Differences in oxidative response of subpopulations of neutrophils from healthy subjects and patients with rheumatoid arthritis.
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Objectives To determine whether blood neutrophils from healthy individuals and blood and synovial fluid neutrophils from patients with rheumatoid arthritis (RA) responded differently to priming agonists and stimuli of the oxidative burst and, if so, whether this was a property of a subpopulation of neutrophils.Methods Continuous flow electrophoresis was used to separate neutrophils into subpopulations based upon quantitative differences in net negative surface charge. The generation of superoxide anion (O2-) was used as a measure of oxidative activity using 10(-7) mol/l N-formyl-methionylleucyl-phenylalanine (FMLP) as the stimulating agonist and 10(-8) mol/l platelet activating factor (PAF) as the priming agent.Results The production of O2- by blood and synovial fluid neutrophils from RA patients in response to FMLP was greater than that observed with control blood neutrophils (p < 0.001). Priming of normal blood neutrophils with PAF increased their FMLP induced oxidative burst (p < 0.001), but PAF treatment had no effect on rheumatoid neutrophils. Neutrophils from synovial fluid of RA patients were less electronegative than paired blood samples and exposure of blood neutrophils to FMLP but not PAF reduced their surface charge. Continuous flow electrophoresis isolated three neutrophil subpopulations: cells of least surface electronegativity were ascribed to pool P1 and cells of greatest surface electro-negativity to P3. Normal blood neutrophils from P3, but not P1, showed increased oxidative activity after PAF priming (twofold increase; p < 0.01), whereas the responsiveness of rheumatoid blood and synovial fluid neutrophils from P1 and P3 was not modified by PAF treatment under the same conditions.Conclusion It is suggested that most of the circulating neutrophils in RA are already in a state of readiness to generate O2- upon activation by an inflammatory stimulus. This is in contrast to normal blood neutrophils, which have both responsive and non-responsive subpopulations with respect to priming agonists.
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In RA, neutrophils are primed to respond to fMet peptides, shown by high oxidative burst to fMLP ex vivo.
“In this disease, neutrophils are primed to respond to fMet peptides, as shown by the high oxidative burst of neutrophils in response to fMLP, a prototypic bacterial fMet peptide, ex vivo180.”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [180]
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The role of mitochondria in rheumatic diseases
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- Authors
- Eggleton, P., Wang, L., Penhallow, J., Crawford, N., & Brown, K. A.
- Affiliations
- University of Oxford (GB)
- ORCID
- Eggleton, P
- Venue
- Annals of the Rheumatic Diseases
- Publisher
- Elsevier BV
- Published
- 1995-11
- Volume
- 54
- Issue
- 11
- Pages
- 916-923
- ISSN
- 0003-4967 (ISSN-L)
- PMC
- PMC1010043
- OpenAlex
- W1972948730
- Cited by
- 82
- References
- 32
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 3 · 2020: 4 · 2019: 7 · 2018: 5 · 2017: 3 · 2016: 4 · 2015: 2 · 2014: 1 · 2013: 2 · 2012: 2
- FWCI
- 1.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of the Rheumatic Diseases (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- rheumatoid arthritis, neutrophils, neutrophil subpopulations, respiratory burst, superoxide, platelet-activating factor, fMLP, surface charge, neutrophil priming
- MeSH terms
- Arthritis, Rheumatoid, Cell Separation, Electrophoresis, Humans, Neutrophils, Platelet Activating Factor, Superoxides, Synovial Fluid, Respiratory Burst, Neutrophil Activation
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