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Intracellular Oxidative Activation in Synovial Fluid Neutrophils from Patients with Rheumatoid Arthritis But Not from Other Arthritis Patients
JAN CEDERGREN, TONY FORSLUND, TOMMY SUNDQVIST, and THOMAS SKOGH
ABSTRACT. Methods. Peripheral blood and SF samples were obtained from 26 gonarthritis patients (13 RA, 13 non-RA) attending the rheumatology unit for therapeutic joint aspiration. Isolated neutrophils were stimulated by a formylated tripeptide (fMLF) or by microbeads coated with collagen-I. Formation of superoxide-anion-derived reactive oxygen species (ROS) was studied by luminol-enhanced chemiluminescence. Paired samples of blood and SF neutrophils from patients with active arthritis were compared with blood neutrophils from patients in remission and from 47 healthy blood donors. Results. SF neutrophils from patients with RA, but not from non-RA patients, showed high baseline intracellular ROS production. Blood neutrophils from arthritis patients in remission existed in a primed state as revealed by more rapid oxidative response after collagen-bead challenge and a more pronounced response after fMLF stimulation compared to healthy blood donors. Blood neutrophils from RA patients with ongoing gonarthritis, however, did not differ from healthy blood donors concerning oxidative activation, whereas blood neutrophils from non-RA patients with gonarthritis showed a significantly lower peak ROS production. Conclusion. A novel finding with pathogenetic implications in our study is that SF neutrophils from patients with RA, but not other arthritides, are activated and produce ROS intracellularly. This implies that synovial neutrophils in RA are engaged in the processing of endocytosed material. (First Release Oct 15 2007; J Rheumatol 2007;34:2162-70) Key Indexing Terms:
NEUTROPHILS
From the Division of Rheumatology and the Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Linköping University, Linköping, Sweden. Supported by grants from the Swedish Rheumatism Association, the Swedish Research Council (project K2006-74X-14594-04-3), Linköping University Hospital Research Foundations, King Gustav V 80-year foundation, and the county council of Östergötland. J. Cedergren, MD, Division of Rheumatology; T. Forslund, PhD, Division of Medical Microbiology; T. Sundqvist, PhD, Professor of Medical Microbiology; T. Skogh, MD, PhD, Professor of Rheumatology. Address reprint requests to Dr. J. Cedergren, Division of Rheumatology, Linköping University Hospital, SE-581 85 Linköping, Sweden. E-mail: jan.cedergren@lio.se Accepted for publication July 5, 2007. |
