Helicobacter pylori Dampens HLA-II Expression on Macrophages via the Up-Regulation of miRNAs Targeting CIITA

Macrophages have a major role in infectious and inflammatory diseases, and the available data suggest that Helicobacter pylori persistence can be explained in part by the failure of the bacterium to be killed by professional phagocytes. Macrophages are cells ready to kill the engulfed pathogen, through oxygen-dependent and -independent mechanisms; however, their killing potential can be further augmented by the intervention of T helper (Th) cells upon the specific recognition of human leukocyte antigen (HLA)-II–peptide complexes on the surface of the phagocytic cells. As it pertains to H. pylori, the bacterium is engulfed by macrophages, but it interferes with the phagosome maturation process leading to phagosomes with an altered degradative capacity, and to megasomes, wherein H. pylori resists killing. We recently showed that macrophages infected with H. pylori strongly reduce the expression of HLA-II molecules on the plasma membrane and this compromises the bacterial antigen presentation to Th lymphocytes. In this work, we demonstrate that H. pylori hampers HLA-II expression in macrophages, activated or non-activated by IFN-γ, by down-regulating the expression of the class II major histocompatibility complex transactivator (CIITA), the “master control factor” for the expression of HLA class II genes. We provided evidence that this effect relies on the up-regulation of let-7f-5p, let-7i-5p, miR-146b-5p, and -185-5p targeting CIITA. MiRNA expression an...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research

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Conclusions. In this population with high rates of gastric cancer, we found that just over half of the H. pylori contained an intact cagPAI and 40 % had the vacA s1/i1/m1 genotype. Infection with these strains was associated with a more severe gastropathy. PMID: 32011229 [PubMed - as supplied by publisher]
Source: Journal of Medical Microbiology - Category: Microbiology Authors: Tags: J Med Microbiol Source Type: research
AbstractHelicobacter pylori is an important human pathogen that causes gastritis, gastric and duodenal ulcers, and gastric cancer. O-polysaccharides ofH. pylori lipopolysaccharide (LPS) are composed of ( β1→3)-poly(N-acetyllactosamine) (polyLacNAc) decorated with multiple α-L-fucose residues. In many strains, their terminal LacNAc units are mono- or difucosylated to mimic Lewis X (Lex) and/or Lewis Y (Ley) oligosaccharides. The studies in rhesus macaques as a model of human infection byH. pylori showed that this bacterium adapts to the host during colonization by expressing host Lewis antigens. Here, we cha...
Source: Biochemistry (Moscow) - Category: Biochemistry Source Type: research
Authors: Annibale B, Esposito G, Lahner E Abstract SUMMARYIntroduction: Atrophic gastritis (AG) is a complex syndrome which arise as consequence of H. pylori infection or in the context of gastric autoimmunity. It often deserves a benign course, but may lead to potentially life-threatening complications: cancer and anaemia. This review aims to address traditional and innovative knowledge on this often under-diagnosed disorder.Areas covered: This review covers clinical presentation, risk factors, diagnosis and management of AG and provides an updated resource for clinicians to get insight in this challenging disorde...
Source: Expert Review of Gastroenterology and Hepatology - Category: Gastroenterology Tags: Expert Rev Gastroenterol Hepatol Source Type: research
This study investigated the molecular targets of the component herbs of QLSP in preventing precancerous lesions based on network pharmacology. Network pharmacology analysis revealed that the 6 herbs regulated multiple CAG-related genes, among which the most important were cancer-related pathway (apoptosis, p53, and VEGF) and epithelial cell signaling in Helicobacter pylori infection. Further animal experiments showed that the expression of survivin and p53 in precancerous lesions of CAG rats was significantly increased which was suppressed by QLSP. Moreover, telomerase activity was inhibited in precancerous lesions of CAG ...
Source: Evidence-based Complementary and Alternative Medicine - Category: Complementary Medicine Tags: Evid Based Complement Alternat Med Source Type: research
Forty-five years have passed since Correa et  al1 proposed their hypothesis on the histopathological cascade leading to gastric adenocarcinoma claiming that gastric cancer usually resulted from chronic gastritis, subsequently leading to gland loss or atrophy, intestinal metaplasia, dysplasia, and eventually invasive cancer. The most common ri sk factor for gastritis soon revealed to be the colonization with Helicobacter pylori.2 Most infections occur during childhood and remain for life. They are almost invariably associated with chronic gastritis, which may eventually lead to a loss of mucosal glands.
Source: Gastroenterology - Category: Gastroenterology Authors: Tags: Mentoring, Education, and Training Corner Source Type: research
Conclusion: According to our analysis, there was no correlation between coinfection and polymorphisms in genes encoding IL-10 and IL-1RN. We conclude that various factors can be involved in the development of gastric diseases. PMID: 31885568 [PubMed]
Source: Journal of Oncology - Category: Cancer & Oncology Tags: J Oncol Source Type: research
In this study, 43 five- and six-genotype combinations were found among 224 strains. The highest frequencies were observed for vacA s1m2i2d2c2 (85/224, 37.9%), s1m2i2d2c2cagA (48/222, 21.6%), s1m1i1d1c1 (40/224, 17.9%) and s1m1i1d1c1cagA (35/222, 15.8%). Logistic regression analysis showed that vacA s1m1i1d1c1, s1m2i1d2c1, s1m2i2d2c1, and s1m2i2d2c1cagA had a high prevalence in GC patients compared to non-atrophic gastritis patients (p 
Source: Infection, Genetics and Evolution - Category: Genetics & Stem Cells Authors: Tags: Infect Genet Evol Source Type: research
Gastric IL-1β, IL-8, and IL-17A expression in Moroccan patients infected with Helicobacter pylori may be a predictive signature of severe pathological stages. Cytokine. 2019 Dec 23;126:154893 Authors: Outlioua A, Badre W, Desterke C, Echarki Z, El Hammani N, Rabhi M, Riyad M, Karkouri M, Arnoult D, Khalil A, Akarid K Abstract INTRODUCTION: Helicobacter pylori induces acute gastritis that can progress to serious diseases such as gastric cancer. H. pylori interacts with host cells within the gastric mucosa, resulting in activation of multiple innate immune signalling pathways, leading to pro-inflam...
Source: Cytokine - Category: Molecular Biology Authors: Tags: Cytokine Source Type: research
Contributors : Claudia I Rivas-Ortiz ; Stephanie E Morales-Guerrero ; Sergio P de Le ón Rosales ; Armando Gamboa-Dominguez ; Claudia Rangel-Escareño ; Luis F Uscanga-Dominguez ; Germán R Aguilar-Gutiérrez ; David Kershenobich-Stalnikowitz ; Yolanda López-Vidal ; Gonzalo Castillo-RojasSeries Type : Expression profiling by arrayOrganism : Homo sapiensGastric cancer is an important health problem because it is difficult to diagnose and treat in advanced stage. This makes that the prognosis of gastric cancer patients remains scarce. Currently it is known that the cause of gastric cancer is at...
Source: GEO: Gene Expression Omnibus - Category: Genetics & Stem Cells Tags: Expression profiling by array Homo sapiens Source Type: research
Authors: Zhang F, Chen C, Hu J, Su R, Zhang J, Han Z, Chen H, Li Y Abstract Helicobacter pylori (H. pylori) is a gram-negative pathogen that colonizes gastric epithelial cells. The drug resistance rates of H. pylori have dramatically increased, causing persistent infections. Chronic infection by H. pylori is a critical cause of gastritis, peptic ulcers and even gastric cancer. In host cells, autophagy is stimulated to maintain cellular homeostasis following intracellular pathogen recognition by the innate immune defense system. However, H. pylori-induced autophagy is not consistent during acute and chronic infectio...
Source: Oncology Letters - Category: Cancer & Oncology Tags: Oncol Lett Source Type: research
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