Báo cáo y học: "Suppression of the inflammatory response in experimental arthritis is mediated via estrogen receptor α but not estrogen receptor "

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Suppression of the inflammatory response in experimental arthritis is mediated via estrogen receptor α but not estrogen receptor β. | Dulos et al. Arthritis Research Therapy 2010 12 R101 http content 12 3 R101 RESEARCH ARTICLE Open Access Suppression of the inflammatory response in experimental arthritis is mediated via estrogen receptor a but not estrogen receptor p John Dulos Peter Vijn Cindy van Doorn Claudia L Hofstra Desiree Veening-Griffioen Jan de Graaf Fred A Dijcks and Annemieke MH Boots Abstract Introduction The immune modulatory role of estrogens in inflammation is complex. Both pro- and anti-inflammatory effects of estrogens have been described. Estrogens bind both estrogen receptor ER a and P. The contribution of ERa and ERP to ER-mediated immune modulation was studied in delayed type hypersensitivity DTH and in experimental arthritis Methods ER-mediated suppression of rat adjuvant arthritis AA was studied using ethinyl-estradiol EE and a selective ERP agonist ERB-79 . Arthritis was followed for 2 weeks. Next effects of ER agonists ethinyl-estradiol an ERa selective agonist ERA-63 and a selective ERP agonist ERB-79 on the development of a tetanus toxoid TT -specific delayed type hypersensitivity response in wild type WT and in ERa - or ERP-deficient mice were investigated. Finally EE and ERA-63 were tested for their immune modulating potential in established collagen induced arthritis in DBA 1J mice. Arthritis was followed for three weeks. Joint pathology was examined by histology and radiology. Local synovial cytokine production was analyzed using Luminex technology. Sera were assessed for COMP as a biomarker of cartilage destruction. Results EE was found to suppress clinical signs and symptoms in rat AA. The selective ERP agonist ERB-79 had no effect on arthritis symptoms in this model. In the TT-specific DTH model EE and the selective ERa agonist ERA-63 suppressed the TT-specific swelling response in WT and ERPKO mice but not in ERaKO mice. As seen in the AA model the selective ERP agonist ERB-79 did not suppress inflammation. Treatment with EE or ERA-63 .

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