ArticleAmino acids2016
Arginase 2 deletion leads to enhanced M1 macrophage activation and upregulated polyamine metabolism in response to Helicobacter pylori infection.
Article in Amino acids, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 79 citations in OpenAlex.
- PLB1 enhances adhesion and invasion of Trichosporon asahii to lung epithelial cells: insights into the mechanisms of Cav1/JAK/STAT3-induced arginine metabolism.Respiratory research · 2026Article
- CXCL16 Promotes the Development of Chronic Atrophic Gastritis by Regulating M1 Macrophage Polarisation.Journal of inflammation research · 2026Article
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Dysregulated macrophage immunity inFrontiers in immunology · 2025Review
- Pathophysiology of Arginases in Cancer and Efforts in Their Pharmacological Inhibition.International journal of molecular sciences · 2024Review
- Helicobacter pylori disrupts gastric mucosal homeostasis by stimulating macrophages to secrete CCL3.Cell communication and signaling : CCS · 2024Article
- Current research on the interaction between Helicobacter pylori and macrophages.Molecular biology reports · 2024Review
- Regulator of G protein signaling 1 is a potential target in gastric cancer and impacts tumor-associated macrophages.Cancer science · 2024Article
- Role of Helicobacter pylori virulence factors and alteration of the Tumor Immune Microenvironment: challenges and opportunities for Cancer Immunotherapy.Archives of microbiology · 2024Review
- Effects and mechanisms ofFrontiers in immunology · 2024Review
- Myeloid deletion of talin-1 reduces mucosal macrophages and protects mice from colonic inflammation.Scientific reports · 2023Article
- Inhibition of pro-inflammatory signaling in human primary macrophages by enhancing arginase-2 via target site blockers.Molecular therapy. Nucleic acids · 2023Article
- Integrated bioinformatics analysis for conducting a prognostic model and identifying immunotherapeutic targets in gastric cancer.BMC bioinformatics · 2023Article
- Involvement of Nitric Oxide in Protecting against Radical Species and Autoregulation of M1-Polarized Macrophages through Metabolic Remodeling.Molecules (Basel, Switzerland) · 2023Review
- The role of immunometabolism in macrophage polarization and its impact on acute lung injury/acute respiratory distress syndrome.Frontiers in immunology · 2023Review
- Inflammatory microenvironment in gastric premalignant lesions: implication and application.Frontiers in immunology · 2023Review
- Gastric precancerous lesions:occurrence, development factors, and treatment.Frontiers in oncology · 2023Review
- Host M-CSF induced gene expression drives changes in susceptible and resistant mice-derived BMdMs uponFrontiers in immunology · 2023Article
- The intestinal clock drives the microbiome to maintain gastrointestinal homeostasis.Nature communications · 2022Article
- Enhancing arginase 2 expression using target site blockers as a strategy to modulate macrophage phenotype.Molecular therapy. Nucleic acids · 2022Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
We reported that arginase 2 (ARG2) deletion results in increased gastritis and decreased bacterial burden during Helicobacter pylori infection in mice. Our studies implicated a potential role for inducible nitric oxide (NO) synthase (NOS2), as Arg2 (-/-) mice exhibited increased NOS2 levels in gastric macrophages, and NO can kill H. pylori. We now bred Arg2 (-/-) to Nos2 (-/-) mice, and infected them with H. pylori. Compared to wild-type mice, both Arg2 (-/-) and Arg2 (-/-) ;Nos2 (-/-) mice exhibited increased gastritis and decreased colonization, the latter indicating that the effect of ARG2 deletion on bacterial burden was not mediated by NO. While Arg2 (-/-) mice demonstrated enhanced M1 macrophage activation, Nos2 (-/-) and Arg2 (-/-) ;Nos2 (-/-) mice did not demonstrate these changes, but exhibited increased CXCL1 and CXCL2 responses. There was an increased expression of the Th1/Th17 cytokines, interferon gamma and interleukin 17, in gastric tissues and splenic T-cells from Arg2 (-/-), but not Nos2 (-/-) or Arg2 (-/-) ;Nos2 (-/-) mice. Gastric tissues from infected Arg2 (-/-) mice demonstrated increased expression of arginase 1, ornithine decarboxylase, adenosylmethionine decarboxylase 1, spermidine/spermine N (1)-acetyltransferase 1, and spermine oxidase, along with increased spermine levels. These data indicate that ARG2 deletion results in compensatory upregulation of gastric polyamine synthesis and catabolism during H. pylori infection, which may contribute to increased gastric inflammation and associated decreased bacterial load. Overall, the finding of this study is that ARG2 contributes to the immune evasion of H. pylori by restricting M1 macrophage activation and polyamine metabolism.
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