2005 Fiscal Year Final Research Report Summary
Therapeutic strategy for autoimmune disease at the neuroendocrine-immune interface
Project/Area Number |
16590999
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
膠原病・アレルギー・感染症内科学
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Research Institution | St.Marianna University School of Medicine |
Principal Investigator |
NAGAFUCHI Hiroko St.Marianna Univ.Sch Med, Lecturer, 医学部, 講師 (80278001)
|
Project Period (FY) |
2004 – 2005
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Keywords | rheumatoid arthritis / systemic lupus erythematosus / neuroendocrine immune system / prolactin / growth hormone / luslin-growth factor / neuropeptide |
Research Abstract |
I investigated about the role of neuroendocrine-immune system in autoimmune disease. I found that synovial cells and T cells in patients with rheumatoid arthritis (RA) produced prolactin, IL-6 and TNFα. Prolactin induced TNFα, IL-6 and IL-8 production from RA synovium and enhanced proliferation of fibroblast-like synovial cells. Prolactin induced MMP-3 production and inhibited TIMP-1 production in RA synovial cells. Prolactin receptors were expressed in the surface of macrophage-like synovial cells, fibroblast-like synovial cells, and synovium-infiltraring T cells. Bromocriptine, which inhibites the secretion of prolactin from endocrine cells and immune cells, inhibited prolactin production in RA synovium, and then IL-6,IL-8 production in RA synovium. Bromocriptine also inhibited RA synovial cell proliferation. These results suggested that prolactin involved bone-carilage distruction in RA pathgenesis. I found that NGF involved the pathogenesis in RA synovium. Furthermore, I studied the expression of hormome and neuropeptides in RA synovium and their production in serum in patients with RA, systemic lupus erythematosusu (SLE), and vasculitis. I found the presence of Growth hormone, TRH, and TSH producing cells in RA synovium. Growth hormone, prolactin and IGFBP-3 production increased in serum in some patients with RA, SLE and vasculitis. These results suggested that neuroendocrine-immune system involved the pathogenesis in autoimmune disease. Further examination is necessary about them.
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Research Products
(2 results)