Lamina Propria Of Gastric Mucosa Research Articles

Histopathological features of glandular atrophy of the lamina propria of the gastric mucosa during its occurrence and development

ObjectiveTo explore the histopathological features of glandular atrophy of the lamina propria of gastric mucosa during its occurrence and development.MethodWe performed detailed histological observation and immunohistochemical examination on the endoscopic biopsy and ESD endoscopic resection specimens of 896 patients with glandular atrophy of the lamina propria of gastric mucosa. The EnVision two-step method was used for immunohistochemical staining, and the slices were incubated with primary antibody CK7, CK20, villin, CDX2, MUC5AC, MUC6, p53 and ki-67. Hematoxylin staining was performed and observed under the microscope and statistically analyzed.ResultsIn the initial stage of glandular atrophy of the lamina propria, the proliferation area of the deep gastric pits, and the isthmus and neck of the gastric glands are characterized by roughly normal structure of the glandular structure, increased mesenchyme, and widened space between glands. Subsequently, the gland becomes smaller in volume and less in number, especially at the base, in the gastric glandular part of the gastric unit. The disease at this stage has higher incidence, and occurs more often in the elderly who account for 64.0% (573/896) of our study group. The disease in this stage may exhibit some lesions that are physiologic (age-related degeneration) while others are pathological. Therefore, this condition is called simple glandular atrophy of the lamina propria of the gastric mucosa. When the gastric mucosal epithelium is subjected to infection or repeated infections, chemical stimuli, immune factors, and genetic factors, it can lead to the proliferation and transformation of stem cells in the proliferation area of the deep gastric pits, and the isthmus and neck of the gastric glands, forming single ducts, multiple ducts, or a proliferation of patchy cells. Then, atypical hyperplasia (intraepithelial neoplasia) presents, finally leading to gastric adenocarcinoma.ConclusionUnderstanding the histopathological characteristics of glandular atrophy of the lamina propria of gastric mucosa is of great significance in controlling the occurrence and development of gastric cancer.

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.

Gastric Stem Cells Are Targeted in Upper Gastrointestinal GVHD

Introduction: Graft-versus-host disease (GVHD) is the major obstacle to perform allogeneic hematopoietic stem cell transplantation (SCT). We previously demonstrated that intestinal stem cells (ISCs) were targeted in lower gastrointestinal (GI) GVHD (Takashima et al, J Exp Med. 2011). However, it remains to be investigated whether gastric stem cells (GSCs) could be targeted in upper GI GVHD. We evaluated if leucine-rich repeat-containing G protein-coupled receptor (Lgr) 5+ GSCs, which replenish antrum and pyloric epithelium, could be damaged in GVHD. Wnt agonist R-Spondin 1 (R-Spo1), which binds to Lgr5, protects ISCs and ameliorates GVHD. We also evaluated if R-Spo1 could protect Lgr5+GSCs against GVHD.Methods: B6D2F1 mice (H-2b/d) were transplanted with 5 × 106 splenocytes plus 5 × 106 bone marrow cells from allogeneic B6 (H-2b) or syngeneic B6D2F1 donors following lethal X-ray total body irradiation on day 0 and histological evaluation of the pylorus and antrum of stomach and flow cytometric analysis of infiltrating donor T cells in the stomach were performed on day +7 after SCT. Recipients of SCT were intravenously injected with 100 μg/day of R-Spo1 from days -3 to -1 and days +1 to +3 after SCT, or naïve mice were injected with 200 µg/day of R-Spo1 for six days.Results: We investigated the fate of GSCs after SCT in Lgr5-creERT2 / eGFP B6D2F1 recipients. Immunofluorescent studies demonstrated development of gastric GVHD with significant donor T-cell infiltration in the lamina propria of gastric mucosa and cleaved-caspase-3+ apoptotic epithelial cells in the stomach of allogeneic animals, but not in syngeneic controls (Figure A). Numbers of Lgr5+ GSCs were significantly decreased in allogeneic recipients compared to those in syngeneic controls on day +7, suggesting that gastric GVHD targets Lgr5+ GSCs (Figure B). We then evaluated effects of R-Spo1 on GSCs. When injected to naïve B6D2F1 mice for 6 days, R-Spo1 significantly prolonged the crypt depth with an increase in numbers of Ki-67+ proliferating epithelial cells in the stomach. Fate mapping analysis using Lgr5-creERT2/eGFP × Rosa26Tomato mice, in which Lgr5+ GSCs and their progenies are labeled with tdTomato and Lgr5+ GSCs are labeled with eGFP, showed that R-Spo1 did not increase eGFP+ GSCs but significantly increased Ki67+ cells and tdTomato+ epithelial cells. These data suggested that R-Spo1 stimulated differentiation of Lgr5+ GSCs into mucosal epithelial cells. We then tested if GVHD prophylaxis with R-Spo1 protects GSCs and ameliorates gastric GVHD after allogeneic SCT. Immunofluorescent analysis showed that brief administration of R-Spo1 significantly suppressed infiltration of donor T-cells and epithelial apoptosis, and protected GSCs from GVHD 7 days after allogeneic SCT (Figure A, B).Conclusion: Lgr5+ GSCs are targeted in upper GI GVHD and R-Spo1 protects GSCs against GVHD after allogeneic SCT.Figure: After allogeneic SCT, cleaved-caspase-3+ apoptotic epithelium was significantly increased (A), and number of Lgr5+ GSCs was significantly decreased on day +7 (B). R-Spo1 inhibited epithelial apoptosis (A) and Lgr5+ GSC loss (B). [Display omitted] DisclosuresTeshima:Astellas: Research Funding; Kyowa-Hakko Kirin: Research Funding; Takeda: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; Novartis: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; Pfeizer: Research Funding; Chugai: Research Funding; Bristol-Myers Squibb: Research Funding.

The therapeutic effect of zerumbone on chronic gastritis via antioxidant mechanisms.

Effects of zerumbone on chronic gastritis remain unclear. The purpose of this study was to investigate the mechanism of the protective effect of zerumbone on the treatment of chronic gastritis in rats. The animal models of chronic gastritis in rats were established, and the surface damage of gastric mucosa was observed by gross anatomy; the changes of gastric mucosal tissue and surface morphology were observed by pathological sections of gastric mucosal tissues; the expressions of heme oxygenase-1 (HO-1) and nuclear factor E2-related factor 2 (Nrf-2) proteins of gastric mucosal tissues in each group were detected by western blot analysis; the activities of superoxide dismutase (SOD) and catalase (CAT) as well as the contents of reduced glutathione (GSH) and malondialdehyde (MDA) in gastric mucosal tissues were detected by kits. The results indicated that zerumbone could significantly relieve red and swelling as well as erosion of the gastric mucosal tissues in rats with chronic gastritis; zerumbone could significantly ameliorate the loose arrangement of cells in the lamina propria of gastric mucosa, epithelial cell deformation and abscission, and inflammatory cell infiltration. The results of western blot analysis showed that compared with the model group, zerumbone could significantly upregulate the expression of HO-1 and Nrf-2 in gastric mucosal tissues. Compared with the model group, the activities of SOD and CAT as well as GSH levels in gastric mucosal tissues of rats in the zerumbone groups were obviously increased, but MDA contents were significantly decreased. Zerumbone has a protective effect on chronic gastritis in rats, which is achieved by improving the antioxidant capacity of gastric mucosal tissues through inhibiting lipid peroxidation.

Glutathione levels modulation as a strategy in host-parasite interactions-insights for biology of cancer.

OPINION article Front. Pharmacol., 05 August 2014Sec. Experimental Pharmacology and Drug Discovery Volume 5 - 2014 | https://doi.org/10.3389/fphar.2014.00180

The "cavitary" type of angiogenesis by gastric cancer. Morphological characteristics and prognostic value.

The “cavitary” type of angiogenesis in patients with gastric cancer (GC) is described for the first time. Material and methods: The samples of tumour and adjacent gastric mucosa (GM) in 73 patients with GC who had undergone radical surgery were being studied. The sections were stained with hematoxylin and eosin (H&E) and immunohistochemically (IGH) using antibodies to CD34. Results: А new type of vessel formation consists of the appearance of cavitary structures (CS) in tumours and the adjacent GM, which are then lined by endothelial cells and merged into the blood vessels of the organ. We believe that the CS can be formed by means: 1) of the abruption of layers of epithelial cells (both normal and tumoral) from their underlying foundation and their desquamation into the lumen of the “obliterated” gastric glands (GG); 2) of the dilatation of the GG and thinning of their walls; 3) of the formation of “cavity” directly in the lamina propria of GM or in the tumoral stroma. It was noted that only the presence of multiple “cavitary” vessels (CV) of type-1 had been associated with the decrease of 3-year overall survival (OR=15,0, 95%CI=2,96-76,31) and relapse-free survival (OR=14,93, 95%CI=4,34-51,38). We also observed the improvement of the long-term outcomes in patients with GC having received antibacterial therapy (AT) before surgery that can be associated with its influence on the formation of CV type-1. Conclusion: The described new type of angiogenesis is of great clinical importance.

Iron medication-induced gastric mucosal injury

Severe gastrointestinal erosion, ulcer, necrosis and strictures after an acute iron overdose are well described. However, gastric mucosal injury in patients receiving therapeutic iron has received only scant recognition despite its wide use. We report a case of iron medication-induced gastric mucosal injury in a 76-year-old male who presented with iron deficiency anemia and had been taking ferrous sulfate tablet for 4 years. Esophagogastroduodenoscopy (EGD) revealed a pale, villous appearing flat lesion along the lesser curvature of gastric body. Histopathologic examination of EGD biopsies of the flat lesion showed brown crystalline materials deposited in the lamina propria of gastric mucosa, which was accompanied with fibrosis, chronic inflammation, and foreign body reaction. The crystalline materials were covered and admixed with gastric epithelium. Prussian blue iron stain confirmed that the brown crystalline materials were iron. The iron and hemosiderin accumulation was also seen in cytoplasm of epithelial cells and lumen of fundic gastric glands. The recognition and reporting by pathologists of iron-induced changes in EGD biopsies will alert clinicians to this underrecognized but easily correctable complication by alternative forms of iron therapy, such as liquid preparation.

SabA Is the H. pylori Hemagglutinin and Is Polymorphic in Binding to Sialylated Glycans

Adherence of Helicobacter pylori to inflamed gastric mucosa is dependent on the sialic acid–binding adhesin (SabA) and cognate sialylated/fucosylated glycans on the host cell surface. By in situ hybridization, H. pylori bacteria were observed in close association with erythrocytes in capillaries and post-capillary venules of the lamina propria of gastric mucosa in both infected humans and Rhesus monkeys. In vivo adherence of H. pylori to erythrocytes may require molecular mechanisms similar to the sialic acid–dependent in vitro agglutination of erythrocytes (i.e., sialic acid–dependent hemagglutination). In this context, the SabA adhesin was identified as the sialic acid–dependent hemagglutinin based on sialidase-sensitive hemagglutination, binding assays with sialylated glycoconjugates, and analysis of a series of isogenic sabA deletion mutants. The topographic presentation of binding sites for SabA on the erythrocyte membrane was mapped to gangliosides with extended core chains. However, receptor mapping revealed that the NeuAcα2–3Gal-disaccharide constitutes the minimal sialylated binding epitope required for SabA binding. Furthermore, clinical isolates demonstrated polymorphism in sialyl binding and complementation analysis of sabA mutants demonstrated that polymorphism in sialyl binding is an inherent property of the SabA protein itself. Gastric inflammation is associated with periodic changes in the composition of mucosal sialylation patterns. We suggest that dynamic adaptation in sialyl-binding properties during persistent infection specializes H. pylori both for individual variation in mucosal glycosylation and tropism for local areas of inflamed and/or dysplastic tissue.

Immunohistochemical demonstration of human circulating antibodies against lamina propria of gastric mucosa

This paper describes a fluorescent pattern of human antibodies circulating in the serum of a 57 year old patient with lymphogranulomatosis. Following incubation with different FITC-labeled anti-human IgG sera including F(ab)2-fragments and with antibodies to human IgA, IgM, IgD, IgE as well as guinea pig serum and FITC-labeled anti-guinea pig serum (for proof the complement binding), it can be assumed that this is a non complement binding IgG antibody directed first of all against the rat gastric mucosal lamina propria (in the cardia and corpus and weaker in the pylorus region). The titre was 1:640. 1:80 diluted serum did not react with duodenum, jejunum, colon, tongue, oesophagus, parotid gland, trachea, lung, heart, diaphragm, liver, spleen, or kidneys. Among others, the species specificity and the antigen binding sides remain to establish.

The interaction between Walker tumour cells and mucosa cells in the lamina propria of gastric mucosa in rats. The tumour behaviour in previously X-irradiated mucosa compared to normal mucosa.

One series of 12 rats was exposed to X-irradiation (1500 R) of the stomach 19 days before implantation of Walker tumour cells in the gastric mucosa, and the frequency of tumour take and the extent of tumour growth after 10 days were compared with a second series with the same tumour implantation, but without X-ray exposure. In a third series simple gastric ulcers without tumour were produced by clamping the gastric wall with a heated (80 degrees) surgical needle holder, and the animals were killed 5-7 day later. All the rats were given injections of vinblastine sulfate 3 hours and of 3H-TDR 1 hour before sacrifice. In viewfields with diameter 180 mu the vinblastine-arrested mitoses and labelled cells on the tumour side of the tumour/mucosa border were calculated as percentages of all tumour cells. In the mucosa the total number of proliferating cells was counted at various distances from the border of the tumour or ulcer. No clear differences in the frequency of tumour take and the extent of tumour growth were found between the X-irradiated and the normal rat stomachs, and it is concluded that the X-ray exposure 3 weeks prior to tumour implantation did not reduce the normal mucosal resistance to tumour growth. The percentage of arrested mitoses and labelled cells in the tumour decreased one view field away from the mucosal border, and the number of proliferating cells in the mucosa bordering on the tumours showed a gradual fall with increasing distance up to 0.8-1.0 mm from the tumour border; within these distances, however, the numbers were much higher than at corresponding distances from edges of the ulcers. The Walker tumour thus seems to stimulate cell proliferation in mucosa to a much greater extent than a simple ulcer does. The causes of this phenomenon and the possible roles of "chalones" or "anti-chalones" are discussed.