ArticleThe Journal of experimental medicine2021
Helicobacter pylori metabolites exacerbate gastritis through C-type lectin receptors.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Comprehensive Integration of Genome-Wide Association and Gene Expression Studies Reveals Novel Gene Signatures and Potential Therapeutic Targets forFrontiers in immunology · 2021Pooled it
- Review
- [Molecular mechanisms of chronic gastric mucosal inflammation induced byZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Review
- Unravelling mechanisms regulating Mincle activation.Communications biology · 2026Review
- C-Type lectin receptors as key modulators of intestinal inflammation: insights into IBD pathogenesis and therapy.FEMS microbiology letters · 2026Review
- Progress in immunotherapy forFrontiers in cellular and infection microbiology · 2026Review
- The association of the advanced lung cancer inflammation index with the risk ofFrontiers in cellular and infection microbiology · 2026Article
- Agarwood essential oils alleviate hypoxia-induced gastric and small intestinal injury.AMB Express · 2025Article
- Targeting CLEC4E in immunosuppressive tumour-associated macrophages via BET inhibition.Clinical and translational medicine · 2025Article
- Trimming the fat: a brief review of lipids at the host-pathogen interface.Infection and immunity · 2025Review
- Antibiotic stress affects the secretion and physicochemical features of extracellular vesicles produced by Helicobacter pylori.The Journal of antimicrobial chemotherapy · 2025Article
- Vacuolar sterol β-glucosidase EGCrP2/Sgl1 deficiency in Cryptococcus neoformans: Dysfunctional autophagy and Mincle-dependent immune activation as targets of novel antifungal strategies.PLoS pathogens · 2025Article
- Dysregulated macrophage immunity inFrontiers in immunology · 2025Review
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- Efficient lipidomic approach for the discovery of lipid ligands for immune receptors by combining LC-HRMS/MS analysis with fractionation and reporter cell assay.Analytical and bioanalytical chemistry · 2024Article
- Metabolic and Lipid Biomarkers for Pathogenic Algae, Fungi, Cyanobacteria, Mycobacteria, Gram-Positive Bacteria, and Gram-Negative Bacteria.Metabolites · 2024Review
- Effect ofFrontiers in oncology · 2024Review
- Subinhibitory concentrations of antibiotics affect development and parameters ofFrontiers in pharmacology · 2024Article
- Article
- Construction of a Bacterial Lipidomics Analytical Platform: Pilot Validation with Bovine Paratuberculosis Serum.Metabolites · 2023Article
Corrections and comments
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Authors and funding
21 authors at 10 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori causes gastritis, which has been attributed to the development of H. pylori-specific T cells during infection. However, the mechanism underlying innate immune detection leading to the priming of T cells is not fully understood, as H. pylori evades TLR detection. Here, we report that H. pylori metabolites modified from host cholesterol exacerbate gastritis through the interaction with C-type lectin receptors. Cholesteryl acyl α-glucoside (αCAG) and cholesteryl phosphatidyl α-glucoside (αCPG) were identified as noncanonical ligands for Mincle (Clec4e) and DCAR (Clec4b1). During chronic infection, H. pylori-specific T cell responses and gastritis were ameliorated in Mincle-deficient mice, although bacterial burdens remained unchanged. Furthermore, a mutant H. pylori strain lacking αCAG and αCPG exhibited an impaired ability to cause gastritis. Thus H. pylori-specific modification of host cholesterol plays a pathophysiological role that exacerbates gastric inflammation by triggering C-type lectin receptors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.