ArticleFrontiers in immunology2017
Glutathione Fine-Tunes the Innate Immune Response toward Antiviral Pathways in a Macrophage Cell Line Independently of Its Antioxidant Properties.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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.
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Who cites it
45 citing papers in PubMed, 89 citations in OpenAlex.
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- Hydroxysafflor Yellow A modulation of metabolite networks and inhibition of JAK2/STAT1 pathway in sepsis.Scientific reports · 2025Article
- The spatiotemporal heterogeneity of reactive oxygen species in the malignant transformation of viral hepatitis to hepatocellular carcinoma: a new insight.Cellular & molecular biology letters · 2025Review
- Glutathione and neurodegenerative diseases: immunopharmacological implications.Frontiers in pharmacology · 2025Review
- Role of disulfide death in cancer (Review).Oncology letters · 2025Review
- The Effect of the Lysine Acetylation Modification of ClpP on the Virulence ofMolecules (Basel, Switzerland) · 2024Article
- ROS signaling in innate immunity via oxidative protein modifications.Frontiers in immunology · 2024Review
- Targeted serum proteomics of longitudinal samples from newly diagnosed youth with type 1 diabetes distinguishes markers of disease and C-peptide trajectory.Diabetologia · 2023Article
- A Review of the Potential of Nuclear Factor [Erythroid-Derived 2]-like 2 Activation in Autoimmune Diseases.Brain sciences · 2023Review
- The Triple Crown: NO, CO, and HPharmacology & therapeutics · 2023Review
- Polymorphisms of theLife (Basel, Switzerland) · 2023Article
- Molecular Genetics of Abnormal Redox Homeostasis in Type 2 Diabetes Mellitus.International journal of molecular sciences · 2023Review
- Characterisation of key biomarkers in diabetic ulcers via systems bioinformatics.International wound journal · 2023Article
- Putrescine supplementation shifts macrophage L-arginine metabolism related-genes reducing Leishmania amazonensis infection.PloS one · 2023Article
- Acidic ascites inhibits ovarian cancer cell proliferation and correlates with the metabolomic, lipidomic and inflammatory phenotype of human patients.Journal of translational medicine · 2022Article
- Utility of NO and HNitric oxide : biology and chemistry · 2022Review
- Chemical Composition, Antioxidant and Antiproliferative Activities ofMolecules (Basel, Switzerland) · 2022Article
- Recent Developments in the Understanding of Immunity, Pathogenesis and Management of COVID-19.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutathione (GSH), a major cellular antioxidant, is considered an inhibitor of the inflammatory response involving reactive oxygen species (ROS). However, evidence is largely based on experiments with exogenously added antioxidants/reducing agents or pro-oxidants. We show that depleting macrophages of 99% of GSH does not exacerbate the inflammatory gene expression profile in the RAW264 macrophage cell line or increase expression of inflammatory cytokines in response to the toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS); only two small patterns of LPS-induced genes were sensitive to GSH depletion. One group, mapping to innate immunity and antiviral responses (Oas2, Oas3, Mx2, Irf7, Irf9, STAT1, il1b), required GSH for optimal induction. Consequently, GSH depletion prevented the LPS-induced activation of antiviral response and its inhibition of influenza virus infection. LPS induction of a second group of genes (Prdx1, Srxn1, Hmox1, GSH synthase, cysteine transporters), mapping to nrf2 and the oxidative stress response, was increased by GSH depletion. We conclude that the main function of endogenous GSH is not to limit inflammation but to fine-tune the innate immune response to infection.
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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.