ArticleJCI insight2020
Arginine metabolic control of airway inflammation.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
30 citing papers in PubMed, 70 citations in OpenAlex.
- l-Arginine supplementation in severe asthma.JCI insight · 2020Trial
- Untargeted metabolomics profiling of childhood asthma: linking metabolic pattern to disease severity.Molecular and cellular pediatrics · 2026Article
- Article
- Effects of T2-high asthma heterogeneity and inhaled corticosteroid on airway and metabolic profiles: A multi-omic approach.Journal of translational internal medicine · 2026Article
- Distinct regulatory elements of SLC6A14 expression contribute to modification of cystic fibrosis phenotypes.Human genetics · 2026Article
- Article
- Metabolomic and immunological signatures of asthma severity in children.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2025Article
- Targeting Arginine Metabolism in Immune Cells for the Treatment of Pulmonary Inflammatory Diseases.Current allergy and asthma reports · 2025Review
- Pulmonary vascular remodeling in Fra-2 transgenic mice is driven by type 2 inflammation and accompanied by pulmonary vascular hyperresponsiveness.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Arginine-mediated inhibition of macrophage apoptosis byFrontiers in immunology · 2025Article
- Article
- Calcium Signaling in Airway Epithelial Cells: Current Understanding and Implications for Inflammatory Airway Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- A novel quinoline with airway relaxant effects and anti-inflammatory properties.Respiratory research · 2024Article
- Metabolomics in Animal Models of Bronchial Asthma and Its Translational Importance for Clinics.International journal of molecular sciences · 2023Review
- L-Arginine, as an essential amino acid, is a potential substitute for treating COPD via regulation of ROS/NLRP3/NF-κB signaling pathway.Cell & bioscience · 2023Article
- Lung pericytes as mediators of inflammation.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Phenotypic characteristics of asthma and morbidity are associated with distinct longitudinal changes in L-arginine metabolism.BMJ open respiratory research · 2023Article
- Regulated Arginine Metabolism in Immunopathogenesis of a Wide Range of Diseases: Is There a Way to Pass between Scylla and Charybdis?Current issues in molecular biology · 2023Review
- Immune Metabolism in TH2 Responses: New Opportunities to Improve Allergy Treatment - Disease-Specific Findings (Part 1).Current allergy and asthma reports · 2023Review
- Preclinical Four-Dimensional Functional Lung Imaging and Quantification of Regional Airflow: A New Standard in Lung Function Evaluation in Murine Models.American journal of respiratory cell and molecular biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Inducible nitric oxide synthase (iNOS) and arginase-2 (ARG2) share a common substrate, arginine. Higher expression of iNOS and exhaled NO are linked to airway inflammation in patients. iNOS deletion in animal models suggests that eosinophilic inflammation is regulated by arginine metabolism. Moreover, ARG2 is a regulator of Th2 response, as shown by the development of severe eosinophilic inflammation in ARG2-/- mice. However, potential synergistic roles of iNOS and ARG2 in asthma have not been explored. Here, we hypothesized that arginine metabolic fate via iNOS and ARG2 may govern airway inflammation. In an asthma cohort, ARG2 variant genotypes were associated with arginase activity. ARG2 variants with lower arginase activity, combined with levels of exhaled NO, identified a severe asthma phenotype. Airway inflammation was present in WT, ARG2-/-, iNOS-/-, and ARG2-/-/iNOS-/- mice but was greatest in ARG2-/-. Eosinophilic and neutrophilic infiltration in the ARG2-/- mice was abrogated in ARG2-/-/iNOS-/- animals. Similarly, angiogenic airway remodeling was greatest in ARG2-/- mice. Cytokines driving inflammation and remodeling were highest in lungs of asthmatic ARG2-/- mice and lowest in the iNOS-/-. ARG2 metabolism of arginine suppresses inflammation, while iNOS metabolism promotes airway inflammation, supporting a central role for arginine metabolic control of inflammation.
Indexed as
Identifiers
What OpenQuestion holds
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.