An inflammatory reaction, essential for defence against infection and
for wound repair, may also induce irreversible tissue damage. It appea
rs that the central nervous system has developed its own immunosuppres
sive strategy in order to limit the destructive effects of inflammatio
n. To clarify this point, we have characterized in one unique model of
inflammation induced in the rat by intracerebral lipopolysaccharide i
njection the kinetics of the inflammatory reaction, the participation
of immunitary and glial cells and of three growth factors. Among these
molecules, brain-derived neurotrophic factor mRNA expression was foun
d decreased following LPS injection. No striking differences were obse
rved in the brain parenchyma after stab lesion or inflammatory lesion
apart from an increase in the number of monocytes/macrophages recruite
d early to the lesion area. Macrophages were later accumulated around
the lesion when astroglia and microglia reactions occurred. Some of th
e macrophages and microglia expressed major histocompatibility complex
class II antigens on their surface whereas no T or B lymphocytes were
observed in the brain parenchyma. However, a subpopulation of CD3- an
d CD4-negative CD8-positive cells, likely natural killer cells, was ob
served around the lesion site; this recruitment was inhibited by the h
ighest dose of LPS. This study therefore supports the hypothesis of a
suppression of some aspects of cell-mediated immunity in the brain, me
chanisms which need to be further characterized.