ArticleAmino acids2012
Arginine and polyamines in Helicobacter pylori-induced immune dysregulation and gastric carcinogenesis.
Article in Amino acids, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 62 citations in OpenAlex.
- Metabolic reprogramming as a key regulator in Helicobacter pylori-infected gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Review
- Exploring compositional and predicted functional alterations of gut microbiota in H. pylori infection.Scientific reports · 2025Article
- Narrative review on bacteria-derived metabolites in the pathogenesis of ulcerative colitis.Clinical microbiology reviews · 2025Review
- Challenges and Prospects for Eradication ofPathogens (Basel, Switzerland) · 2025Review
- Modulating Gut Microbiota with Dietary Components: A Novel Strategy for Cancer-Depression Comorbidity Management.Nutrients · 2025Review
- Heterogeneity of T cells regulates tumor immunity mediated by Helicobacter pylori infection in gastric cancer.BMC cancer · 2025Article
- Integrated analysis of single-cell and bulk transcriptomes reveals the prognostic value of polyamine metabolism biomarkers and immune microenvironment features in gastric cancer.Frontiers in immunology · 2025Article
- Enhancing the radiosensitivity of colorectal cancer cells by reducing spermine synthase through promoting autophagy and DNA damage.World journal of gastrointestinal oncology · 2024Review
- Specific TLR-mediated HSP70 activation plays a potential role in host defense against the intestinal parasiteFrontiers in microbiology · 2023Article
- Altered L-Arginine Metabolic Pathways in Gastric Cancer: Potential Therapeutic Targets and Biomarkers.Biomolecules · 2021Article
- Abnormal arginine metabolism is associated with prognosis in patients of gastric cancer.Translational cancer research · 2021Article
- The impact of ICOSCancer immunology, immunotherapy : CII · 2021Article
- Polyamines and related signaling pathways in cancer.Cancer cell international · 2020Review
- α-Difluoromethylornithine reduces gastric carcinogenesis by causing mutations inProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Polyamine metabolism and cancer: treatments, challenges and opportunities.Nature reviews. Cancer · 2018Review
- Spermine Alleviates Acute Liver Injury by Inhibiting Liver-Resident Macrophage Pro-Inflammatory Response Through ATG5-Dependent Autophagy.Frontiers in immunology · 2018Article
- Ferritin H Deficiency in Myeloid Compartments Dysregulates Host Energy Metabolism and Increases Susceptibility toFrontiers in immunology · 2018Article
- Workshop Report: Modulation of Antitumor Immune Responses by Dietary and Microbial Metabolites.Journal of the National Cancer Institute · 2017Article
- Arginase of Helicobacter Gastric Pathogens Uses a Unique Set of Non-catalytic Residues for Catalysis.Biophysical journal · 2017Article
- Oxidative and nitrosative stress defences of Helicobacter and Campylobacter species that counteract mammalian immunity.FEMS microbiology reviews · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
L-arginine (L-Arg) is metabolized by nitric oxide synthase and arginase enzymes. The gastric pathogen Helicobacter pylori causes peptic ulcer disease and gastric cancer. We have shown that alterations in L-Arg availability and metabolism into polyamines contribute significantly to the dysregulation of the host immune response to this infection. Nitric oxide (NO) derived from inducible NO synthase (iNOS) can kill H. pylori. There are multiple mechanisms leading to failure of this process, including competition for L-Arg substrate by H. pylori arginase, and induction of host macrophage arginase II (Arg2) and ornithine decarboxylase (ODC). Generation of spermine by ODC inhibits iNOS translation and NO-mediated H. pylori killing. Expression of ODC is dependent on formation of a unique AP-1 complex, leading to upregulation of c-Myc as a transcriptional enhancer. Macrophage apoptosis is mediated by oxidation of spermine via the enzyme spermine oxidase (SMO) that generates hydrogen peroxide (H(2)O(2)), and thus oxidative stress-induced mitochondrial membrane polarization. Our studies have demonstrated that apoptosis occurs through a pERK → pc-Fos/c-Jun → c-Myc → ODC → SMO pathway. In gastric epithelial cells, activation of oxidative stress by H. pylori is dependent on SMO induction and results in both apoptosis and DNA damage, such that inhibition or knockdown of SMO markedly attenuates these events. In summary, L-Arg metabolism by the arginase-ODC pathway and the activation of SMO leads to H. pylori-induced DNA damage and immune dysregulation through polyamine-mediated oxidative stress and impairment of antimicrobial NO synthesis. Our studies indicate novel targets for therapeutic intervention in H. pylori-associated diseases, including gastritis, ulcer disease, and gastric cancer.
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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.