The role of somatostatin in the pathophysiology of rheumatoid arthritis.
Involvement of neuro-endocrineimmune interactions in the development of pathologic responses has been suggested in patients with rheumatoid arthritis (RA). Recently we studied the production of an inhibitory neuropeptide-somatostatin (SOM)--and somatostatin receptor (SOMR) expression in RA synovium and its function in patients with RA. We found that physiologic concentrations of SOM inhibited the proliferation of RA synovial cells. Proinflammatory cytokine and matrix metalloproteinase (MMP) production by RA synovial cells were also inhibited by SOM. Subtype 1 and subtype 2 SOMR were expressed on fibroblast-like synovial cells, and the expression of subtype 2 SOMR was up-regulated with the proinflammatory cytokine treatment of the synovial cells in RA patients. RA fibroblast-like cells synthesized SOM by themselves, suggesting that SOM may act as an autocrine regulator of synovial cell functions in RA patients. SOM and SOM analogues have also been reported to be effective in the treatment of patients with RA. In summary, SOM inhibited aberrant synovial cell functions in patients with RA, suggesting a possible clinical application of this neuropeptide.
Sakane
T
T
Department of Immunology, St. Marianna University School of Medicine, Kanagawa, Japan.
Suzuki
N
N
D001172:Arthritis, Rheumatoid / Q000378:metabolism / Q000503:physiopathology*; D002478:Cells, Cultured; D006801:Humans; D017481:Receptors, Somatostatin / Q000378:metabolism; D013004:Somatostatin / Q000494:pharmacology / Q000502:physiology*; D013583:Synovial Membrane / Q000166:cytology / Q000187:drug effects / Q000378:metabolism
D017481:Receptors, Somatostatin; D013004:Somatostatin