ArticleLife sciences2016
Aryl hydrocarbon receptor influences nitric oxide and arginine production and alters M1/M2 macrophage polarization.
Article in Life sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 75 citations in OpenAlex.
- The gut microbiota-tryptophan metabolism-immune axis in inflammatory bowel disease: Mechanisms and therapeutic prospects.Human vaccines & immunotherapeutics · 2026Review
- Aryl hydrocarbon receptor pharmacology-mechanisms, ligands, and therapeutic potential.Pharmacological reviews · 2026Review
- Integrated multi-omics analysis reveals a gut microbiota-tryptophan metabolism axis contributes to sex differences in a β-aminopropionitrile-induced aortic dissection mouse model.Biology of sex differences · 2026Article
- Aryl hydrocarbon receptor: a potential target for natural products in the treatment of inflammatory bowel disease.Frontiers in immunology · 2026Review
- Aryl Hydrocarbon Receptor in Health and Disease.MedComm · 2025Review
- Metabolic reprogramming of immune cells in the battle against intracellular bacterial chronic infections: novel mechanisms and breakthroughs.Molecular biology reports · 2025Review
- Targeting heat shock protein 90 with usnic acid relieves immune suppression via aryl hydrocarbon receptor-mediated mechanisms in lung cancer.Molecular biomedicine · 2025Article
- Tissue macrophages: origin, heterogenity, biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- The role of the AHR in host-pathogen interactions.Nature reviews. Immunology · 2025Review
- AhR governs lipid metabolism: the role of gut microbiota.Frontiers in microbiology · 2025Review
- Unveiling the Immune effects of AHR in tumors: a decade of insights from bibliometric analysis (2010-2023).Discover oncology · 2024Article
- Indoxyl sulphate-TNFα axis mediates uremic encephalopathy in rodent acute kidney injury.Acta pharmacologica Sinica · 2024Article
- Mechanisms underlying aryl hydrocarbon receptor-driven divergent macrophage function.Toxicological sciences : an official journal of the Society of Toxicology · 2024Review
- Genistein Promotes M2 Macrophage Polarization via Aryl Hydrocarbon Receptor and Alleviates Intestinal Inflammation in Broilers with Necrotic Enteritis.International journal of molecular sciences · 2024Article
- The Aryl Hydrocarbon Receptor: Impact on the Tumor Immune Microenvironment and Modulation as a Potential Therapy.Cancers · 2024Review
- Aryl hydrocarbon receptor: current perspectives on key signaling partners and immunoregulatory role in inflammatory diseases.Frontiers in immunology · 2024Review
- The aryl hydrocarbon receptor controls mesenchymal stromal cell-mediated immunomodulation via ubiquitination of eukaryotic elongation factor-2 kinase.Cell death & disease · 2023Article
- Advances in the study of macrophage polarization in inflammatory immune skin diseases.Journal of inflammation (London, England) · 2023Review
- Bridging of host-microbiota tryptophan partitioning by the serotonin pathway in fungal pneumonia.Nature communications · 2023Article
- Constitutive aryl hydrocarbon receptor facilitates the regenerative potential of mouse bone marrow mesenchymal stromal cells.World journal of stem cells · 2023Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
aimsThe aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the toxicity of environmental pollutants. It is also implicated in the regulation of the immune system. Ahr-null macrophages overproduce several proinflammatory cytokines following LPS-mediated stimulation, suggesting that AHR affects the balance between the inflammatory M1 and anti-inflammatory M2 phenotypes. Therefore, the present study aimed to examine whether the loss of AHR modifies macrophage polarization. MATERIALS AND
methodsPeritoneal macrophages from wild-type and Ahr-null mice were differentiated into M1 or M2 phenotype by treatment with LPS/IFNγ or IL-4, and several M1 and M2 markers were determined by qPCR and ELISA assays. Macrophage phagocytic capacity was determined through phagocytosis of yeast and Leishmania major infection assays. Nitric oxide (NO) and urea production, and arginase activity were also determined. KEY
findingsWhen macrophages were polarized to the M1 phenotype, Ahr-null cells presented a mixed response; higher levels of IL-1β, IL-6, IL-12, and TNFα were observed after IFNγ- and LPS-mediated activation. However, Ahr-null cells also exhibited decreased NO production and phagocytic capacity. When macrophage was polarized to the M2 phenotype, Ahr-null cells exhibited lower levels of Fizz1, Ym1, and IL-10. In contrast, arginase activity was increased when compared to wild-type macrophages. In addition, macrophages from Ahr-null mice were more susceptible to L. major infection. SIGNIFICANCE: Disruption of the Ahr gene alters macrophage polarization when compared to WT macrophage. These changes may affect the development and resolution of several diseases such as bacterial or parasitic infections.
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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.