Gastric Mucosa In Chronic Gastritis Research Articles

CDX2 protein distribution in the gastric mucosa in chronic gastritis by a semi-quantitative index and its reproducibility

Introduction The Cdx2 gene provides an intestinal differentiation of epithelial cells and plays an oncosupressive role. An indirect method of the Cdx2 gene expression assessment is the immunohistochemical study of its product, the CDX2 protein. Therefore, the common approach to the immunohistochemical study of the CDX2 protein hasn’t been developed yet. A semi-quantitative CDX2 index based on the percentage of CDX2-positive cells in the tissue specimen, the staining intensity and an expression pattern has been proposed.The purpose of the study was to assess the reproducibility of the semi-quantitative CDX2 index calculation in chronic atrophic gastritis stages I-IV.Materials and methods 20 chronic atrophic gastritis cases (5 cases for each stage of the gastritis according to the Operative link for gastritis assessment system) were taken according to the Maastricht V protocol and examined by the immunohistochemical method (CDX2, clone EPR2764Y, ready to use). The reproducibility of the CDX2 semi-quantitative index was assessed by five pathologists. An agreement between observed raters was measured by the kappa statistics.Results The Cohen’s κ value is 0,8 for unweighted κ and 0,97 for weighted κ (extremely high level of agreement) for the semi-quantitative CDX2 index calculation.Discussion The least reproducible parameter used for the semi-quantitative CDX2 index calculation the percentage of CDX2-positive cells because of the subjective assessment. The Cohen’s weighted κ value was higher compared to the unweighted κ because of the close yet not similar CDX2 semi-quantitative index values calculated by pathologists.Conclusion The semi-quantitative CDX2 index can be used to rank CDX2 expression and has a high level of reproducibility.

PDCD4 and CDX-2 as immunohistochemical markers of gastric mucosa atrophy in chronic gastritis

Introduction Diagnosis of the gastric mucosa atrophy represents an important problem, the solution of which depends on the possibility of secondary prevention of gastric cancer. A possible way of solution is the use of immunohistochemical markers - proteins associated with cellular remodeling of gastric mucosa, PDCD4 and CDX2.The aim of the work is to evaluate the possibility of using immunohistochemical markers PDCD4 and CDX-2 to diagnose atrophy of the gastric mucosa in chronic gastritis and increase the informative value of biopsy examination.Materials and method The object of the study was 155 cases of biopsy examination of the gastric mucosa of patients with chronic gastritis (5 fragments per case − 775 biopsy specimens). A comparative semi-quantitative assessment of immunohistochemical expression of CDX2, PDCD4 at different stages of chronic gastritis was performed. Spearman correlation coefficient was used to assess correlation relationship.Results There were no statistically significant differences in the level of PDCD4 in studied samples depending on the stage of chronic gastritis, p=0.06. Statistically significant increase of CDX2sum index in progressing stage of chronic atrophic gastritis (p=0.005), demonstrated a pronounced positive correlation r=0.70 (p<0.01).Discussion According to the results obtained, it is shown that the decline in PDCD4 protein does not occur with the progression of atrophy severity. Complementary use of immunohistochemical marker CDX2 is able to give an idea of the presence and severity of both metaplastic and absolute atrophic changes in the gastric mucosa.Conclusion Equally high level of PDCD4 protein index in the gastric mucosa at different stages of chronic gastritis excludes the possibility of its use as an immunohistochemical marker of atrophy. Semi-quantitative immunohistochemical index of CDX2 protein can be used as an additional marker in decision support system for assessment of atrophic changes in gastric mucosa.

Morphofunctional state of the gastric mucosa in children with chronic gastritis and the persistence of Epstein-Barr virus

The aim is to establish the effect of the persistence of the Epstein-Barr virus on the morphofunctional state of the gastric mucosa in chronic gastritis in children. Methods. 324 children aged 6—16 years with chronic gastritis were examined. We analyzed clinical and anamnestic data, the results of esophagogastroduodenoscopy with biopsy, genetic typing of Hp with the identification of pathogenicity genes VacA, CagA, IceA, BabA. The persistence of the Epstein-Barr virus was determined by the detection of its DNA in the materials of gastrobiopsy. The titer of class G antibodies to gastric parietal cells was studied in 110 patients.The results of the study. In children with chronic gastritis, Epstein-Barr virus was detected in the gastric mucosa in 49.1% of cases. In these patients, its colonization by highly pathogenic Hp strains was detected 1.8 times more often than in patients who had no infection with this virus. The persistence of the Epstein-Barr virus contributed to an increase in the severity of inflammation, the appearance of signs of indefinite atrophy of the mucous membrane and in the absolute majority of children was not accompanied by an increase in the titer of antibodies to the parietal cells of the stomach.Conclusion. The persistence of Epstein-Barr virus in the gastric mucosa in chronic Hp-associated gastritis contributes to its infection with highly pathogenic Hp strains and severe inflammation. No data have been obtained indicating the role of Epstein-Barr virus in the formation of atrophic or autoimmune gastritis in childhood.

Клинические проявления и эндоскопически-гистологические изменения у детей с хроническим гастритом, индуцированным Helicobacter pylori, с разной токсигенностью

Актуальность. Инфекция Helicobacter pylori является важным фактором хронического гастрита (ХГ) и дуо­денальной язвы у детей. За последнее десятилетие установлена разная вирулентность штаммов H.pylori, которая зависит от его генов токсигенности. Цель: изучить клинические проявления, эндоскопические и гистологические изменения слизистой оболочки желудка (СОЖ) у детей с хроническим гастритом, индуцированным H.pylori, с разной его токсигенностью. Материалы и методы. Проведено клинико-инструментальное обследование 136 детей с хроническим гастритом, индуцированным H.pylori, в возрасте 7–17 лет (основная группа) и 30 здоровых детей этого же возраста (контрольная группа). Пациенты были разделены на 2 группы: IА группу составили 72 ребенка с хроническим гастритом, индуцированным H.pylori CagA «+»; IБ группу — 64 ребенка с хроническим гастритом, индуцированным H.pylori CagA «–», по результатам определения суммарных антител IgG к антигену CagA сыворотки крови и/или определения антигена CagA в биоптатах СОЖ методом полимеразной цепной реакции. Изучали и анализировали клинические проявления, эндоскопические и гистологические изменения слизистой оболочки желудка. Статистическая обработка проводилась с помощью пакета статистических программ Statgrafics 16.0. Результаты. У детей с ХГ, индуцированным H.pylori CagA «+» (IА группа), клинические проявления болевого абдоминального и диспептического синдромов существенно не отличаются от таковых у детей с ХГ, индуцированным H.pylori CagA «–» (ІБ группа). Не выявлены существенные эндоскопические изменения в виде эритематозной гастропатии и антральной нодулярности как у детей с ХГ, индуцированным H.pylori CagA «+», так и у детей с ХГ, индуцированным H.pylori CagA «–». Гистологические изменения в ІА и ІБ группах были разные: детям с ХГ, индуцированным H.pylori CagA «+», свойственны II и I степень активности воспаления и ІІ, І, ІІІ степени обсемененности Н.pylori слизистой оболочки желудка, а детям с ХГ, индуцированным H.pylori CagA «–», свойственны I, II степень активности воспаления слизистой оболочки желудка и II и I степень обсемененности Н.pylori. Выводы. Клиническими проявлениями ХГ, индуцированного H.pylori, у детей в стадии обострения является эпигастральная боль, симптомы диспепсии и хронического интоксикационного синдрома. Эндоскопическими проявлениями являются эритематозная гастропатия и/или антральная нодулярнисть. У детей с ХГ, индуцированным H.pylori СagA «+», и у детей с ХГ, индуцированным H.pylori СagA «–», по клиническим и эндоскопическим проявлениям существенного различия не выявлено. Гистологическим изменением СОШ при ХГ, индуцированном H.pylori, в стадии обострения является диффузная лимфоцитарно-плазмоцитарная инфильтрация собственной пластинки СОЖ с нарушением эпителия. При ХГ, индуцированным H.pylori СagA «+», преобладает II и III степень обсеменения H.pylori в сочетании с I и II степенью активности воспаления СОЖ. При ХГ, индуцированном H.pylori СagA «–», преобладает II и I степень обсеменения H.pylori СОЖ. У детей с ХГ, индуцированным H.pylori, целесообразно диагностировать его токсигенность CagA «+» для оценки H.pylori CagA-статуса ребенка.

Analysis of gastroscopy results among healthy people undergoing a medical checkup: a retrospective study

BackgroundThe association of upper gastrointestinal endoscopic findings with sex, age, and Helicobacter pylori infection in asymptomatic healthy people is unclear. The aim of this study was to retrospectively determine the associations of upper gastrointestinal endoscopic findings in asymptomatic healthy people with sex, age, and H. pylori infection.MethodsA retrospective study was conducted on 2923 patients from a health examination center in Xiangya Hospital between September 2015 and September 2019. Data on sex, age, H. pylori infection, and gastroscopy results were collected.ResultsAmong 2923 asymptomatic patients who underwent gastroscopy, 2911 (99.59%) had abnormal results. The top three results were chronic gastritis (95.11%), peptic ulcer (17.45%), and duodenitis (9.17%). Inflammation of the gastric mucosa in chronic gastritis was more severe in the H. pylori-positive group. The incidence of peptic ulcer decreased with increasing age and was higher in men, patients aged < 30 years, and H. pylori-positive patients. The incidence of polyps was higher in women (9.54%) than in men (5.94%), and the incidence in individuals aged ≥60 years (11.63%) was higher than that in those aged < 60 years (6.83%). The pathological results of gastric polyps depended on the location of the lesion.ConclusionThe incidence of abnormal upper gastrointestinal endoscopic results is high in asymptomatic healthy people undergoing a check-up and is associated with sex, age, and H. pylori infection. Gastroscopy should be considered part of a routine health check.

The Mechanisms of Sijunzi Decoction in the Treatment of Chronic Gastritis Revealed by Network Pharmacology.

Chronic gastritis is characterized by inflammation in the gastric mucosa with a vicious circle in inflammatory cells and inflammatory mediators. Stomach adenocarcinoma would occur in the metaplastic gastric mucosa of chronic gastritis. Sijunzi decoction is a famous classical formula for the treatment of chronic gastritis. Although previous studies revealed some functions of Sijunzi decoction in treating chronic gastritis, the underlying mechanisms have not been illustrated clearly. In this study, we used network pharmacology to investigate the mechanism of Sijunzi decoction in treating chronic gastritis. Firstly, online datasets TCMSP, SWISS, and DisGeNET were used to investigate the functional mechanism of Sijunzi decoction against chronic gastritis and 18 genes were identified as targets of Sijunzi decoction in chronic gastritis. These 18 genes can be categorized into immunologically related genes and cancer-related genes. GO analysis showed that the 18 target genes were mainly enriched in angiogenesis, nitric oxide biosynthetic process, ERK1 and ERK2 cascade, cellular response to drug, and MAPK cascade. So, Sijunzi decoction alleviated chronic gastritis by inhibiting the local inflammatory response. Furthermore, we also investigated the impact of Sijunzi decoction on the peripheral blood leukocytes with our own RNA sequencing (RNA-seq) data of 11 chronic superficial gastritis patients. 102 differentially expressed genes (DEGs) were identified by comparing RNA-seq data of chronic superficial gastritis patients with healthy control groups. After performing a functional analysis on 102 DEGs and Sijunzi decoction potential targets and taking the intersection of these pathways, we found that platelet activation, angiogenesis, and pathways in cancer were candidate target pathways regulated by Sijunzi decoction. Thus, Sijunzi decoction also alleviates chronic gastritis by suppressing inflammatory response of peripheral blood leukocytes. Our results showed that Sijunzi decoction can ameliorate the local gastric inflammation and inflammations in peripheral blood leukocytes and might also reduce the incidence of stomach cancer in chronic gastritis.

Rotective effect of Fengliao-Changweikang extracts, a traditional Chinese herbal medicine formula,on mucosa in rat with chronic gastritis

Background: Fengliao-Changwei-Kang(FCK), the Chinese patent drug, is a famous traditional Chinese herbal medicine formula. It has a significant effect on the clinic treatment of gastrointestinal diseases including gastritis, enteritis and diarrhea for many years. However, there is few research on the protective effects of FCK on the gastric mucosa of chronic gastritis (CG) model rat. Objective: The present study aimed to explore the effects of FCK extract on mucosa in rats with Chronic Gastritis.Materials and Methods: 50 SD mice were randomly divided into 5 groups with 10 in each group（five per sex). The groups are respectively control group, model group, low, middle and high FCK extracts (FCK I, II and III) group. The CG rat model was induced by synthetic methods. FCK I, II and III group were administrated with FCK extracts at 2.16g• kg, 4.32g• kg, 8.94g• kg once per day for 21 consecutive days, and the control group and model group were administrated the same volume of distilled water at 10mL/kg once per day. 16 hours after the last administration, the rats were anesthetized and their blood and stomach were drawn from vena cava and abdominal cavity. The serum levels of EGF was measured by enzyme linked immunosorbent assay(ELISA) method, the expression of growth factor receptor (EGFR) in gastric mucosa was detected by immunohistochemical method, and the mRNA expressions of NF-κB p65 was detected in-situ hybridization.Results: The inflammation grades and the expressions of NF-κB p65 mRNA in gastric mucosa of the model group were markedly higher than those of the control group (P&lt;0.05). The inflammation grades of gastric mucosa and the expressions of NF-κB p65 mRNA in gastric mucosa the FCK extract group are significantly lower than those of the model group, and the FCK extract group at 8.64g/kg could greatly increase the serum levels of EGF and the expressions of EGFR in gastric mucosa. High EGF level was found in FCK extract group at 4.32g/kg, but low in FCK extract groups at 2.16g/kg. There were no marked differences among the rats from control group, model group and FCK extract group on ratio of Ll/L2 (P&gt;0.05).Conclusions: FCK extract could alleviate mucosal inflammation by down regulating the expressions of NF-κB p65 mRNA and promote tissue repair by up regulating EGFR expression in gastric mucosa cell.Keywords: chronic gastritis; fengliao-changwei-kang extract; epidermal growth factor receptor; nuclear factor kappa B.

PROTECTIVE EFFECT OF FENGLIAO-CHANGWEIKANG EXTRACTS, A TRADITIONAL CHINESE HERBAL MEDICINE FORMULA,ON MUCOSA IN RAT WITH CHRONIC GASTRITIS

Background: Fengliao-Changwei-Kang(FCK), Chinese patent drug, is a famous traditional Chinese herbal medicine formula, which is effectively used to cure gastrointestinal disease including gastritis, enteritis and diarrhea in the clinic for many years. However, little research has been focused on the protective effects of FCK on the gastric mucosa of chronic gastritis (CG) model rat.&#x0D; Objective: The present study aimed to explore the effects of FCK extract on mucosa in rats with Chronic Gastritis.&#x0D; Materials and Methods: The CG rat model was induced by synthetic methods. The serum levels of EGF was measured by enzyme linked immunosorbent assay(ELISA) method, the expression of growth factor receptor (EGFR) in gastric mucosa was detected by immunohistochemical method, the mRNA expressions of NF-κB p65 was detected in-situ hybridization.&#x0D; Results: In the model group, the inflammation grades of gastric mucosa and the expressions of NF-κB p65 mRNA in gastric mucosa were markedly higher than those of the control group (P0.05).&#x0D; Conclusions: FCK extract could alleviate mucosal inflammation by down regulating the expressions of NF-κB p65 mRNA and promote tissue repair by up regulating EGFR expression in gastric mucosa cell.

Association of Helicobacter pylori and iNOS production by macrophages and lymphocytes in the gastric mucosa in chronic gastritis.

Helicobacter pylori is one of the most common causes of chronic gastritis. With the development of the disease cellular inflammatory infiltrates composed of lymphocytes, plasma cells, and macrophages are formed in epithelium and lamina propria of the stomach. These cells are capable of secreting a number of active substances, including inducible nitric oxide synthase (iNOS). We examined the relationship between H. pylori and secretion of iNOS by cells of inflammatory infiltrates in chronic gastritis by light microscopy and immunohistochemistry. The data obtained indicate that stimulation of H. pylori immune system cells of the host organism during development of chronic gastritis causes increase in number of macrophages and lymphocytes in the inflammatory infiltrate of the gastric mucosa. This is accompanied with increased expression of inducible NO-synthase with excess free radicals in the tissues, which leads to secondary alterations and exacerbates the inflammation with impaired regeneration processes.

Reduced Expression of Sulfatides and Galactosylceramide 3′-Sulfotransferase in the Gastric Mucosa of Chronic Gastritis

Sulfatides highly expressed in the normal gastric mucosa play important roles in gastric mucosal protection. However, it is unknown whether the sulfatides expression changes in chronic gastritis. Sulfatides expression levels were examined with immunohistochemical staining in 77 specimens obtained from resected human stomachs, followed by the measurement of optical density of the staining under digital microscopy. For mRNA expression analysis of GalCer (galactosylceramide)-sulfotransferase and arylsulfatase A using a quantitative real time reverse transcription-polymerase chain reaction, 64 biopsy specimens were endoscopically taken from the gastric corpus of out patients. Mucosal changes were scored under microscopic observations according to the updated Sydney System classification. The sulfatides expression decreased along with the progression of mucosal atrophy and lymphocytes infiltration, and was barely observed in intestinal metaplasia. The mRNA expression of GalCer-sulfotransferase, a biosynthetic enzyme for sulfatides, also decreased along with the progression of mucosal atrophy and lymphocytes infiltration. In contrast, mRNA expression of arylsulfatase A, which degrades sulfatides, was not altered. Expression of sulfatides and GalCer-sulfotransferase in the gastric mucosa of chronic gastritis is selectively reduced according to the mucosal atrophy and inflammation. Decreased expression of sulfatides may attribute to the deterioration of mucosal protection in chronic gastritis.

Gastric mucosal fibrosis: a novel explanation for dyspepsia

The etiology of functional dyspepsia has not been discerned yet which has led to inadequate treatment of this disease. It remains a common disorder with expensive and yet often ineffective therapy. We propose that the pathogenesis of this disease lies in the histological and ultrastructural changes inflicted on the gastric mucosa in chronic gastritis and fibrosis. This hypothesis, if substantiated will provide for therapy which will be based on the pathogenesis of the disease and which will be cheaper and easily available to most. It will also add impetus to the early eradication of Helicobacter pylori, which would prevent chronic gastritis and hence gastric fibrosis.

Enhanced expression of inducible nitric oxide synthase in chronic gastritis with intestinal metaplasia.

Nitric oxide produced by inducible nitric oxide synthase (iNOS) has been claimed to be involved in gastritis; however, its characteristics are largely unknown. We assessed (1) iNOS expression in the human gastric mucosa in chronic gastritis and (2) the cytokines associated with iNOS expression. Gastric biopsy specimens were obtained from patients with chronic gastritis. Total RNA was isolated and reverse transcription-polymerase chain reaction (PCR) was performed semiquantitatively using specific primer sets for iNOS, interleukin (IL)-1beta, IL-8, IL-6, interferon-y, tumor necrosis factor-alpha (TNF-alpha), TNF receptors, IL-6 receptors, and sucrase, respectively. Helicobacter pylori infection was examined by the PCR assay. Reverse transcription-PCR analysis showed that expression of iNOS was detected in 10 of 23 samples. Expression of iNOS mRNA was closely correlated with expression of TNF-alpha and was observed frequently in subjects with intestinal metaplasia. The Helicobacter pylori gene was detected by PCR assay in all iNOS-positive cases. These results indicate that iNOS is predominantly expressed in the gastric mucosa with intestinal metaplasia and H. pylori infection. TNF-alpha is thought to be an important cytokine associated with iNOS expression.

Relation of Helicobacter pylori to the human gastric mucosa in chronic gastritis of the antrum.

The spatial relations between bacteria and the affected tissues can indicate pathogenic mechanisms. This study was undertaken to define the spatial relation of Helicobacter pylori to the human gastric mucosa. Antibodies against gastric mucus and ruthenium red were used to stabilise the glycoprotein structure of the mucus and glycocalyces in antral biopsy specimens from eight patients infected with H pylori. The location of organisms and ultrastructural features were assessed using systematic scanning and transmission electron microscopy: 92 (2)% (mean (SE] of H pylori were in the pit mucus, and 7 (3)% were in the surface mucus; 60 (12)% of H pylori were close to epithelial cells, with only 5 (2)% located near the epithelial intercellular junctions. Fine filamentous strands extended between organisms and nearby epithelial cells, with few organisms in membrane to membrane contact. H pylori were not observed between, beneath, or within cells of the gastric mucosa. The preferred location of H pylori in the gastric antrum is within the pit mucus close to the epithelial cell surface, with no evidence that they have a direct toxic effect on the mucosa.

慢性萎縮性胃炎における組織性カリクレインの消長

We measured amount of tissue kallikrein of gastric mucosa in 39 patients of chronic gastritis by sandwich type enzyme linked immunosorbent assay (S-ELISA) . Amount of tissue kallikrein was 9.1±4.4 ng/g tissue (mean±S.E.) in gastric mucosa of gastric glands, and was about twenty five times as much as it in the parts of atrophic gastric mucosa of them. The quantity of kallikrein was in proportion to age and the extent of atrophic gastritis. It was speculated that tissue kallikrein would participate in inflammatory atrophic change of gastric mucosa in chronic gastritis.

Cells with features of chief and parietal cells in the human gastric mucosa in chronic gastritis

Cells with features of chief and parietal cells in the human gastric mucosa in chronic gastritis

3H-thymidine autoradiographic studies on the human gastric mucosa of chronic gastritis and normal stomach —New incubation method using physical pressure—

3H-thymidine autoradiographic studies on the human gastric mucosa of chronic gastritis and normal stomach —New incubation method using physical pressure—