ArticleRedox biology2020
Activation leads to a significant shift in the intracellular redox homeostasis of neutrophil-like cells.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Formation of the intradimer disulfide bond in human calprotectin maintains metal-withholding function and tunes proteolytic susceptibility.Chemical science · 2026Article
- Redox Biology and Insulin-like Growth Factor-Binding Protein-6: A Potential Relationship.Biology · 2025Review
- Two redox-responsive LysR-type transcription factors control the oxidative stress response of Agrobacterium tumefaciens.Nucleic acids research · 2025Article
- Neutrophil-activating Peptide 2 as a Novel Modulator of Fibrin Clot Properties in Patients with Atrial Fibrillation.Translational stroke research · 2024Article
- Exploring Immune Redox Modulation in Bacterial Infections: Insights into Thioredoxin-Mediated Interactions and Implications for Understanding Host-Pathogen Dynamics.Antioxidants (Basel, Switzerland) · 2024Review
- The role of glutathione in periplasmic redox homeostasis and oxidative protein folding in Escherichia coli.Redox biology · 2023Article
- Review
- Article
- Abundant Monovalent Ions as Environmental Signposts for Pathogens during Host Colonization.Infection and immunity · 2021Review
- The effects of neutrophil-generated hypochlorous acid and other hypohalous acids on host and pathogens.Cellular and molecular life sciences : CMLS · 2021Review
- NETosis as a Pathogenic Factor for Heart Failure.Oxidative medicine and cellular longevity · 2021Review
- In Vivo Imaging with Genetically Encoded Redox Biosensors.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils produce a cocktail of oxidative species during the so-called oxidative burst to attack phagocytized bacteria. However, little is known about the neutrophils' redox homeostasis during the oxidative burst and there is currently no consensus about the interplay between oxidative species and cellular signaling, e.g. during the initiation of the production of neutrophil extracellular traps (NETs). Using the genetically encoded redox sensor roGFP2, expressed in the cytoplasm of the neutrophil-like cell line PLB-985, we saw that stimulation by both PMA and E. coli resulted in oxidation of the thiol residues in this probe. In contrast to the redox state of phagocytized bacteria, which completely breaks down, the neutrophils' cytoplasmic redox state switched from its intital -318 ± 6 mV to a new, albeit higher oxidized, steady state of -264 ± 5 mV in the presence of bacteria. This highly significant oxidation of the cytosol (p value = 7 × 10
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Registered trials
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