Link between optic nerve regrowth failure and macrophage stimulation in mammals.

The adult mammalian central nervous system (CNS) fails to regenerate its axons following injury. A comparison between its postinjury response and that of axons of nervous systems capable of regeneration reveals major differences with respect to inflammation. In regenerative systems, a large number of macrophages rapidly invade the injured site during the first few hours and days after the injury. Following their activation/differentiation through interaction with the host tissue, they play a central role in tissue healing through phagocytosis of cell debris and communication with cellular and molecular elements of the damaged tissue. Relative to the peripheral nervous system (PNS), macrophage recruitment in the adult mammalian CNS is delayed and is restricted in amount and activity. It was recently proposed that in injured mammalian CNS tissue, implantation of macrophages stimulated by prior co-culture with segments of peripheral (sciatic) nerves can compensate, at least in part, of the restricted postinjury inflammatory reaction. In the present study, this experimental paradigm is further explored and shows that there is no conflict between the systemic use of anti-inflammatory compounds and treatment with stimulated macrophages to promote regrowth of neuronal tissue.