Macrophages and astroglial interactions in repair to brain injury.
The response to brain injury appears to involve a well-coordinated interaction between microglia, extrinsic macrophages and glial cells. The proliferation of glial cells at the site of the injury appears necessary to reseal the brain. Most data support the view that glial cell (and fibroblast and endothelial cell) proliferation is driven by IL-1-like factors liberated by the invaded macrophages. Although less well established, most data, including our own suggest that glial cells contribute to the neutrotrophic response found after brain injury. In vitro evidence suggests that glial cell-mediated production of neurotrophic factors may also depend, like glial cell proliferation, on actions of interleukins (e.g., IL-1) at the site of the injury. Moreover, evidence of in vivo experiments, showing that immunosuppressants inhibit the glial response and that inhibition of glial proliferation suppresses the neurotrophic response are in line with this view. Restoration of the damaged brain site may also be compatible with the lack of T and B cell infiltration at the lesioned site. Factors such as prostaglandins and TGF-beta released from glial cells may be involved in controlling and counteracting a threatening immune attack. In conclusion, tissue repair in the brain appears to be centered around regulatory properties of glial cell proliferation, enhancement of neuronal growth and inhibition of a local immune response.
Berkenbosch
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Department of Pharmacology, Medical Faculty, Free University, Amsterdam, The Netherlands.
D000818:Animals; D001253:Astrocytes / Q000502:physiology*; D001812:Blood-Brain Barrier; D001930:Brain Injuries / Q000503:physiopathology*; D002450:Cell Communication; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D007375:Interleukin-1 / Q000096:biosynthesis; D008264:Macrophages / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains
D000949:Histocompatibility Antigens Class II; D007375:Interleukin-1