The central nervous system (CNS) does not regenerate partly due to the slow clearance of debris from the degenerated myelin sheath by Wallerian degeneration. The mechanism underlying the inefficiency in myelin clearance is not clear. Here we showed that endogenous proBDNF may inhibit the infiltration of ED1+ inflammatory cells after spinal cord injury. After injury, proBDNF and its receptors sortilin and p75NTR are expressed in the spinal cord as determined by Western blots and immunocytochemistry. ProBDNF and mature BDNF were released from macrophages in vitro. Macrophages in vivo (ED1+) and isolated in vitro (CD11b+) express moderate levels of proBDNF, sortilin and p75NTR. ProBDNF suppressed the migration of isolated macrophages in vitro and the antibody to proBDNF enhanced the migration. Suppression of proBDNF in vivo by administering the antiserum to the prodomain of BDNF after spinal cord injury (SCI) increased the infiltration of macrophages and increased number of neurons in the injured cord. BBB tests showed that the treatment of the antibody to proBDNF improved the functional recovery after spinal cord injury. Our data suggest that proBDNF is a suppressing factor for macrophage migration and infiltration and may play a detrimental role after SCI.
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