ArticleRheumatology (Oxford, England)2016
Neutrophils from patients with SAPHO syndrome show no signs of aberrant NADPH oxidase-dependent production of intracellular reactive oxygen species.
Article in Rheumatology (Oxford, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Current and future advances in practice: SAPHO syndrome and chronic non-bacterial osteitis (CNO).Rheumatology advances in practice · 2024Review
- Serum-derived extracellular vesicles inhibit osteoclastogenesis in active-phase patients with SAPHO syndrome.Therapeutic advances in musculoskeletal disease · 2021Article
- Article
- Synovitis, acne, pustulosis, hyperostosis, and osteitis syndrome: review and update.Therapeutic advances in musculoskeletal disease · 2020Review
- Enhanced migration and adhesion of peripheral blood neutrophils from SAPHO patients revealed by RNA-Seq.Orphanet journal of rare diseases · 2019Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveWe aimed to investigate if aberrant intracellular production of NADPH oxidase-derived reactive oxygen species (ROS) in neutrophils is a disease mechanism in the autoinflammatory disease SAPHO syndrome, characterized by synovitis, acne, pustulosis, hyperostosis and osteitis, as has previously been suggested based on a family with SAPHO syndrome-like disease.
methodsNeutrophil function was explored in a cohort of four patients with SAPHO syndrome, two of whom were sampled during both inflammatory and non-inflammatory phase. Intracellular neutrophil ROS production was determined by luminol-amplified chemiluminescence in response to phorbol myristate acetate.
resultsCells from all patients produced normal amounts of ROS, both intra- and extracellularly, when compared with internal controls as well as with a large collection of healthy controls assayed in the laboratory over time (showing an extensive inter-personal variability in a normal population). Further, intracellular production of ROS increased during the inflammatory phase. Neutrophil activation markers were comparable between patients and controls.
conclusionDysfunctional generation of intracellular ROS in neutrophils is not a generalizable feature in SAPHO syndrome. Secondly, serum amyloid A appears to be a more sensitive inflammatory marker than CRP during improvement and relapses in SAPHO syndrome.
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