Antigastric autoantibodies in Helicobacter pylori infection: implications of histological and clinical parameters of gastritis.
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ABSTRACT:
SUBMITTER: Faller G
PROVIDER: S-EPMC1891571 | biostudies-other | 1997 Nov
REPOSITORIES: biostudies-other
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Project description:Background:Helicobacter pylori (H. pylori) is a common and universally distributed bacterial infection. However, in children, active gastritis and ulcer are rarely seen. Objectives:The aims of this study were to establish the prevalence of H. pylori infection and to compare the clinical, endoscopic, and histopathological findings between infected and noninfected pediatric patients at Makassed General Hospital. Methods:Patients aged between 1 month and 17 years who underwent upper gastrointestinal endoscopy from January 2011 to January 2017 were included. The diagnosis of H. pylori was confirmed by a CLO test and/or its presence on biopsy specimens. Demographic data, clinical characteristics, endoscopic and histopathological findings, and gastritis score were recorded retrospectively. Results:During the study period, 651 children underwent upper gastrointestinal endoscopy. The main indication was abdominal pain (61%). The prevalence of H. pylori infection was 16.5%. The infection was most commonly seen among children aged between 6 and 10 years (43%). A large number of family members were associated with increased risk of infection (4.8 ± 1.5 versus 5.2 ± 1.8; p < 0.05). Epigastric pain was more associated with H. pylori (61.3% versus 14.6% in noninfected patients; p < 0.05). Nodular gastritis was commonly seen in infected patients (41.5% vs. 7.9%; p < 0.05). Mild and moderate gastritis was seen more in infected versus noninfected patients (mild: 53.8% vs. 14%; moderate: 27.4% vs. 2.4%, respectively). Conclusion:Although epigastric pain was associated with H. pylori, other diagnoses should be considered since the infection are rarely symptomatic in children. Antral nodularity was associated with H. pylori infection; however, its absence does not preclude the diagnosis.
| S-EPMC7238322 | biostudies-literature
Project description:The molecular mechanism responsible for Helicobacter pylori infection-mediated gastritis and carcinogenesis is not yet clear. Increased evidence suggests that chronic gastritis and elevated gastric epithelial cell (GEC) apoptosis are crucial events during stomach carcinoma transformation. PUMA is a potent proapoptotic Bcl-2 protein and mediates acute tissue injury. In this study, we aimed to investigate the role of PUMA in GEC apoptosis and inflammation induced by H. pylori infection. As a result, we found that PUMA expression was elevated in gastritis tissues compared with uninvolved tissues, and it was correlated with the severity of apoptosis and gastritis. In mice, PUMA mRNA and protein were markedly induced in GECs upon induction of gastritis by H. pylori. PUMA-deficient mice were highly resistant to apoptosis and gastritis induced by H. pylori. Furthermore, the transcription factor NF-?B p65 binds to PUMA promoter to activate PUMA transcription after H. pylori infection. In addition, NF-?B inhibitor could rescue H. pylori-induced apoptosis and gastritis. Finally, H. pylori-induced activation of p-p65 and PUMA was mediated via Toll-like receptor 2 (TLR2) and blocked in TLR2 knockout mice. Taken together, these results verified the pro-inflammatory effect of PUMA in H. pylori-infected gastric tissue. Moreover, TLR2/NF-?B-mediated transcriptional regulation of PUMA contributes to the pathogenesis of H. pylori-infected gastritis.
| S-EPMC7033162 | biostudies-literature
Project description:The interleukin-17 (IL-17) family of cytokines (IL-17A to IL-17F) is involved in many inflammatory diseases. Although IL-17A is recognized as being involved in the pathophysiology of Helicobacter pylori-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specimens. IL-17C mRNA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsy specimens. This was confirmed by quantitative reverse transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in H. pylori-infected gastric biopsy specimens was predominantly localized to epithelial and chromogranin A-positive endocrine cells. IL-17C mRNA levels were also significantly greater among cagA-positive than cagA-negative H. pylori infections (P = 0.012). In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with cagA-positive infections compared to cells infected with either cagA-negative or cag pathogenicity island (PAI) mutant. Chemical inhibition of I?B kinase (IKK), mitogen-activated protein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion, H. pylori infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of H. pylori-induced diseases remains to be determined.
| S-EPMC5607407 | biostudies-literature
Project description:AimTo investigate and elucidate the molecular mechanism underlying varioliform gastritis for early detection, prevention and intervention of gastric cancer.MethodsA combination of two-dimensional gel electrophoresis and mass spectrometry was used to detect the differentially expressed proteins between varioliform gastritis and matched normal mucosa. The selected proteins were confirmed by Western blotting and reverse transcription polymerase chain reaction (RT-PCR) in additional samples and the function of some proteins in varioliform gastritis was analyzed by bio-method preliminarily.ResultsWe identified 21 differentially expressed proteins in varioliform gastritis, and compared them with matched normal mucosa. Eleven proteins were upregulated and ten downregulated in varioliform gastritis when compared with the same proteins in individual-matched normal gastric mucosa. These proteins are related to metabolism, oxidation, cytoskeleton, apoptosis, signal transduction and other aspects of cells. Two novel proteins, thioredoxin domain-containing protein 5 (TXNDC5) upregulated in varioliform gastritis, and neuropolypeptide h3 [phosphatidylethanolamine-binding protein 1 (PEBP1)] downregulated in varioliform gastritis, were further investigated. Their expressions were validated by Western blotting and RT-PCR in 12 cases of varioliform gastritis which was matched with normal mucosa. The expression level of PEBP1 in varioliform gastritis was significantly lower (P < 0.05) while that of TXNDC5 was significantly higher than that in matched normal gastric mucosa (P < 0.05).ConclusionThere are some changes of protein expression in varioliform gastritis. Downregulation of PEBP1 and upregulation of TXNDC5 are involved in the development of varioliform gastritis.
| S-EPMC2915426 | biostudies-literature
Project description:ObjectiveThe present study aims to investigate the effect of Helicobacter pylori (Hp) infection on gastric mucosal microbiota in patients with chronic gastritis.MethodsHere recruited a population of 193 patients with both chronic gastritis and positive rapid urease, including 124 patients with chronic atrophic gastritis (CAG) and 69 patients with chronic non-atrophic gastritis (nCAG). Immunoblotting was used to detect four serum Hp antibodies (UreA, UreB, VacA and CagA) to determine the types of virulent Hp-I and avirulent Hp-II infections. Gastric microbiota was profiled by 16S rRNA gene V3-V4 region, and R software was used to present the relationship between the microbial characteristics and the type of Hp infection.ResultsIn the stomach of patients with Hp-positive gastritis, the dominant gastric bacterial genera included Ralstonia (23.94%), Helicobacter (20.28%), Pseudonocardia (9.99%), Mesorhizobium (9.21%), Bradyrhizobium (5.05%), and Labrys (4.75%). The proportion of Hp-I infection was significantly higher in CAG patients (91.1%) than in nCAG patients (71.0%) (P < 0.001). The gastric microbiota richness index (observed OTUs, Chao) was significantly lower in CAG patients than in nCAG patients (P <0.05). Compared with avirulent Hp-II infection, virulent Hp-I infection significantly decreased the Shannon index in CAG patients (P <0.05). In nCAG patients, Hp-I infected patients had lower abundances of several dominant gastric bacteria (Aliidiomarina, Reyranella, Halomonas, Pseudomonas, Acidovorax) than Hp-II infected patients. Meanwhile, in CAG patients, Hp-I infected patients occupied lower abundances of several dominant oral bacteria (Neisseria, Staphylococcus and Haemophilus) than Hp-II infected patients. In addition, bile reflux significantly promoted the colonization of dominant oral microbiota (Veillonella, Prevotella 7 and Rothia) in the stomach of CAG patients. There was no significant symbiotic relationship between Helicobacter bacteria and non-Helicobacter bacteria in the stomach of nCAG patients, while Helicobacter bacteria distinctly linked with the non-Helicobacter bacteria (Pseudolabrys, Ralstonia, Bradyrhizobium, Mesorhizobium and Variovorax) in CAG patients.ConclusionsVirulent Hp infection alters the gastric microbiota, reduces microbial diversity, and enhances the symbiotic relationship between the Helicobacter bacteria and non-Helicobacter bacteria in patients with chronic gastritis. The data provides new evidence for treating Hp infection by improving the gastric microbiota.
| S-EPMC10470091 | biostudies-literature
Project description:ObjectiveTo present results of the Kyoto Global Consensus Meeting, which was convened to develop global consensus on (1) classification of chronic gastritis and duodenitis, (2) clinical distinction of dyspepsia caused by Helicobacter pylori from functional dyspepsia, (3) appropriate diagnostic assessment of gastritis and (4) when, whom and how to treat H. pylori gastritis.DesignTwenty-three clinical questions addressing the above-mentioned four domains were drafted for which expert panels were asked to formulate relevant statements. A Delphi method using an anonymous electronic system was adopted to develop the consensus, the level of which was predefined as ≥80%. Final modifications of clinical questions and consensus were achieved at the face-to-face meeting in Kyoto.ResultsAll 24 statements for 22 clinical questions after extensive modifications and omission of one clinical question were achieved with a consensus level of >80%. To better organise classification of gastritis and duodenitis based on aetiology, a new classification of gastritis and duodenitis is recommended for the 11th international classification. A new category of H. pylori-associated dyspepsia together with a diagnostic algorithm was proposed. The adoption of grading systems for gastric cancer risk stratification, and modern image-enhancing endoscopy for the diagnosis of gastritis, were recommended. Treatment to eradicate H. pylori infection before preneoplastic changes develop, if feasible, was recommended to minimise the risk of more serious complications of the infection.ConclusionsA global consensus for gastritis was developed for the first time, which will be the basis for an international classification system and for further research on the subject.
| S-EPMC4552923 | biostudies-literature
Project description:We used 10X 5' single cell RNA sequencing (scRNAseq) technology to examine the transcriptional profiles of distinct gastric metaplastic cell types within the gastric corpus of mice chronically infected with Helicobacter pylori or chronically inflamed with autoimmune gastritis and humans with autoimmune gastritis.
2024-09-25 | GSE271866 | GEO
Project description:Chronic atrophic gastritis (CAG) is a very common gastritis and one of the major precursor lesions of gastric cancer, one of the most common cancers worldwide. The molecular mechanism underlying CAG is unclear, but its elucidation is essential for the prevention and early detection of gastric cancer and appropriate intervention. A combination of two-dimensional gel electrophoresis and mass spectrometry was used in the present study to analyze the differentially expressed proteins. Samples from 21 patients (9 females and 12 males; mean age: 61.8 years) were used. We identified 18 differentially expressed proteins in CAG compared with matched normal mucosa. Eight proteins were up-regulated and 10 down-regulated in CAG when compared with the same amounts of proteins in individually matched normal gastric mucosa. Two novel proteins, proteasome activator subunit 1 (PSME1), which was down-regulated in CAG, and ribosomal protein S12 (RPS12), which was up-regulated in CAG, were further investigated. Their expression was validated by Western blot and RT-PCR in 15 CAG samples matched with normal mucosa. The expression level of RPS12 was significantly higher in CAG than in matched normal gastric mucosa (P < 0.05). In contrast, the expression level of PSME1 in CAG was significantly lower than in matched normal gastric mucosa (P < 0.05). This study clearly demonstrated that there are some changes in protein expression between CAG and normal mucosa. In these changes, down-regulation of PSME1 and up-regulation of RPS12 could be involved in the development of CAG. Thus, the differentially expressed proteins might play important roles in CAG as functional molecules.
| S-EPMC3854201 | biostudies-literature
Project description:BackgroundInnate immunity was found to be associated with both persistence of Helicobacter pylori (H. pylori) infection and increased risk of gastric cancer.AimTo identify the risk factors associated with H. pylori infection and to establish the role of TLR9 rs352140 in suppressing or promoting inflammation related to this infection in children.MethodsWe performed a study of 155 children with digestive symptoms, who were divided into two groups according to the histopathological exam: Group 1 - 48 children with H. pylori-induced chronic gastritis, and Group 2 - control group.ResultsRural area and poor living conditions were significantly associated with H. pylori chronic gastritis (P = 0.0042/P < 0.0001). Both positive immunoglobulin A anti H. pylori and the rapid urease test were significantly associated with H. pylori infection (P < 0.0001). Significantly higher values of leukocytes and neutrophils within the peripheral blood were found in children with H. pylori chronic gastritis (P = 0.111/P = 0.284). We found a significant positive correlation between the variant TT genotype of TLR9 rs352140 polymorphism and both leucocytes and neutrophils (P = 0.0225/P = 0.0292).ConclusionVariant TT genotype carriers of the TLR9 rs352140 gene polymorphism might have a more severe degree of inflammation.
| S-EPMC8362532 | biostudies-literature
Project description:Background & aimsThe association between cellular senescence and Helicobacter pylori-induced atrophic gastritis is not clear. Here, we explore the role of cellular senescence in H pylori-induced atrophic gastritis and the underlying mechanism.MethodsC57BL/6J mice were infected with H pylori for biological and mechanistic studies in vivo. Gastric precancerous lesions from patients and mouse models were collected and analyzed using senescence-associated beta-galactosidase, Sudan Black B, and immunohistochemical staining to analyze senescent cells, signaling pathways, and H pylori infection. Chromatin immunoprecipitation, luciferase reporter assays, and other techniques were used to explore the underlying mechanism in vitro.ResultsGastric mucosa atrophy was highly associated with cellular senescence. H pylori promoted gastric epithelial cell senescence in vitro and in vivo in a manner that depended on C-X-C motif chemokine receptor 2 (CXCR2) signaling. Interestingly, H pylori infection not only up-regulated the expression of CXCR2 ligands, C-X-C motif chemokine ligands 1 and 8, but also transcriptionally up-regulated the expression of CXCR2 via the nuclear factor-κB subunit 1 directly. In addition, CXCR2 formed a positive feedback loop with p53 to continually enhance senescence. Pharmaceutical inhibition of CXCR2 in an H pylori-infected mouse model attenuated mucosal senescence and atrophy, and delayed further precancerous lesion progression.ConclusionsOur study showed a new mechanism of H pylori-induced atrophic gastritis through CXCR2-mediated cellular senescence. Inhibition of CXCR2 signaling is suggested as a potential preventive therapy for targeting H pylori-induced atrophic gastritis. GEO data set accession numbers: GSE47797 and GSE3556.
| S-EPMC7859172 | biostudies-literature