慢性胃炎粘膜内CD3+细胞,S-100+树突状细胞和nNOS表达与幽门螺旋杆菌感染的关系研究

目的　探讨幽门螺旋杆菌 (Hp)与慢性胃炎粘膜内CD3+ 细胞 ,S 10 0 + 树突状细胞和nNOS表达之间的关系。方法　用免疫细胞化学方法 ,检测Hp+ 和Hp 胃炎患者及正常人的胃窦部活检标本。结果　Hp+ 胃炎组胃窦粘膜内CD3+ 细胞和S 10 0 + 树突状细胞数量明显高于Hp-胃炎和正常组 ,且有显著性差异 (P <0 0 1和P <0 0 5 ) ,而nNOS呈高表达 ,与Hp-胃炎组相比有显著性差异 (P <0 0 1)。结论　Hp+ 胃炎患者胃窦粘膜内CD3+ 细胞和S 10 0 + 树突状细胞的增加是机体对Hp的免疫应答 ,而nNOS在Hp+ 胃炎组的高表达可能与Hp感染有密切关系。     

人慢性胃炎与神经内分泌G、D细胞关系的研究

探讨神经内分泌G、D细胞与慢性胃炎的关系,用免疫细胞化学方法对52例慢性胃炎及9例对照者进行胃窦粘膜内G、D细胞密度计数。结果显示慢性胃炎病人的G、D细胞数均低于对照组,特别是萎缩性胃炎G、D细胞显著减少,同时还发现不同组别、不同程度的萎缩性胃炎,其G细胞的数量均大于D细胞,G／D细胞的比值在中、重度性胃炎与其它组相比有显著性差异（P＜0.01）。资料还显示G、D细胞的计数不仅可以判断胃窦粘膜的萎缩程度,而且可作为观察临床疗效的一项重要指标。     

慢性胃炎患者粘膜内EGF和TFF1的表达及G细胞的相关研究

目的探讨EGF和TFF1在慢性胃炎患者胃窦粘膜内的表达及G细胞相关研究.方法免疫细胞化学.结果 EGF和TFF1在慢性胃炎粘膜内的表达与正常对照组相比均有减弱或消失,而且有显著性差异(P<0.01).在萎缩性胃炎的肠化区EGF和TFF1均为阴性,但与其相邻的腺体内TFF1仍为阳性反应.G细胞数目在Hp 和Hp-组之间无显著性差异,与正常对照组比较亦无差异(P>0.05);但萎缩性胃炎的G细胞显著减少,与正常对照组有差异(P<0.01).结论慢性胃炎粘膜内的EGF和TFF1表达减弱或消失与Hp或其它致病原有关.肠化区内的TFF1消失,可能与细胞恶变有关.Hp 组患者的G细胞无增加.     

人慢性胃炎粘膜内CD3+细胞,S-100+树突状细胞和nNOS表达的意义

采用免疫细胞化学方法探讨胃粘膜内 CD3+细胞 ,S- 10 0 +树突状细胞和 n NOS的表达与慢性胃炎的关系及意义。检测标本均取自胃窦部活检的胃粘膜组织。结果显示 CD3+细胞主要分布于粘膜上皮、腺上皮和固有膜内 ,而 S- 10 0 +树突状细胞则主要位于固有膜内 ,正常组与浅表性胃炎组和萎缩性胃炎组 ,浅表性胃炎组与萎缩性胃炎组细胞数量有显著性差异(P<0 .0 1) ,n NOS阳性反应主要位于粘膜上皮和腺上皮的基底部 ,但各组之间 n NOS的表达程度不同 ,特别是萎缩性胃炎与浅表性胃炎有显著性差异 (P<0 .0 1) ,我们认为 ,对 CD3+细胞 ,S- 10 0 +树突状细胞和 n NOS的检测 ,不仅有助于判断胃炎的病变程度和临床疗效 ,而且也为胃炎的治疗提供新的启示     

人慢性胃炎胃粘膜内胃泌素及其mRNA的表达和意义

目的　探讨慢性胃炎胃粘膜对细胞内胃泌素 (G)及其mRNA的表达和意义。方法　标本均来自活检的胃窦部粘膜组织 ,用免疫细胞化学和原位杂交技术。结果　对照组G细胞及GmRNA阳性细胞数 ,与浅表性胃炎组比较无显著性差异 (P >0 0 5 ) ,而与萎缩性胃炎组比较则有显著性差异 (P <0 0 1) ,不论对照组还是胃炎组的G细胞数量与GmRNA阳性细胞均有平行关系。结论　证明浅表性和萎缩性胃炎的胃泌素基因的转录和蛋白表达功能保存完好 ,因此检测G细胞的数量及GmRNA不仅可以帮助了解胃炎的萎缩程度 ,而且能判断临床疗效。     

不同临床类型乙型病毒感染者外周血T细胞亚群与血清HBVDNA载量及HBeAg滴度相关性分析

目的：探讨慢性乙型肝炎病毒（HBV）感染患者外周血T细胞亚群与血清HBVDNA载量及HbeAg滴度的关系。方法：选取103名HBV感染患者和20名健康者为研究对象。流式细胞术检测外周血T细胞亚群,聚合酶链式反应及酶免疫分析法分别检测血清HBVDNA载量及HbeAg滴度。结果：慢性乙型肝炎患者和慢性HBV携带者外周血CD3可、CD4T淋巴细胞亚群百分数低于健康对照组,结果有统计学意义（P〈0．05或0．01;而CD8＋T细胞亚群则呈现相反趋势,结果亦有统计学意义（P〈0．05或0．01）。HBeAg阴性组中,HBVDNA水平与CD8T细胞亚群百分数呈正相关（r=0．567,P〈0．01）,与CD47CD8＋T细胞亚群百分数比值呈负相关（r=-0．601,P〈0．01）,而与CD3＋T、CD4＋T细胞亚群百分数无相关性。HBeAg阳性组中,HBVDNA水平及HbeAg滴度与cD3＋1r、cD41、CD8叮细胞百分数及CD47CD8＋T细胞百分数均无相关性（P〉0．05）。结论：不同临床类型的慢性乙型肝炎病毒感染患者外周血T细胞亚群存在不同程度细胞免疫功能降低和细胞免疫调节异常。HbeAg阴性的HBV感染患者,其血清HBVDNA水平与外周血T淋巴细胞免疫存在相关性。     

人慢性胃炎粘膜内CD3+细胞,S-100+树突状细胞和nNOS表达的意义

采用免疫细胞化学方法探讨胃粘膜内CD3+细胞,S-100+树突状细胞和nNOS的表达与慢性胃炎的关系及意义.检测标本均取自胃窦部活检的胃粘膜组织.结果显示CD3+细胞主要分布于粘膜上皮、腺上皮和固有膜内,而S-100+树突状细胞则主要位于固有膜内,正常组与浅表性胃炎组和萎缩性胃炎组,浅表性胃炎组与萎缩性胃炎组细胞数量有显著性差异( P<0.01),nNOS阳性反应主要位于粘膜上皮和腺上皮的基底部,但各组之间nNOS的表达程度不同,特别是萎缩性胃炎与浅表性胃炎有显著性差异(P<0.01),我们认为,对CD3+ 细胞,S-100 +树突状细胞和nNOS的检测,不仅有助于判断胃炎的病变程度和临床疗效,而且也为胃炎的治疗提供新的启示.     

幽门螺杆菌对PCNA及HSP60在慢性胃炎中的表达的影响

目的研究HSP60与PCNA在幽门螺杆菌感染慢性胃炎组织中的表达及其意义。方法免疫细胞化学检测Hp 和Hp-慢性胃炎患者胃窦粘膜内的PCNA和HSP60。结果PCNA在浅表性胃炎以弱阳性或阳性表达为主,在萎缩性胃炎以阳性或强阳性表达为主。与Hp-患者相比,Hp 患者胃粘膜PCNA的表达显著增强,两者之间差异显著(P<0·05);HSP60在Hp 患者浅表性胃炎、萎缩性胃炎的阳性率分别为40·0%和76·9%,Hp 患者胃粘膜HSP60的表达比Hp-患者强(P<0·05)。结论幽门螺杆菌的感染增强了PCNA、HSP60在胃粘膜中的表达,与胃粘膜的病理特征有密切的关系,两者可能是胃粘膜病变趋势或临床病理特征的重要指标。     

猴头菌颗粒治疗慢性萎缩性胃炎作用机制研究

目的：观察猴头菌提取物颗粒对大鼠慢性萎缩性胃炎的治疗效果。方法：SD大鼠分为5组,即正常对照组、模型对照组、维酶素治疗组、猴头菌颗粒小剂量组、猴头菌颗粒大剂量组;除正常对照组外,其余大鼠用热盐水灌胃方法制作慢性萎缩性胃炎模型：模型制成后连续给药28天;处死动物后通过制备病理切片和利用试剂盒测定胃粘膜氨基己糖、前列腺素E2（PGE2）含量,由此观察猴头菌提取物颗粒对慢性萎缩性胃炎的治疗作用。结果：猴头菌颗粒治疗组大鼠胃粘膜G、D细胞数量和氨基己糖、PGE2含量高于模型对照组,尤以猴头菌颗粒大剂量组,最为显著（P〈0．01）。结论：猴头菌颗粒对大鼠慢性萎缩性胃炎有明显的治疗作用。     

系统性红斑狼疮患者外周血调节性T细胞、Foxp3和IL-6的表达

目的探讨系统性红斑狼疮（ systemic lupus erythematosus, SLE）患者外周血CD4^＋ CD25^＋调节性T细胞（regulatory T cells,Tregs）、roxp3 mRNA和血浆IL-6表达的意义。方法对38例SLE患者和16例正常人采用流式细胞术检测外周血CD4^＋ CD25^＋ T regs百分率,RT-PCR检测roxp3 mRNA表达,ELISA法检测IL-6水平。结果①SLE活动组和非活动组的CD4^＋ CD25^＋ Tregs水平均显著低于正常对照组（P〈0．01）;②SLE活动组的roxp3 mRNA表达水平明显低于正常对照组（P〈0．05）;③SLE活动组和非活动组血浆的IL-6水平均显著高于正常对照组（P〈0．01）,而且活动组显著高于非活动组（P〈0．05）;④38例SLE患者的CD4^＋ CD25^＋Tregs水平与SLEDAI评分呈显著性负相关（P〈0．01）,F0xp3mRNA水平与CD4^＋ CD25^＋Tregs呈显著性正相关（P〈0．01）,血浆IL-6水平与SLEDAI评分之间呈显著性正相关（P〈0．01）,血浆IL-6水平与CD4^＋ CD25^＋Tregs／CD4^＋细胞比值呈显著负相关（P〈0．05）。结论CD4^＋ CD25^＋Tregs和Foxp3以及IL-6可能在SLE的发生和发展中发挥重要作用。     

人和大鼠胃窦部神经内分泌细胞分布和形态学的比较研究

目的探讨人和大鼠胃窦部神经内分泌细胞的分布和形态学特征。方法采用免疫细胞化学方法,检测人和大鼠胃窦部粘膜内生长抑素细胞(D细胞)、胃泌素细胞(G细胞)、5-羟色胺细胞(5-HT细胞)、嗜铬粒素A细胞(CgA细胞)的分布。结果人和大鼠的G、D细胞的特征是都具有细胞突起,但是在细胞密度及其分布上是不同的;5-HT细胞的分布在两组稍有不同,在大鼠胃窦部,大多数5-HT细胞位于腺体基部,而人的5-HT细胞主要在间质,少数位于腺上皮内;在两组中,CgA细胞几乎布满整个胃粘膜,其数量也高于其他神经内分泌细胞,CgA细胞形态多样,胞质内充满细小颗粒。结论1)人与大鼠的G、D细胞通常都伴有突起,但其分布不同。2)5-HT细胞形态多样,分布于间质和腺上皮内。3)CgA细胞特征是胞质内充满细小颗粒,细胞形态多样,几乎布满整个粘膜。     

Inflammatory changes in the gastric mucosa of patients with idiopathic non-ulcer dyspepsia and the effect of colloid bismuth treatment on the course of inflammation]

The studies were aimed at the assessment of the coexistence of non-ulcer dyspepsia with chronic gastritis and Campylobacter pylori infection, and of the effect of therapy with De-Nol on the course of such disease. The studies involved 50 patients with non-ulcer dyspepsia. Prior to and after the treatment with De-Nol samples of the mucosa collected from the antrum and corpus of the stomach have been examined histologically with urease test indicating C. pylori infection. Chronic gastritis of the antral mucosa membrane and/or mucosa of the corpus of the stomach has been found in 36 patients, and normal mucosa in 14 patients. Therapy with De-Nol produced statistically significant improvement. Totally histological improvement has been noted in 77.1% of patients with inflammation of the antral mucous membrane and in 64.3% of patients with inflammation of the corporeal gastric mucosa. Campylobacter pylori has been eradicated in all patients with chronic gastritis. De Nol eliminates or significantly lowers an inflammation in the antrum and/or corpus of the stomach. Its action is related to the eradication of Campylobacter pylori infection.     

Oxidative phosphorylation and its coupling to mitochondrial creatine and adenylate kinases in human gastric mucosa

Energy metabolism in gastrobiopsy specimens of the antral and corpus mucosa, treated with saponin to permeabilize the cells, was studied in patients with gastric diseases. The results show twice lower oxidative capacity in the antral mucosa than in the corpus mucosa and the relative deficiency of antral mitochondria in complex I. The mucosal cells expressed mitochondrial and cytosolic isoforms of creatine kinase and adenylate kinase (AK). Creatine (20 mM) and AMP (2 mM) markedly stimulated mitochondrial respiration in the presence of submaximal ADP or ATP concentrations, and creatine reduced apparent Km for ADP in stimulation of respiration, which indicates the functional coupling of mitochondrial kinases to oxidative phosphorylation. Addition of exogenous cytochrome c increased ADP-dependent respiration, and the large-scale cytochrome c effect (>or=20%) was associated with suppressed stimulation of respiration by creatine and AMP in the mucosal preparations. These results point to the impaired mitochondrial outer membrane, probably attributed to the pathogenic effects of Helicobacter pylori. Compared with the corpus mucosa, the antral mucosa exhibited greater sensitivity to such type of injury as the prevalence of the large-scale cytochrome c effect was twice higher among the latter specimens. Active chronic gastritis was associated with decreased respiratory capacity of the corpus mucosa but with its increase in the antral mucosa. In conclusion, human gastric mucosal cells express the mitochondrial and cytosolic isoforms of CK and AK participating in intracellular energy transfer systems. Gastric mucosa disease is associated with the altered functions of these systems and oxidative phosphorylation.     

Reactive Nitrogen Species Mediate DNA Damage in Helicobacter pylori-Infected Gastric Mucosa

Background:  Reactive oxygen species (ROS) and reactive nitrogen species (RNS) can play an important role in cellular injury and carcinogenesis of gastric epithelial cells infected with Helicobacter pylori . 8-OH-deoxy guanosine (8-OHdG) and 8-nitroguanine (8-NG) are markers for ROS- and RNS-mediated DNA oxidation, respectively. In this study, RNS-mediated DNA damage in gastric mucosa was observed directly using a newly developed antibody to 8-NG to clarify how H. pylori infection causes nitrative DNA damage to gastric epithelial cells.
Methods:  Immunohistochemistry with anti-8-OHdG and anti-8-NG antibodies was performed on gastric tissue samples from 45 patients (25 men and 20 women) with H. pylori -positive gastritis and 19 patients (11 men and 8 women) exhibiting successful H. pylori eradication. Histologic factors for gastric mucosal inflammation were graded according to the guidelines of the Updated Sydney system.
Results:  In corpus mucosa, 8-OHdG and 8-NG production were significantly associated with the degree of glandular atrophy, infiltration of chronic inflammatory cells and intestinal metaplasia in the glandular epithelial cells. Successful H. pylori eradication resulted in a significant reduction of chronic inflammatory cell infiltration and neutrophilic activity. Mean 8-OHdG production was lower after H. pylori eradication in both corpus and antral mucosa ( p  = .022 and .049, respectively). However, the reduction in 8-NG exhibited was more pronounced than the reduction of 8-OhdG ( p  = .004 and .007, respectively).
Conclusions:  Helicobacter pylori infection can induce inflammatory cells infiltration, which evokes DNA damage of gastric epithelial cells through ROS and RNS production. 8-NG might be a more sensitive biomarker than 8-OHdG for H. pylori -induced DNA damage in gastric mucosa.     

Serotonin-producing enterochromaffin (EC) cells of gastrointestinal mucosa in dexamethasone-treated rats

The aim of our study was to investigate the morphological, immunohistochemical and ultrastructural changes of rat serotonin-producing enterochromaffin (EC) cells of gastrointestinal mucosa in dexamethasone-treated rats (D). After 12-daily intraperitoneal administration of 2 mg/kg dexamethasone, rats developed diabetes similar to human diabetes type 2. Stomach, small and large intestines were examined. Large serotonin positive EC cells appeared in the corpus mucosa epithelium of D group of rats, although these cells were not present in control (C) rats. Both volume fraction and the number of EC cells per mm(2) of mucosa were significantly increased only in the duodenum. However, the number of EC cells per circular sections of both antrum and small intestine was increased, but reduced both in the ascending and descending colon in D group. The dexamethasone treatment caused a strong reduction in number of granules in the antral EC cells, while it was gradually increased beginning from the jejunum to descending colon. The mean granular content was reduced in the antral EC cells but increased in the jejunal EC cells in D group. In conclusion, the present study showed that morphological changes in gut serotonin-producing EC cells occurred in diabetic rats.     

The pathological examinations of gastric mucosa in patients with Helicobacter pylori-positive and -negative pernicious anemia

Background. The basic histopathological finding in gastric mucosa is chronic atrophic gastritis in patients with pernicious anemia.
Materials and Methods. We evaluated the frequency of Helicobacter pylori and pathological examinations of gastric mucosa in pernicious anemia (n = 30) by endoscopical findings and biopsy. The results were compared with gastric mucosa specimens of patients with H. pylori –positive nonulcer dyspepsia (n = 36) and H. pylori –negative nonulcer dyspepsia (n = 21).
Results. H. pylori was diagnosed in 12 patients (40%) with pernicious anemia. Fundal biopsy examinations showed atrophic gastritis in 30 patients (100%), intestinal metaplasia in 13 patients (43.3%), lymphoid follicle in 15 patients (50%), and dysplasia in 6 patients (20%). Antral biopsy examinations showed atrophic gastritis in 8 patients (26.6%), intestinal metaplasia in 8 patients (26.6%), lymphoid follicle in 8 patients (26.6%), and dysplasia in 3 patients (10%). The frequency of fundal inflammation, atrophy, intestinal metaplasia, lymphoid follicle, and dysplasia and antral intestinal metaplasia and mild antral dysplasia were found to be higher in those in the pernicious anemia group than in the nonulcer dyspeptic patients. Antral inflammation, atrophy, and moderate and severe antral dysplasia were found to be higher in those in the nonulcer dyspeptic group.
Conclusions. Particularly, fundal precancerous lesions were found to be more frequent in patients with pernicious anemia independent of H. pylori.     

The influence of the different morphological changes on gastric mucosa on somatostatin cell number in antrum mucosa and serum somatostatin

The aim of our paper was to investigate the influence of the different morphological changes on gastric mucosa on somatostatin D-cell number in antral mucosa and serum Somatostatin. We analyzed according to Sydney classification to what extent the severity of gastritis affect the observed hormonal values. somatostatin D-cell number in antral mucosa and serum Somatostatin values were compared between three groups of patients; mild, moderate and severe chronic gastritis. The average number of somatostatin cell in biopsy sample of antrum mucosa was 30.41 +/- 35.38 (N = 17) in the case of middle form, 18.69 +/- 26.65 (N = 56) in moderate and in severe case of chronic gastritis 5.23 +/- 5.93 (N = 7) cells in mm2 of mucosa. The level of somatostatin in the serum of middle form gastritis were 26.43 +/- 28.76, moderate 19.95 +/- 35.93 and severe 17.88 +/- 17.66 pg/mL. In order to determine the number of somatostatin cells in antrum mucosa and serum somatostatin with present morphological changes of mucosa, it might helpful to exclude the patients with non-ulcer dyspepsia, but with the higher risk of premalignant and malignant changes.     

Cell-specific processing of chromogranin A in endocrine cells of the rat stomach.

The rat stomach is rich in endocrine cells. The acid-producing (oxyntic) mucosa contains ECL cells, A-like cells, and somatostatin (D) cells, and the antrum harbours gastrin (G) cells, enterochromaffin (EC) cells and D cells. Although chromogranin A (CgA) occurs in all these cells, its processing appears to differ from one cell type to another. Eleven antisera generated to different regions of rat CgA, two antisera generated to a human (h) CgA sequences, and one to a bovine (b) CgA sequence, respectively, were employed together with antisera directed towards cell-specific markers such as gastrin (G cells), serotonin (EC cells), histidine decarboxylase (ECL cells) and somatostatin (D cells) to characterize the expression of CgA and CgA-derived peptides in the various endocrine cell populations of the rat stomach. In the oxyntic mucosa, antisera raised against CgA(291-319) and CGA(316-321) immunostained D cells exclusively, whereas antisera raised against bCgA(82-91) and CgA(121-128) immunostained A-like cells and D cells. Antisera raised against CgA(318-349) and CgA(437-448) immunostained ECL cells and A-like cells, but not D cells. In the antrum, antisera against CgA(291-319) immunostained D cells, and antisera against CgA(351-356) immunostained G cells. Our observations suggest that each individual endocrine cell type in the rat stomach generates a unique mixture of CgA-derived peptides, probably reflecting cell-specific differences in the post-translational processing of CgA and its peptide products. A panel of antisera that recognize specific domains of CgA may help to identify individual endocrine cell populations.     

Gastric inflammatory markers and interleukins in patients with functional dyspepsia, with and without Helicobacter pylori infection

Helicobacter pylori is the most important cause of gastritis, peptic ulcers and the development of gastric cancer. The chronic active inflammation is dominated by neutrophils, macrophages, lymphocytes and plasma cells. Several interleukins (IL-8, IL-10 and IFN-gamma) are involved in the inflammatory process in the gastric mucosa. The aim of this study was to investigate the gastric inflammation in patients with functional dyspepsia. Fifty-three consecutive patients were included and antral biopsies were obtained for histology, culture and immunohistochemistry. The sections were examined for the interleukins IL-4, IL-6, IL-8, IL-10 and IFN-gamma as well as for the cell markers CD4, CD8, CD14, Cd19, CD25 and CD30. Only CD4 and CD19 were significantly increased in patients with increased gastric inflammation and increased density of H. pylori. However, several of the examined markers (IFN-gamma, IL-8, IL-10 and CD14) showed a non-significant trend to be increased in patients with extensive gastric inflammation and high density of H. pylori. Therefore, an arbitrary index (IM11) for all the 11 immunological markers was made as an average value for each of the four morphological groups. For the four morphologically different groups of patients the values were 0.49, 0.77, 0.86 and 1.25, respectively. Significant increases in the index from none to moderate antral inflammation as well as the density of H. pylori were found (p<0.001). By using an index of inflammatory markers trends can be summarized and thereby significant which may be of importance when gastric inflammation is investigated in children and patients with functional dyspepsia.