Malon Jennifer, Grlickova-Duzevik Eliza, Vaughn James, Beaulac Holly, Vunk Tyler R, Cao Ling
Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, Biddeford, ME.
Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME.
J Neuroimmunol. 2015 Feb 15;279:64-70. doi: 10.1016/j.jneuroim.2015.01.010. Epub 2015 Jan 27.
C57BL/6 (B6) mice develop peripheral neuropathy post-LP-BM5 infection, a murine model of HIV-1 infection, along with the up-regulation of select spinal cord cytokines. We investigated if calcitonin gene-related peptide (CGRP) contributed to the development of peripheral neuropathy by stimulating glial responses. An increased expression of lumbar spinal cord CGRP was observed in vivo, post-LP-BM5 infection. Consequently, in vitro CGRP co-treatments led to a microglial content-dependent attenuation of viral loads in spinal cord mixed glia infected with selected doses of LP-BM5. This inhibition was neither caused by the loss of glia nor induced via the direct inhibition of LP-BM5 by CGRP.
C57BL/6(B6)小鼠在感染LP-BM5后会出现周围神经病变,LP-BM5是一种HIV-1感染的小鼠模型,同时特定脊髓细胞因子会上调。我们研究了降钙素基因相关肽(CGRP)是否通过刺激神经胶质反应促进周围神经病变的发展。在体内,LP-BM5感染后观察到腰脊髓CGRP表达增加。因此,在体外,CGRP共同处理导致感染选定剂量LP-BM5的脊髓混合神经胶质中病毒载量呈小胶质细胞含量依赖性衰减。这种抑制既不是由神经胶质损失引起的,也不是由CGRP直接抑制LP-BM5诱导的。