ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Immune evasion by Helicobacter pylori is mediated by induction of macrophage arginase II.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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.
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Who cites it
58 citing papers in PubMed, 82 citations in OpenAlex.
- The arginase-polyamine signaling axis in immune cells: Implications for immune modulation and host-pathogen interactions.iScience · 2026Review
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- Research progress on monocyte/macrophage in the development of gastric cancer.Future oncology (London, England) · 2025Review
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Dysregulated macrophage immunity inFrontiers in immunology · 2025Review
- Polyamines: the pivotal amines in influencing the tumor microenvironment.Discover oncology · 2024Review
- Effects and mechanisms ofFrontiers in immunology · 2024Review
- BRD4 Regulates Glycolysis-Dependent Nos2 Expression in Macrophages Upon H pylori Infection.Cellular and molecular gastroenterology and hepatology · 2024Article
- Determination of Heterogeneous Proteomic and Metabolomic Response in anti-TNF and anti-IL-6 Treatment of Patients with Rheumatoid Arthritis.Life (Basel, Switzerland) · 2023Article
- Host M-CSF induced gene expression drives changes in susceptible and resistant mice-derived BMdMs uponFrontiers in immunology · 2023Article
- Gastric precancerous lesions:occurrence, development factors, and treatment.Frontiers in oncology · 2023Review
- Innate Immunity Crosstalk withInternational journal of molecular sciences · 2022Review
- Cystathionine γ-lyase exacerbates Helicobacter pylori immunopathogenesis by promoting macrophage metabolic remodeling and activation.JCI insight · 2022Article
- Transcriptome analysis of Echinococcus granulosus sensu stricto protoscoleces reveals differences in immune modulation gene expression between cysts found in cattle and sheep.Veterinary research · 2022Article
- Targeting cancer-specific metabolic pathways for developing novel cancer therapeutics.Frontiers in immunology · 2022Review
- Effects ofFrontiers in immunology · 2022Review
- Monocytic-Myeloid Derived Suppressor Cells Suppress T-Cell Responses in Recovered SARS CoV2-Infected Individuals.Frontiers in immunology · 2022Article
- The Efficacy of Cancer Immunotherapies Is Compromised byFrontiers in immunology · 2022Review
- Arginine Signaling and Cancer Metabolism.Cancers · 2021Review
- The role of polyamines in gastric cancer.Oncogene · 2021Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Helicobacter pylori infection persists for the life of the host due to the failure of the immune response to eradicate the bacterium. Determining how H. pylori escapes the immune response in its gastric niche is clinically important. We have demonstrated in vitro that macrophage NO production can kill H. pylori, but induction of macrophage arginase II (Arg2) inhibits inducible NO synthase (iNOS) translation, causes apoptosis, and restricts bacterial killing. Using a chronic H. pylori infection model, we determined whether Arg2 impairs host defense in vivo. In C57BL/6 mice, expression of Arg2, but not arginase I, was abundant and localized to gastric macrophages. Arg2(-/-) mice had increased histologic gastritis and decreased bacterial colonization compared with wild-type (WT) mice. Increased gastritis scores correlated with decreased colonization in individual Arg2(-/-) mice but not in WT mice. When mice infected with H. pylori were compared, Arg2(-/-) mice had more gastric macrophages, more of these cells were iNOS(+), and these cells expressed higher levels of iNOS protein, as determined by flow cytometry and immunofluorescence microscopy. There was enhanced nitrotyrosine staining in infected Arg2(-/-) versus WT mice, indicating increased NO generation. Infected Arg2(-/-) mice exhibited decreased macrophage apoptosis, as well as enhanced IFN-γ, IL-17a, and IL-12p40 expression, and reduced IL-10 levels consistent with a more vigorous Th1/Th17 response. These studies demonstrate that Arg2 contributes to the immune evasion of H. pylori by limiting macrophage iNOS protein expression and NO production, mediating macrophage apoptosis, and restraining proinflammatory cytokine responses.
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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.