Article ID Journal Published Year Pages File Type
3063954 Journal of Neuroimmunology 2015 7 Pages PDF
Abstract

•There was a significant upregulation of spinal cord CGRP in murine AIDS infection.•CGRP reduced viral load in mixed glia in a microglial content-dependent manner.•CGRP's anti-retroviral effect requires interaction between CGRP and host cell.

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.

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