Neuro-endocrine-immune axis in rheumatoid arthritis.
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概要
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Objective. To elucidate the role of neurologic, endocrine, and immune system interactions in the development of pathologic responses in patients with rheumatoic arthritis (RA), we studied neuropeptide production and neuropeptide receptor expression in RA synovium and its function in patients with RA.<BR>Methods. The effects of neuropeptides on proinflammatory cytokine (interleukir (IL) -6 and IL-8) and collagenase production by RA synovial cells were estimated by enzyme-linked immunosorbent assay, and their messenger RNA expression was assessed by reverse transcription-polymerase chain reaction (RT-PCR) using-limiting dilutions of the complementary DNA. The expression of receptors for neuropeptides by RA synovial cells was also studied by RT-PCR and radioreceptor assays. Local production of neuropeptides was estimated by RT-PCR and immunohistochemical staining. Functions of some neuropeptides for the synovial cells were studied by using antagonists for the peptides.<BR>Results. Some neuropeptides inhibited proliferation of and proinflammatory cytokine and matrix metalloproteinase (MMP) production by RA synovial cells both at the level of mRNA expression and at the protein level, and another neuropeptides did rather upregulate them. Expression of receptors for the neuropeptides studied on RA synovial cells was confirmed by RT-PCR and radio-receptor assays. Functions of the neuropeptide receptors were inhibited by their receptor antagonists. Some, but not all, neuropeptides inhibited nuclear translocation and phosphorylation of transcription factor, cyclic AMP responsive element binding protein (CREB), in RA synovial cells, while prolactin acted via translocation of STAT-5 to nuclei in RA synovial cells.<BR>Conclusion. Neuropeptides upregulated or downregulated synovial cell functions, suggesting regulation of inflammatory responses by neuropeptides in patients with RA and possible clinical application of certain neuropeptides.
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