Tuyển tập các báo cáo nghiên cứu khoa học quốc tế về bệnh thú y đề tài: Increased expression of osteopontin in the spinal cords of Lewis rats with experimental autoimmune neuritis | J. Vet. Sci. 2004 5 4 289-293 JOURNAL OF Veterinary Science Increased expression of osteopontin in the spinal cords of Lewis rats with experimental autoimmune neuritis Changjong Moon Taekyun Shin Department of Veterinary Medicine Cheju National University Jeju 690-756 Korea To investigate the pattern of expression of osteopontin OPN in tissues of the central nervous system CNS responding to peripheral immunological stimulation the expression of OPN was studied in the spinal cord of rats with experimental autoimmune neuritis EAN . In this model system the sciatic nerves and spinal nerve roots are the target organs of EAN and the spinal cord is a remote organ that may be indirectly affected. OPN was constitutively expressed in some astrocytes adjacent to the pia mater and neurons in normal rats. In rats with EAN OPN was increased in the same cells and in some inflammatory cells including macrophages in the subarachnoid space. Expression of CD44 a receptor of OPN was weak in normal spinal cord tissue and increased in the entire spinal cord parenchyma in rats with EAN as well as in inflammatory cells. These findings suggest that inflammatory cells as well as reactive astrocytes are major sources of OPN and CD44 in the spinal cord of rats with EAN. Further study is needed to elucidate the functional role of OPN in the spinal cord affected by EAN. Key words Experimental autoimmune neuritis osteopontin CD44 spinal cord Introduction Experimental autoimmune neuritis EAN is a T-cell-mediated autoimmune disease of the peripheral nervous system that is used as a model of human demyelinating diseases 17 . The clinical course of EAN is characterized by weight loss ascending progressive paralysis and spontaneous recovery. It has been proposed that inflammatory mediators produced in the affected spinal nerve roots and sciatic nerves are involved in the pathogenesis of EAN 22 . Although the major lesions of Corresponding author Tel 82-64-754-3363 Fax 82-64-756-3354 E-mail .
