Production of PAF-acether by synovial fluid neutrophils in rheumatoid arthritis
| Autor: | A. Dulioust, C. Gregoir, A. Arnoux, C. J. Menkès, P. Hilliquin |
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| Rok vydání: | 1995 |
| Předmět: |
Allergy
medicine.medical_specialty Platelet Aggregation Neutrophils Immunology Phospholipid Arthritis In Vitro Techniques Arthritis Rheumatoid Pathogenesis chemistry.chemical_compound Internal medicine Synovial Fluid medicine Humans Synovial fluid Platelet Activating Factor Calcimycin Pharmacology Ionophores Platelet-activating factor business.industry respiratory system medicine.disease Rheumatology chemistry Rheumatoid arthritis lipids (amino acids peptides and proteins) business |
| Zdroj: | Inflammation Research. 44:313-316 |
| ISSN: | 1420-908X 1023-3830 |
| DOI: | 10.1007/bf01796260 |
| Popis: | PAF-acether (PAF) is a pro-inflammatory phospholipid molecule potentially involved in the pathogenesis of arthritis. PAF and related metabolites have been isolated in the synovial fluid from patients with arthritis. The aim of this study was to determine fluid and blood in patients with rheumatoid arthritis. Blood neutrophils from normal donors were also studied for their capacity to form PAF. Neutrophils were stimulated with the calcium ionophore A23187 (2 microM) for 1 to 60 min. PAF released in the medium and PAF associated to cells were measured. In synovial fluid neutrophils. PAF production began as soon as 1 min of stimulation (16.1 +/- 6.3 pmol per 1 x 10(6) cells) and reached a maximum at 20 min: 29.2 +/- 2.8 pmol per 1 x 10(6) cells (mean +/- SEM, n = 5). The amount of PAF released in the supernatant increased with the length of stimulation, similar amounts of PAF were produced by blood neutrophils isolated from the joint had a lower capacity to produce PAF than blood neutrophils from the same patients. The present results demonstrate the synthesis and release of PAF by synovial fluid neutrophils. They suggest that neutrophils may be source of PAF locally present in the joint. Newly synthesized PAF could participate in the amplification of the local inflammatory reaction. |
| Databáze: | OpenAIRE |
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