ArticleFree radical biology & medicine2013
Glutathione reductase is essential for host defense against bacterial infection.
Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 53 citations in OpenAlex.
- lncRNA-mRNA Co-expression Network Unveils Neutrophil Metabolic Reprogramming in Human Sepsis.Inflammation · 2026Article
- The transsulfuration pathway suppresses the embryonic lethal phenotype of glutathione reductase mutants in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2025Article
- Integrated transcriptomics and metabolomics analysis reveal the regulatory mechanisms underlying the combined effects of heat and glucose starvation on carotenoid biosynthesis in Rhodotorula glutinis YM25079.Biotechnology for biofuels and bioproducts · 2025Article
- Glutathione reductase modulates endogenous oxidative stress and affects growth and virulence in Avibacterium paragallinarum.Veterinary research · 2025Article
- Development and validation of a machine learning-driven mitochondrial gene signature for the diagnosis of breast cancer.Frontiers in immunology · 2025Article
- Symbiotic T6SS affects horizontal transmission ofISME communications · 2025Article
- Modulation of Innate Immune Memory Dynamics by Subcellular Reactive Oxygen Species.Antioxidants & redox signaling · 2023Review
- Diversity of arterial cell and phenotypic heterogeneity induced by high-fat and high-cholesterol diet.Frontiers in cell and developmental biology · 2023Article
- Redox regulation of the immune response.Cellular & molecular immunology · 2022Review
- The interaction mechanism of nickel ions with L929 cells based on integrative analysis of proteomics and metabolomics data.Regenerative biomaterials · 2022Article
- Preclinical insights into fucoidan as a nutraceutical compound against perfluorooctanoic acid-associated obesityFrontiers in nutrition · 2022Article
- Glutathione Reductase Is Associated with the Clinical Outcome of Septic Shock in the Patients Treated Using Continuous Veno-Venous Haemofiltration.Medicina (Kaunas, Lithuania) · 2021Observational
- Prolonged Transcriptional Consequences in Survivors of Sepsis.International journal of molecular sciences · 2021Article
- Genomic Analysis of Natural RoughInternational journal of molecular sciences · 2020Article
- Biodegradable Nickel Disulfide Nanozymes with GSH-Depleting Function for High-Efficiency Photothermal-Catalytic Antibacterial Therapy.iScience · 2020Article
- Glutathione Reductase Promotes Fungal Clearance and Suppresses Inflammation during SystemicJournal of immunology (Baltimore, Md. : 1950) · 2019Article
- A parent-of-origin analysis of paternal genetic variants and increased risk of conotruncal heart defects.American journal of medical genetics. Part A · 2018Article
- Group BFrontiers in cellular and infection microbiology · 2017Article
- Article
- Reactive oxygen species and antioxidant defense in human gastrointestinal diseases.Integrative medicine research · 2016Review
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Glutathione reductase (Gsr) catalyzes the reduction of glutathione disulfide to glutathione, a major cellular antioxidant. We have recently shown that Gsr is essential for host defense against the gram-negative bacteria Escherichia coli in a mouse model of sepsis. Although we have demonstrated that Gsr is required for sustaining the oxidative burst and the development of neutrophil extracellular traps, the role of Gsr in other phagocytic functions remains unclear. It is also unclear whether Gsr-deficient mice exhibit host defense defects against gram-positive bacteria. In this study, we characterized the effects of Gsr deficiency on the innate immune responses to a gram-positive bacterium, group B Streptococcus, and to the gram-negative bacterial cell wall component lipopolysaccharide (LPS). We found that, like E. coli, group B Streptococcus resulted in a substantially more robust cytokine response and a markedly higher morbidity and mortality in Gsr-deficient mice than in wild-type mice. The increased morbidity and mortality were associated with greater bacterial burden in the Gsr-deficient mice. Interestingly, Gsr-deficient mice did not exhibit a greater sensitivity to LPS than did wild-type mice. Analysis of the neutrophils of Gsr-deficient mice revealed impaired phagocytosis. In response to thioglycollate stimulation, Gsr-deficient mice mobilized far fewer phagocytes, including neutrophils, macrophages, and eosinophils, into their peritoneal cavities than did wild-type mice. The defective phagocyte mobilization is associated with profound oxidation and aggregation of ascitic proteins, particularly albumin. Our results indicate that the oxidative defense mechanism mediated by Gsr is required for an effective innate immune response against bacteria, probably by preventing phagocyte dysfunction due to oxidative damage.
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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.