幽门螺杆菌对体外感染胃黏膜上皮细胞TGF-β1 B7-H1表达的影响

目的 探讨适当菌量幽门螺杆菌(H.pylori)对体外感染胃黏膜上皮细胞转化生长因子β1(TGF-β1)、B7-H1 mRNA表达的影响及其诱导TGF-β1表达的菌体因素,为支持H.pylori通过诱导胃黏膜上皮细胞表达TGF-β1及B7-H1,抑制宿主免疫功能,参与H.pylori免疫逃逸提供依据.方法 (1)选用1.0×109CFU/ml(低浓度)、4.0×109 CFU/ml(中浓度)、8.0×109 CFU/ml(高浓度)H.pylori国际标准毒力菌株NCTC 11637活菌悬液分别感染体外培养胃黏膜上皮细胞,建立不同共孵育时间(0 h、0.5 h、1 h、1.5 h、2 h、4 h、8 h、12 h)H.pylori体外感染细胞模型,设立未加H.pylori的胃黏膜上皮细胞对照组,以酶联免疫吸附法(ELISA)检测感染及对照细胞各时间点培养上清TGF-β1含量,原位杂交法检测不同浓度感染及对照细胞共培养12 h B7-H1 mRNA的表达.(2)同时用H.pylori中浓度灭活菌悬液与体外培养胃黏膜细胞共孵育,测定共孵育细胞2 h、12 h培养细胞上清的TGF-β1含量.(3)用超声粉碎并经离心获取的H.pylori菌体成分上清、沉淀以及煮沸后上清、沉淀分别作用体外培养胃黏膜细胞,测定2 h、12 h培养细胞上清TGF-β1含量.结果 (1)H.pylori活菌悬液3种浓度各时间组胃黏膜上皮细胞培养上清TGF-β1含量均较对照组明显增高(P<0.05),各浓度时间组TGF-β1表达量有栩似的动态趋势,但尤以中浓度组TGF-β1表达量最高(P<0.05).(2)中浓度H.pylori灭活菌株组与同浓度活菌组细胞培养上清TGF-β1含量差异无统计学意义(P>0.05).(3)H.pylori菌体成分上清组较对照组和沉淀组细胞培养上清TGF-β1表达增高(P<0.01);上清煮沸组较未煮沸组明显降低(P<0.01);沉淀煮沸组与未煮沸组差异无统计学意义(P>0.05).(4)高、中、低浓度组感染细胞12 h B7-H1 mRNA的表达均较对照组增高(P<0.05),以中浓度组表达最高,并与高、中、低浓度组12 h感染细胞上清TGF-β1含量呈正相关(rs=0.628,P<0.01).结论 H.pylori可直接诱导胃黏膜上皮细胞分泌TGF-β1,其诱导因素为可溶性不耐热菌体成分;H.pylori同样可诱导胃黏膜上皮细胞B7-H1 mRNA表达增高,且B7-H1 mRNA表达与TGF-β1呈正相关.推测H.pylori通过诱导TGF-β1、B7-H1高表达,抑制宿主免疫应答,参与H.pylori免疫逃逸.     

小檗碱减轻幽门螺杆菌诱导的人胃黏膜上皮细胞损伤

目的:探讨小檗碱(Ber)对幽门螺杆菌(Hp)诱导的人胃黏膜上皮细胞GES-1损伤的保护作用及机制。方法:采用Hp感染GES-1细胞,加入小檗碱(5,10和20μmol/L)和细胞外调节蛋白激酶(ERK1/2)抑制剂PD98059(20μmol/L)共培养。MTT法检测细胞活力,流式细胞术检测细胞凋亡,ELISA法检测细胞白细胞介素(IL)-1β及IL-8的水平,比色法检测细胞乳酸脱氢酶(LDH)活性并以Western blot法检测细胞Bax、Bcl-2、p-ERK1/2的蛋白水平。结果:与对照组比较,Hp可抑制GES-1细胞活力、促进GES-1细胞凋亡、诱导GES-1细胞分泌IL-1β和IL-8、增加LDH活性、增加GES-1细胞内p-ERK1/2及Bax蛋白水平并降低Bcl-2蛋白水平,差异均有统计学显著性(P0.05);与Hp感染组比较,中、高剂量小檗碱均可逆转Hp对GES-1细胞活力、细胞凋亡、细胞IL-1β及IL-8分泌、LDH活性和GES-1细胞内p-ERK1/2、Bax及Bcl-2蛋白水平的影响,差异均有统计学显著性(P0.05);与高剂量小檗碱组比较,PD98059联合小檗碱可进一步逆转Hp对GES-1细胞上述指标的影响,差异均有统计学显著性(P0.05)。结论:小檗碱可通过抗炎、增加细胞活力和抗凋亡来减轻Hp诱导的GES-1细胞损伤,其机制可能与抑制ERK1/2通路有关。     

胃黏膜中两种形态幽门螺杆菌感染的临床病理学意义

目的 探讨不同形态幽门螺杆菌(helicobacter pylori,HP)感染的临床病理学意义.方法 采用HE、HP检测(银染法)及免疫组化SP法检测171例胃黏膜活检标本,观察不同形态HP在黏膜中的定植数量及部位,同时观察胃黏膜病变的相关病理学指标.结果 球形HP感染者中,伴螺旋状HP感染者黏膜糜烂率及炎症活动率分别为72.1%(49/68)、79.4%(54/68),均高于螺旋状HP阴性者[阳性率分别为19.2%(19/99)、29.3%(29/99)],单纯球形HP感染者黏膜糜烂率及炎症活动率分别为36.0%(9/25)、44.0%(11/25),亦均高于球形HP阴性者[阳性率分别为15.4%(12/78)、26.9%(21/78)],螺旋状及单纯球形HP阳性者间质淋巴细胞数量均明显多于阴性者,HP数量与炎症严重程度呈正相关.结论 与螺旋状HP一样,球形HP对胃黏膜具有致病性,但较螺旋状HP弱.     

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。     

幽门螺杆菌对胎儿胃粘膜上皮细胞的粘附作用研究

实验选用６至７个月龄的胎儿胃粘膜组织进行有关幽门螺杆菌的粘附部位及菌株间粘附能力差异的研究，发现ＣＡＰＭ Ｄ３２株与ＮＣＴＣ １１６３７株的粘附部位相似，Ｈｐ对胃窦及胃体下部粘膜组织具有很强的粘附能力，而对胃体上部及胃底部粘膜组织的粘附能力很差或不能粘附；而ＣＡＰＭ Ｚ－４株则对胃体、胃窦及胃底部粘膜上皮组织均表现出很强的粘附能力；表明Ｈｐ的粘附存在明显的部位特异性，不同Ｈｐ菌株间在粘附同一胎儿胃     

一种新的检测胃黏膜幽门螺杆菌荧光定量PCR法

幽门螺杆菌(Helicobacter pylori,HP)是全球最常见的人类感染菌之一,其被认为是慢性胃炎、消化性溃疡的主要原因,且与胃癌的发生密切相关[1,2]。WHO将HP列为第1类致病因子。因此快速准确地检测HP感染对大众健康具有重要意义。实时荧光定量PCR(fluorogenic quantitative polymerase chain reaction,FQ-PCR)技术具有高灵敏度和高特异性的优点,并能对细菌进行定量,国内外已有多项研究应用FQ-PCR法检测HP不同的基因片段。本文以HP尿素酶     

胃癌高发区幽门螺杆菌对胃上皮细胞系GES1蛋白质组的影响

目的探究胃癌高发区分离的幽门螺杆菌(H.pylori-400)对正常胃上皮细胞系GES1细胞蛋白质组的影响。方法 C-13呼气实验阳性患者胃镜下取下胃黏膜,分离、培养并鉴定H.pylori-400。将H.pylori-400与GES1细胞按50∶1的比例共培养,提取细胞RNA,RT-qPCR法检测炎性因子IL-8、IL-1β和TNF-α的mRNA表达。收集共培养细胞蛋白,用高效液相色谱-质谱联用检测蛋白质组的改变,lable-free进行定量分析。选择差异表达蛋白进行GO和KEGG富集分析,并筛选出其中的关键基因(Hub)。结果在胃癌高发区(河北井陉地区)分离培养并鉴定出H.pylori-400,其能够促进胃上皮细胞GES1的IL-8,IL-1β和TNF-α炎性因子的mRNA表达。GES1感染H.pylori-400后,373个蛋白发生显著变化(|Fold change|≥2),其中143个蛋白降低,230个蛋白升高。这些差异表达蛋白经富集分析后表明,H.pylori-400可能通过调节细胞周期、T细胞免疫活性以及P53通路调节炎性因子分泌,进而导致肿瘤发生。结论胃癌高发区分离的H.p...     

幽门螺杆菌对胎儿胃粘膜上皮细胞的粘附用研究

实验选用６至７个月龄的脑儿胃粘膜组织进行有关幽门螺杆菌（Ｈｐ）的粘附部位及菌株间粘附能力差异的研究，发现ＣＡＰＭＤ３２株与ＮＣＴＣ１１６３７株的粘附部位相似，Ｈｐ对胃窦及胃体下部粘膜组织具有很强的粘附能力，而对胃体上部及胃底部粘膜组织的粘附能力很差或不能粘附；而ＣＡＰＭ Ｚ－４株则对胃体、胃窦及胃底部粘膜上皮组织均表现出很强的粘附能力；表明Ｈｐ的粘附存在明显的部位特异性，不同Ｈｐ菌株间在粘附同一胎儿胃粘膜组织时表现出明显的差异，Ｈｐ与胃粘膜上皮细胞间的粘附过程比较复杂，至少包括两种类型，参与Ｈｐ粘附的粘附素和相应受体不止一种。结果提示Ｈｐ相关性慢性胃炎的好发部位及严重程度除与人胃粘膜组织不同部位细菌粘附受体的表达存在明显的差异外，还决定于Ｈｐ的粘附素的种类和粘附特性。不但首次在机体和细菌两个方面揭示了Ｈｐ相关性慢性胃炎的发病规律，也为进一步开展该菌疫苗的研制、开展对Ｈｐ感染及其相关疾病的防治提供了重要线索。     

CagA对幽门螺杆菌诱导胃黏膜上皮细胞分泌IL-8水平的影响

目的：利用小分子干扰RNA（siRNA）探讨CagA在幽门螺杆菌诱导胃黏膜上皮细胞分泌IL-8中的作用。 方法： 设计5条siRNA，采用电穿孔法转入CagA+幽门螺杆菌 NCTC11637,与胃黏膜上皮细胞共培养后测定IL-8水平，并以 RT-PCR、Western blotting法检测穿孔前、后不同时点细菌的CagA表达。采用CagA-株NCTC11639作对照。 结果： CagA+NCTC11637诱导胃黏膜上皮细胞分泌IL-8水平明显高于CagA-NCTC11639［（1 200.00±32.51) ng/L vs (100.00±8.58） ng/L］（P<0.01）。siRNAⅢ转化的幽门螺杆菌诱导胃黏膜上皮细胞分泌IL-8 水平显著低于转化前［(400.00±17.35)ng/L vs （1 200.00±32.51 )ng/L］(P<0.05)；siRNA Ⅲ转化的幽门螺杆菌CagA mRNA水平显著低于转化前, 穿孔后6 h mRNA水平最低为31.3%(0.270/0.861), 抑制率为68.7%。Western blotting显示siRNA Ⅲ组CagA蛋白水平低于穿孔前（P<0.01）；其余4条siRNA未见显著变化。 结论： CagA在幽门螺杆菌诱导胃黏膜上皮细胞分泌IL-8中起重要作用，小分子干扰RNA可能通过抑制CagA基因表达而减少幽门螺杆菌诱导胃黏膜上皮细胞IL-8的分泌。     

幽门螺杆菌诱导人胃上皮细胞(GES-1)自噬的研究

 摘要:目的 观察幽门螺杆菌感染人胃上皮细胞后自噬的发生及变化情况,为进一步研究幽门螺杆菌感染后诱发自噬反应的相关研究奠定基础。方法 采用中性红摄入法确定H. pylori感染细胞的最佳浓度,以此浓度分别感染细胞,通过Western Blot检测感染不同时间LC3与p62的表达情况,免疫荧光染色检测自噬体。使用自噬抑制剂3MA、E64d、 pepstatin A干预后,观察感染后自噬变化情况。结果 H. pylori (22695) 感染GES-1细胞最佳浓度为m.o.i=400。感染后2小时即可观察到自噬的发生,且呈时间依赖性,于8小时到达高峰,24小时开始恢复基础水平。使用3MA阻断自噬,自噬体明显减少,且细胞形态欠佳。使用E64d和pepstatin A处理后自噬也受到一定程度的抑制。结论 H. pylori（22695）能够诱导人胃上皮（GES-1）发生自噬,且可被自噬抑制剂所抑制。     

Gastrospirillum hominis and Helicobacter pylori infection in Thai individuals: Comparison of histopathological changes of gastric mucosa

The presence of Helicobacter pylori (H. pylori ) in the stomach is closely associated with histological signs of chronic active gastritis and peptic ulcer. Another spiral organism named Gastrospirillum hominis (G. hominis ) has led to further interest in the bacterial pathogenesis of gastritis. Due to the low prevalence of G. hominis , it is difficult to evaluate its biological behavior. Recently 16 cases of G. h ominis-associated gastritis were found in 257 Thai individuals, which made it possible to study the biological characteristics of G. hominis and its relationship with gastric mucosal inflammation. The results showed that H. pylori and G. hominis could be easily observed in the lower third of the mucous layer and in the mucosa of the gastric pits by means of toluidlne blue staining. Both bacteria immunostained positive. Helicobacter pylori were usually in the shape of curved bacillary while G. hominis often appeared in spiral configuration. In 257 cases of Thai subjects, 169 cases were found to be H. pylori positive, the detection rate was 65.7%, and 16 cases were G. hominis positive, with a 6.2% detection rate. In G. hominis infection, 43.6% of cases had normal gastric mucosa. Superficial, erosive and atrophlc gastritis cases were 13.2, 10.9 and 12.5%, respectively. Mucosal inflammation was usually severe in H. pylori , but neutrophil polymorph infiltration was often mild and focal in G. hominis Infection. Although no G. hominis infection with carcinoma was shown in our cases, the occurrence of mucosal atrophy, metaplasia and dysplasia was higher in both bacterial infections compared with H. pylori- and G. hominis -negative cases. It is suggested that G. hominis may be partly responsible for the mucosal inflammation and some malignant-associated lesions.     

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.     

Epithelial damage by Helicobacter pylori in gastric ulcers

On review of 136 consecutive biopsies of benign gastric ulcer, Helicobacter pylori was detected in 78 cases (57.3%). The gastric epithelium colonized by Helicobacter pylori showed a characteristic constellation of changes, including loss of apical mucous portion of individual cells, drop-out of epithelial cells, epithelial pits, erosions and cellular tufts, indicative of cellular injury and regeneration. Among the 58 Helicobacter-negative cases, similar changes were not observed in the ulcer edges, except for two cases which exhibited some cellular tufts. Thus, the topographic association of Helicobacter pylori with epithelial damage in the gastric ulcer edges in more than half of the cases suggests that this organism probably plays an aetiological role in ulcerogenesis, at least in these cases. Furthermore, the epithelial changes are so distinctive that they can serve as a helpful histological indicator for the presence of Helicobacter pylori in gastric biopsies.     

Localized accumulation of Russell body-containing plasma cells in gastric mucosa with Helicobacter pylori infection: 'Russell body gastritis'

One of the gastric biopsy specimens taken from a 53-year-old male showed localized accumulation of plasma cells containing Russell bodies, In association with infection of Helicobacter pylori (H. pylori ). An endoscoplc study demonstrated multiple ulcer scars in the antrum. Immunohistochemically, H. pylori Infection was Identified both on the surface of the foveolar epithelial cells and in the cytoplasm of macrophages in the lamina propria mucosae. Plasma cells filled with 'Russell bodies', so-called 'Motts cells', were immunoreactlve for CD45, CD79a and IgG. This seems to be a previously unrecognized tissue reaction in gastric mucosa associated with H. pylori Infection, which we have called 'Russell body gastritis'.     

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。     

幽门螺杆菌感染与胃癌关系的系统评价

目的:探讨幽门螺杆菌(Helicobacter pylori,Hp)感染与胃癌的关系.方法:纳入22篇关于Hp感染与胃癌关系的文献,应用Review Manager 4.2软件进行Meta分析,计算合并优势比(odd ratio,OR)及OR值95%可信区间(confidence interval,CI),倒漏斗图法定性评价发表性偏倚.结果:Meta分析得出Hp感染与胃癌发病合并OR值为2.47(95 %CI为1.74～3.52,χ2 =144.18,P<0.01).本研究倒漏斗分析图形不对称,但经敏感性分析和计算失安全系数证明发表性偏倚的影响较小.结论:Hp感染是胃癌发生的危险因素.     

Helicobacter pylori infection in gastric xanthomas: lmmunohistochemical analysis of 145 lesions

A total of 145 paraffin-embedded biopsy samples of gastric xanthoma were analyzed for the localization of Hellcobacter pylorl (HP) antigens. By the indirect immunoperoxidase method using a polyclonal antibody, HP lnfection was identffied on the surface of foveolar cells In 69 (48%) samples. In 38 (55%) of the 69 lesions, the HP antigens were demonstrated in the cytoplasm of xanthoma cells clustered in the actively inflamed lamina propria mucosae, Among the remalning 76 xanthoma lesions negative for HP lnfection on the epithellal surface, only eight (11%) showed the existence of HP antigens in the foamy histiacytes, and 39 (51 %) revealed mild inflammatory change. Monoclonal antibody study using 75 specimens also gave a comparable result. Pre-embedding lmmunoelectron microscopy using paraffin sections revealed positively labeled rod-shaped bacteria both on the epithelial surface and in the phagosome of the xanthoma cells. These findings strongly suggest that some of the xanthoma lesions are provoked by lamina proprial invasion of surface-infected HP.     

Expression and subcellular distribution of toll-like receptors TLR4, TLR5 and TLR9 on the gastric epithelium in Helicobacter pylori infection

Toll-like receptors (TLRs) expressed by mucosal epithelium play an essential role in the defense against microbes by recognizing conserved bacterial molecules. For the first time TLR4, TLR5 and TLR9 have been microanatomically localized in patients with noninflamed gastric mucosa and Helicobacter pylori gastritis by immunohistochemistry. Because polarized expression of TLRs in apical and basolateral epithelial compartments is thought to modulate mucosal immunity, subcellular TLR distribution by gastric epithelium was investigated using confocal microscopy. TLR4, TLR5 and TLR9 were expressed by gastric epithelium in antrum and corpus of all patients with H. pylori gastritis (n = 14) and with noninflamed gastric mucosa (n = 5). TLR4 was expressed at the apical and the basolateral pole of the gastric epithelium as well in noninflamed gastric mucosa as in H. pylori gastritis. TLR5 and TLR9 expression in the noninflamed gastric mucosa was identical to that of TLR4 with localization at the apical and the basolateral epithelial pole. However, in H. pylori gastritis TLR5 and TLR9 expression on the gastric epithelium changed to an exclusive basolateral localization without detectable expression at the apical pole. In the human stomach, the gastric epithelium expressed TLR4, TLR5 and TLR9, which gives it the possibility to interact with H. pylori. Furthermore, gastric epithelial TLR4 expression is highly polarized in an apical and a basolateral compartment, whereas TLR5 and TLR9 polarization seems to be a process dynamically influenced by H. pylori infection. This polarized and dynamically regulated gastric epithelial expression of TLRs supports a sentinel role for these receptors in the mucosal immunity to H. pylori.     

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.