the gastric microbiota in Mongolian gerbils. The aim of this study was to determine the change in the gastric microbiota after long-term infection with Helicobacter pylori. One year after inoculation with H. pylori, five gerbils were determined as H. pylori-positive and 6 gerbils H. pylori-negative by culture and real time qt PCR methods. The gastric microbiota of each group of gerbils was also compared with that of 6 gerbils uninfected with H. pylori. DNA from the Atopobium cluster, Bifidobacterium spp., Clostridium coccoides group, Clostridium leptum subgroup, Enterococcus spp. and Lactobacillus spp. were detected in the gastric mucus of both infected and uninfected gerbils. In contrast, Eubacterium cylindroides group and Prevotella spp. were detected only in H. pylori-negative gerbils. The numbers of C. leptum subgroup, C. coccoides group and Bifidobacterium spp. in gastric mucus of H. pylori-negative Mongolian gerbils were significantly lower than those in non-infected gerbils. The results obtained suggest that the composition of gastric indigenous microbiota in Mongolian gerbils may be disturbed by long-term infection with H. pylori, and that these changes may in fact inhibit H. pylori infection.     

Increased programmed death-ligand-1 expression in human gastric epithelial cells in Helicobacter pylori infection

B7‐H1 [programmed death‐ligand‐1 (PD‐L1)] is a B7‐family member that binds to programmed death‐1 (PD‐1). Recently, deficiency of PD‐L1 has been demonstrated to result in accelerated gastric epithelial cell damage in gastritis, and PD‐L1 is suggested to play a critical role in regulating T cell homeostasis. Here, we aimed to gain more insight into gastric PD‐L1 expression, regulation and function during Helicobacter pylori infection. PD‐L1 expression in human gastric epithelial cells was analysed using Western blotting, quantitative polymerase chain reaction and fluorescence activated cell sorter analysis. Furthermore, co‐culture experiments of human gastric epithelial cells with primary human T cells or Jurkat T cells were conducted. PD‐L1 expression in primary human gastric epithelial cells was strongly enhanced by H. pylori infection and activated T cells, and augmented markedly by further stimulation with interferon‐γ or tumour necrosis factor‐α. Moreover, PD‐L1 expression in gastric epithelial cells significantly induced apoptosis of T cells. Our results indicate that a novel bidirectional interaction between human gastric epithelial cells and lymphocytes modulates PD‐L1 expression in human gastric epithelial cells, contributing to the unique immunological properties of the stomach.     

幽门螺杆菌对体外培养的胃上皮细胞增殖与凋亡的影响

目的　研究H .pylori对体外培养的胃上皮细胞增殖与凋亡的影响。方法　以SGC 790 1细胞作为H .pylori感染的体外细胞模型 ,用Ki 6 7抗原的免疫组化分析检测了H .pylori标准菌株NCTC 116 37活菌对胃上皮细胞增殖的影响 ,同时用流式细胞术、荧光染色技术检测了细胞凋亡率。结果　H .pylori在较低浓度 (≤ 1.6× 10 5CFU/ml)时对细胞增殖有促进作用 ,而在较高浓度 (≥ 8× 10 5CFU/ml)时抑制细胞增殖。H .pylori以浓度依赖方式诱导胃上皮细胞凋亡 ,Hoechst 332 5 8荧光染色和流式细胞术两种方法所得结果一致。结论　细胞凋亡与增殖间的不平衡亦可部分解释人体感染H .pylori后所表现的多样化结局     

Down-regulation of a morphogen (sonic hedgehog) gradient in the gastric epithelium of Helicobacter pylori-infected Mongolian gerbils

Sonic hedgehog (Shh) is a morphogen involved in many aspects of patterning of the gut during embryogenesis and in gastric fundic gland homeostasis in the adult. Intestinal metaplastic change of the gastric epithelium is associated with the loss of Shh expression, and mice that lack Shh expression show intestinal transformation of the gastric mucosa. The present study was designed to investigate the alteration of Shh expression in the stomach of an experimental model of Helicobacter pylori (H. pylori) colonization. Male Mongolian gerbils were inoculated with H. pylori and examined 4 and 51 weeks later. The level of Shh mRNA expression was determined by quantitative RT-PCR and in situ hybridization. Shh protein expression was determined by immunoblotting and immunohistochemistry. Shh was expressed in the parietal cells, zymogenic cells, and mucous neck cells of the gastric fundic glands of gerbils. Prolonged colonization by H. pylori led to extension of the inflammation from the antrum to the corpus of the stomach, with loss of Shh expression. Loss of Shh expression correlated with loss of parietal cells, disturbed maturation of the mucous neck cell-zymogenic cell lineage, and increased cellular proliferation. Shh expression is significantly reduced in H. pylori-associated gastritis. These data show for the first time that H. pylori infection leads to down-regulation of the expression of a morphogen with an established role (Shh) in gastric epithelial differentiation.     

Homeostatic mass control in gastric non-neoplastic epithelia under infection of Helicobacter pylori: an immunohistochemical analysis of cell growth, stem cells and programmed cell death

We evaluated homeostatic mass control in non-neoplastic gastric epithelia under Helicobacter pylori (HP) infection in the macroscopically normal-appearing mucosa resected from the stomach with gastric cancer, immunohistochemically analyzing the proliferation, kinetics of stem cells and programmed cell death occurring in them. Ki67 antigen-positive proliferating cells were found dominantly in the elongated neck portion, sparsely in the fundic areas and sporadically in the stroma with chronic infiltrates. CD117 could monitor the kinetics of gastric stem cells and showed its expression in two stages of gastric epithelial differentiation, namely, in transient cells from the gastric epithelial stem cells to the foveolar and glandular cells in the neck portion and in what are apparently progenitor cells from the gastric stem cells in the stroma among the infiltrates. Most of the nuclei were positive for ssDNA in the almost normal mucosa, suggesting DNA damage. Cleaved caspase-3-positive foveolar cells were noted under the surface, suggesting the suppression of apoptosis in the surface foveolar cells. Besides such apoptosis of the foveolar cells, in the severely inflamed mucosa apoptotic cells were found in the neck portion where most of the cells were Ki67 antigen-positive proliferating cells. Beclin-1 was recognized in the cytoplasm and in a few nuclei of the fundic glandular cells, suggesting their autophagic cell death and mutated beclin-1 in the nuclei. Taken together, the direct and indirect effects of HP infection on the gastric epithelial proliferation, differentiation and programmed cell death suggested the in-situ occurrence of gastric cancer under HP infection.     

Different cytokine profile and antigen-specificity repertoire in Helicobacter pylori-specific T cell clones from the antrum of chronic gastritis patients with or without peptic ulcer

Helicobacter pylori (Hp) infection almost invariably results in chronic antral gastritis, but only a proportion of patients develop peptic ulcer. Some Hp strains may be more ulcerogenic than others, but some ulcerogenic mechanisms may also depend on the type of the host immune response. In this study, the antigen specificity and the cytokine profile of 53 Hp-specific CD4⁺ T cell clones derived from the antral mucosa of five patients with Hp-induced uncomplicated chronic gastritis (CG) were assessed and compared with those of 34 Hp-specific CD4⁺ T cell clones derived from six Hp-infected patients with chronic gastritis and peptic ulcer (CG-PU). The majority (28/34; 82%) of gastric Hp-specific T cell clones from CG-PU patients expressed the Th1 profile and 17 (all Th1) of the 34 clones were specific for cytotoxin-associated protein (CagA). In contrast, 34 (64%) of the 53 Hp-specific gastric T cell clones derived from CG patients were able to secrete both Th1 and Th2 cytokines (Th0 profile) and only 36% expressed a polarized Th1 profile. The majority (85%) of Hp-specific clones from CG patients recognized Hp antigens other than CagA, since 13/53 (25%) were specific for urease, 6 (11%) for VacA, 6 (11%) for HSP and 20 (38%) for other undefined Hp antigens. Results provide evidence that the type of T helper cell response against Hp may vary according to the antigen involved and suggest that a polarized Th1 response may play a role in the genesis of peptic ulcer, whereas a local Th0 response, including interleukin-4 production, may represent an individual host factor which contributes to lower the degree of gastric inflammation and prevent ulcer complication.     

ATP4A autoimmunity and Helicobacter pylori infection in children with type 1 diabetes

Persistent presence of ATP4A autoantibodies (ATP4AA) directed towards parietal cells is typical for atrophic body gastritis (ABG), an autoimmune disease associated with type 1 diabetes. We assessed whether Helicobacter pylori (Hp) infection might be associated with positivity for ATP4AA in children with type 1 diabetes. Sera were collected from 70 (38♀) type 1 diabetes children [aged 13·2 ± 4·5 years, age at diagnosis 8·8 ± 4·3 years, diabetes duration 4·5 ± 3·8 years, mean HbA1c 7·8 ± 1·6% (62 ± 17·5 mmol/mol)] seen at the regional diabetes clinic in Katowice, Poland. Patients were tested concurrently for Hp infection by means of a 13C urea breath test. ATP4AA were measured using a novel radioimmunoprecipitation assay developed at the Barbara Davies Center for Childhood Diabetes, University of Colorado. ATP4AA were present in 21 [30%, 95% confidence interval (CI) = 19–41%] and Hp infection was detected in 23 (33%, 95% CI = 22–44%) children. There was no statistically significant association between ATP4AA presence and Hp status. ATP4AA presence was not associated with current age, age at type 1 diabetes diagnosis, diabetes duration or current HbA1c. ATP4AA were more prevalent in females [42% (26–58%)] than males [16% (3–28%)], P = 0·016. ATP4A are found in nearly one‐third of children with type 1 diabetes and more common among females. In this cross‐sectional analysis, Hp infection was not associated with autoimmunity against parietal cells.     

cagA基因阳性幽门螺杆菌培养滤液对人胃粘膜上皮细胞系GES-1生长的影响

目的：研究cagA^ 幽门螺杆菌（Hp）培养滤液对人胃粘膜上皮细胞（GES－1）的作用及机制。方法：制备Hp培养滤液，PCR鉴定cagA基因。采用倒置显微镜、电镜、细胞生长曲线、克隆形成实验、单细胞微凝胶电泳及流式细胞仪等，观察Hp (cagA^ ）培养滤液对GES－1细胞的作用。结果：经Hp(cagA^ )培养滤液处理GES－1细胞，细胞核增大、畸形、核染色质变粗、核仁肥大、核分裂。生长曲线可见细胞增生活跃，增殖率195％。克隆形成试验显示细胞克隆形成能力增强，增殖率达到337．5％。流式细胞仪S期细胞比率显著高于对照组。Hp(cagA^ ）培养滤液可使GES－1细胞形成彗星现象。结论：Hp(cagA^ )培养滤液可以导致GES－1细胞的生长特性改变，呈现肿瘤细胞的形态学及生长特征。DNA损伤可能是cagA诱导GES－1细胞生长特性改变的机制之一。     

CagA protein secreted by the intact type IV secretion system leads to gastric epithelial inflammation in the Mongolian gerbil model

Helicobacter pylori causes various gastro-duodenal diseases, including gastric cancer. The CagA protein, an H. pylori virulence factor, induces morphological changes in host cells and may be associated with the development of peptic ulcer and gastric carcinoma. The present study has analysed the role of CagA protein in the pathogenesis of H. pylori infection in the Mongolian gerbil model. Mongolian gerbils were challenged with wild-type H. pylori strain TN2, which has a functional cag pathogenicity island or isogenic mutants with disrupted cagA (DeltacagA) or cagE (DeltacagE) genes. They were sacrificed at 7, 13, and 25 weeks after inoculation. Pathological changes of the gastric mucosa were determined and apoptosis was assessed by the TUNEL assay. Immunohistochemistry for PCNA, phospho-IkappaBalpha, and phospho-Erk was also performed. All of the bacterial strains colonized the gerbil stomach at similar densities; however, the DeltacagA mutant induced milder gastritis than did the wild type. The extent of apoptosis and lymphoid follicle formation in the epithelium appeared to depend on intact cagA. The DeltacagA mutant induced less phosphorylation of IkappaBalpha and Erk, and less expression of interferon-gamma and interleukin-1beta mRNA in the epithelium than did the wild type. It is concluded that CagA protein may be essential for the induction of severe gastritis in the Mongolian gerbil model.     

固有免疫分子DC-SIGN在幽门螺杆菌感染胃黏膜上皮细胞表达意义

探讨固有免疫分子DC-SIGN在幽门螺杆菌(H.pylori)感染的胃上皮细胞表达,及其与胃黏膜损伤的关系.选取经胃镜及组织病理检查确诊的72例慢性胃炎患儿胃黏膜活检标本,采用免疫组化检测胃黏膜上皮细胞DC-SIGN表达.体外建立幽门螺杆菌感染胃上皮细胞模型,采用流式细胞术检测幽门螺杆菌刺激的胃上皮细胞DC-SIGN以...     

Influence of age and duration of infection on bacterial load and immune responses to Helicobacter pylori infection in a murine model

Using a murine model, we previously showed that Helicobacter pylori infects and colonizes offspring via maternal transmission during the nursing period. The aim of this study was to investigate the influence of age and duration of infection on inflammatory and immune responses to H. pylori in infant and adult mice. During the breast-feeding period, the number of bacteria was significantly suppressed in 1-week-old mice infected with H. pylori at an early stage of nursing, compared with adult mice, suggesting that breast-milk induces such low colonization. In addition, these mice had weaker gastric inflammation, especially Th1 cytokine and humoral responses than in mice infected with H. pylori after weaning in spite of elevated levels of Th1 cytokines. Although infant mice showed low inflammatory responses against H. pylori, they produced H. pylori-specific antibodies following vaccination with oral or parenteral adjuvant. Our results suggest the importance of age at the time of primary infection on bacterial load, gastric inflammation and humoral responses in a murine model of H. pylori infection.     

Five month persistence of Helicobacter pylori infection in guinea pigs

Seven Dunkin-Hartley guinea pigs were infected with the Sydney strain of H. pylori (SS1). Gastric histopathology was evaluated and serum antibody response to H. pylori cell-surface proteins was analysed by enzyme immunoassay (EIA) and immunoblot. Tissue and faecal samples from five control animals were analysed for the presence of naturally occurring Helicobacter spp. infection by culture and Helicobacter genus-specific PCR. The H. pylori infection persisted for 5 months, in most animals accompanied by a histologically severe antral gastritis, exhibiting focal degeneration and necrosis of gastric crypt epithelium. Increased numbers of mitotic figures were observed in the gastric epithelium, indicating a regenerative process. Infected animals displayed specific antibodies towards H. pylori cell-surface proteins in immunoblot, whereas EIA was of dubious value creating false-positive results. Serum complement C3 and cholesterol levels appeared to be elevated in infected animals. Helicobacter spp. infection was not detected in the control animals. The persistent infection, accompanied by severe gastritis and a prominent serum antibody response, and the apparent absence of a natural Helicobacter spp. infection makes the guinea pig model useful in H. pylori research.     

Production of IL-12 in gastritis relates to infection with Helicobacter pylori.

Increased production of proinflammatory cytokines, including tumour necrosis factor-alpha (TNF-alpha), IL-1beta, IL-6 and IL-8, has been demonstrated in Helicobacter pylori-associated gastric mucosal inflammation. IL-12, a newly characterized cytokine, is thought to be a key mediator in host responses to bacterial infections. The aim of this study was to investigate differences in cytokine patterns between H. pylori-positive and -negative gastritis and normal mucosa. Secretion of IL-12, TNF-alpha, IL-1beta, IL-6, IL-8 and IL-10 was measured in 176 patients with chronic gastritis in whole biopsy cultures. Gastritis was graded for chronic inflammation or acute inflammatory activity, respectively, according to the Sydney system. Biopsies with similar scores were matched for analysis from H. pylori-infected and non-infected patients. Secretion of IL-12 was significantly increased in H. pylori-associated gastritis in comparison with H. pylori-negative gastritis (P < 0.0001). In contrast, secretion of TNF-alpha, IL-1beta, IL-6, and IL-8 correlated with the degree of inflammation but was not different between H. pylori-positive and -negative patients. Moreover, IL-10 secretion was found to be higher in H. pylori-positive than in H. pylori-negative patients. IL-12 may play a specific role in H. pylori-associated gastric disease, whereas production of the proinflammatory cytokines TNF-alpha, IL-1beta, IL-6 and IL-8 does not seem to be restricted to H. pylori-induced inflammation. The contra-inflammatory cytokine IL-10 may be a contributor to the chronicity of H. pylori-associated gastritis by impairing clearance of the pathogen.     

长链非编码RNA LINC00260抑制幽门螺杆菌感染胃上皮细胞系引起的炎性反应和细胞迁移

目的探讨长链非编码RNA-LINC00260在幽门螺杆菌(HP)感染引起的胃癌中的作用及可能机制。方法实时荧光定量PCR检测LINC00260在HP感染的胃黏膜正常上皮细胞(GES1)中的表达,在胃癌细胞系SGC-7901中通过瞬时转染siRNA敲低LINC00260后与HP共培养,用q PCR检测炎症相关细胞因子肿瘤坏死因子α(TNF-α)、白介素1β(IL-1β)、白介素6(IL-6)及白介素8(IL-8)的表达;在敲低LINC00260的表达后,通过划痕愈合实验,观察对胃癌细胞迁移能力的影响。结果 1)HP感染细胞后,GES1和SGC-7901细胞形态学改变;2)LINC00260在HP感染的胃黏膜正常上皮细胞表达显著下降(P0.05);3)敲低LINC00260可抑制HP引起的炎症相关因子TNF-α、IL-1β、IL-6和IL-8的表达;4)敲低LINC00260抑制胃癌细胞的迁移能力。结论 LINC00260可能是一个癌基因,在HP感染引起的胃癌中发挥重要作用。     

幽门螺杆菌感染与胃黏膜增殖及与胃癌预后的关系

目的 :探讨增殖细胞核抗原 (PCNA)在幽门螺杆菌 (HP)感染的不同胃黏膜增殖性病变演进中的表达情况及其相互关系 ,并着重探讨HP感染对胃癌预后的意义。方法 :对 14 5例经病理证实的不同胃黏膜病变用免疫组化方法检测PCNA标记指数 (LI) ,Warthin Starry(W S)法检测HP感染。结果 :在浅表性胃炎 (CSG)、萎缩肠化性胃炎 (CAG +IM)、异型增生 (DYS)、早期胃癌和进展期胃癌中 ,PCNA LI为 2 4 0 0± 17 88,4 6 5 9± 18 15 ,6 0 5 9± 2 0 2 6 ,5 7 92± 15 15 ,71 0 8± 2 1 2 5。在IM、DYS、胃癌组织均高于CSG(P <0 0 5 )。PCNA阳性表达与胃癌组织类型、浆膜浸润和淋巴结转移密切相关 ,而且Bor rmannIV高于早期胃癌 (P <0 0 5 )。PCNA阳性表达与肠型胃癌HP感染有关。CAG +IM、DYS和GC组PCNA阳性表达中HP感染者高于阴性者。胃癌HP阳性者 5年存期短于HP阴性者。结论 :PCNA基因表达与胃黏膜增殖和恶化有关。HP感染和胃黏膜增殖和恶化有关 ,HP感染与胃癌预后有关。     

Th17细胞及其相关细胞因子在幽门螺杆菌感染中的作用研究

目的 探讨Th17细胞及其相关细胞因子在幽门螺杆菌(H.pylri)感染中的作用.方法 建立幽门螺杆菌感染的小鼠模型,同时设立治疗组与对照组.HE染色评价小鼠胃组织学改变;RT-PCR法检测胃组织IL-17 mRNA、IL-23 mRNA表达水平;ELISA法检测胃组织匀浆上清IL-17、IL-23含量;FCM检测脾脏单细胞悬液中Th17细胞应答情况.结果 与对照组相比,H.pylori感染组小鼠胃组织IL-17、IL-23在mRNA及蛋白水平表达均升高,脾淋巴细胞中Th17细胞比例显著升高;而且H.pylori感染组小鼠IL-17、IL-23 mRNA和蛋白含量以及脾淋巴细胞中Th17细胞比例随感染时间延长而增加;治疗组小鼠IL-17、IL-23表达量及脾淋巴细胞中Th17细胞比率,与治疗前即感染后4周的小鼠相比较均有所下降;感染后不同时期小鼠胃黏膜的炎症程度与IL-17、IL-23的表达量存在正相关.结论 H.pylori感染后可以诱导Th17细胞应答且IL-17、IL-23表达均上调;H.pylori感染后胃炎程度与胃组织1L-17、IL-23含量存在正相关.     

抗幽门螺杆菌血清IgE和胃粘膜肥大细胞在Hp致病中的作用

目的探讨机体免疫反应在幽门螺杆菌（Ｈｐ）致病中的作用。方法采用间接ＥＬＩＳＡ法检测了１４９例患者血清中抗ＨｐＩｇＥ,并用改良甲苯胺蓝染色法检测其胃粘膜中肥大细胞（ＭＣ）。结果①Ｈｐ阳性者血清抗ＨｐＩｇＥ含量、阳性率和胃粘膜中ＭＣ总数及脱颗粒比均显著高于Ｈｐ阴性者（Ｐ＜０．０１）;②不同胃部疾病之间血清抗ＨｐＩｇＥ含量、阳性率和胃粘膜中ＭＣ总数及脱颗粒比有显著差异,活动性胃炎显著高于非活动性胃炎和消化性溃疡（Ｐ＜０．０１）,中重度胃炎显著高于轻度胃炎（Ｐ＜０．００１）;③血清抗ＨｐＩｇＥ阳性者胃粘膜内ＭＣ总数及脱颗粒比均显著高于抗ＨｐＩｇＥ阴性者（Ｐ＜０．０１）,且血清抗ＨｐＩｇＥ含量与胃粘膜内ＭＣ脱颗粒比呈正相关（ｒ＝０．６０,Ｐ＜０．００１）。结论血清抗ＨｐＩｇＥ参与了Ｈｐ的致病过程,其机制可能为刺激ＭＣ脱颗粒,而致胃粘膜损伤。