ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Arginase II restricts host defense to Helicobacter pylori by attenuating inducible nitric oxide synthase translation in macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.
- Infiltration to infection: key virulence players of Helicobacter pylori pathogenicity.Infection · 2024Pooled it
- Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026Review
- Feeding the invaders: how metabolic imbalance shapes infection and biofilm development.FEMS microbiology reviews · 2026Review
- Changes in potential pathogenicity-associated proteins ofFrontiers in microbiology · 2025Article
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- The immunoregulatory role of helper T cells inFrontiers in immunology · 2025Review
- Polyamines: the pivotal amines in influencing the tumor microenvironment.Discover oncology · 2024Review
- Strategies ofFrontiers in cellular and infection microbiology · 2024Review
- Arginine metabolism regulates the pathogenesis of inflammatory bowel disease.Nutrition reviews · 2023Article
- Involvement of Nitric Oxide in Protecting against Radical Species and Autoregulation of M1-Polarized Macrophages through Metabolic Remodeling.Molecules (Basel, Switzerland) · 2023Review
- Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023Article
- Article
- Host Cell Antimicrobial Responses againstInternational journal of molecular sciences · 2022Review
- Incorporating Immunotherapy in the Management of Gastric Cancer: Molecular and Clinical Implications.Cancers · 2022Review
- Cystathionine γ-lyase exacerbates Helicobacter pylori immunopathogenesis by promoting macrophage metabolic remodeling and activation.JCI insight · 2022Article
- Impacts and mechanisms of metabolic reprogramming of tumor microenvironment for immunotherapy in gastric cancer.Cell death & disease · 2022Review
- Statins' Regulation of the Virulence Factors ofAntioxidants (Basel, Switzerland) · 2021Review
- Review
- The Microbiome and the Gut-Liver-Brain Axis for Central Nervous System Clinical Pharmacology: Challenges in Specifying and Integrating In Vitro and In Silico Models.Clinical pharmacology and therapeutics · 2020Review
- Expression of a heroin contextually conditioned immune effect in male rats requires CaMKIIα-expressing neurons in dorsal, but not ventral, subiculum and hippocampal CA1.Brain, behavior, and immunity · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
Helicobacter pylori infection of the stomach causes peptic ulcer disease and gastric cancer. Despite eliciting a vigorous immune response, the bacterium persists for the life of the host. An important antimicrobial mechanism is the production of NO derived from inducible NO synthase (iNOS). We have reported that macrophages can kill H. pylori in vitro by an NO-dependent mechanism, but supraphysiologic levels of the iNOS substrate l-arginine are required. Because H. pylori induces arginase activity in macrophages, we determined if this restricts NO generation by reducing l-arginine availability. Inhibition of arginase with S-(2-boronoethyl)-l-cysteine (BEC) significantly enhanced NO generation in H. pylori-stimulated RAW 264.7 macrophages by enhancing iNOS protein translation but not iNOS mRNA levels. This effect resulted in increased killing of H. pylori that was attenuated with an NO scavenger. In contrast, inhibition of arginase in macrophages activated by the colitis-inducing bacterium Citrobacter rodentium increased NO without affecting iNOS levels. H. pylori upregulated levels of arginase II (Arg2) mRNA and protein, which localized to mitochondria, whereas arginase I was not induced. Increased iNOS protein and NO levels were also demonstrated by small interfering RNA knockdown of Arg2 and in peritoneal macrophages from C57BL/6 Arg2(-/-) mice. In H. pylori-infected mice, treatment with BEC or deletion of Arg2 increased iNOS protein levels and NO generation in gastric macrophages, but treatment of Arg2(-/-) mice with BEC had no additional effect. These studies implicate Arg2 in the immune evasion of H. pylori by causing intracellular depletion of l-arginine and thus reduction of NO-dependent bactericidal activity.
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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.