ArticleBMC immunology2009
Bone marrow cell derived arginase I is the major source of allergen-induced lung arginase but is not required for airway hyperresponsiveness, remodeling and lung inflammatory responses in mice.
Article in BMC immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 33 citations in OpenAlex.
- Regulatory haplotypes in ARG1 are associated with altered bronchodilator response.American journal of respiratory and critical care medicine · 2011Trial
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- A novel quinoline with airway relaxant effects and anti-inflammatory properties.Respiratory research · 2024Article
- An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment.Science immunology · 2022Article
- Arginine Therapy for Lung Diseases.Frontiers in pharmacology · 2021Review
- Hypoargininemia exacerbates airway hyperresponsiveness in a mouse model of asthma.Respiratory research · 2018Article
- Arginase 1 deletion in myeloid cells affects the inflammatory response in allergic asthma, but not lung mechanics, in female mice.BMC pulmonary medicine · 2017Article
- Increased mitochondrial arginine metabolism supports bioenergetics in asthma.The Journal of clinical investigation · 2016Article
- IL-4 and IL-13 signaling in allergic airway disease.Cytokine · 2015Review
- Group V secretory phospholipase A2 is involved in macrophage activation and is sufficient for macrophage effector functions in allergic pulmonary inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
- Resistin-like molecule-α regulates IL-13-induced chemokine production but not allergen-induced airway responses.American journal of respiratory cell and molecular biology · 2012Article
- Adoptive transfer of IL-4Rα+ macrophages is sufficient to enhance eosinophilic inflammation in a mouse model of allergic lung inflammation.BMC immunology · 2012Article
- Contribution of alternatively activated macrophages to allergic lung inflammation: a tale of mice and men.Journal of innate immunity · 2012Article
- Competitive metabolism of L-arginine: arginase as a therapeutic target in asthma.Journal of biomedical research · 2011Article
- Identification of an IFN-γ/mast cell axis in a mouse model of chronic asthma.The Journal of clinical investigation · 2011Article
- Arginase and arginine dysregulation in asthma.Journal of allergy · 2011Article
- The cationic amino acid transporter 2 is induced in inflammatory lung models and regulates lung fibrosis.Respiratory research · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundArginase is significantly upregulated in the lungs in murine models of asthma, as well as in human asthma, but its role in allergic airway inflammation has not been fully elucidated in mice.
resultsIn order to test the hypothesis that arginase has a role in allergic airway inflammation we generated arginase I-deficient bone marrow (BM) chimeric mice. Following transfer of arginase I-deficient BM into irradiated recipient mice, arginase I expression was not required for hematopoietic reconstitution and baseline immunity. Arginase I deficiency in bone marrow-derived cells decreased allergen-induced lung arginase by 85.8 +/- 5.6%. In contrast, arginase II-deficient mice had increased lung arginase activity following allergen challenge to a similar level to wild type mice. BM-derived arginase I was not required for allergen-elicited sensitization, recruitment of inflammatory cells in the lung, and proliferation of cells. Furthermore, allergen-induced airway hyperresponsiveness and collagen deposition were similar in arginase-deficient and wild type mice. Additionally, arginase II-deficient mice respond similarly to their control wild type mice with allergen-induced inflammation, airway hyperresponsiveness, proliferation and collagen deposition.
conclusionBone marrow cell derived arginase I is the predominant source of allergen-induced lung arginase but is not required for allergen-induced inflammation, airway hyperresponsiveness or collagen deposition.
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.