Lipopolysaccharide intracerebral administration induces minimal inflammatory reaction in rat brain.
An inflammatory reaction, essential for defence against infection and for wound repair, may also induce irreversible tissue damage. It appears that the central nervous system has developed its own immunosuppressive strategy in order to limit the destructive effects of inflammation. To clarify this point, we have characterized in one unique model of inflammation induced in the rat by intracerebral lipopolysaccharide injection 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 found decreased following LPS injection. No striking differences were observed in the brain parenchyma after stab lesion or inflammatory lesion apart from an increase in the number of monocytes/macrophages recruited early to the lesion area. Macrophages were later accumulated around the lesion when astroglia and microglia reactions occurred. Some of the 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- and CD4-negative CD8-positive cells, likely natural killer cells, was observed around the lesion site; this recruitment was inhibited by the highest dose of LPS. This study therefore supports the hypothesis of a suppression of some aspects of cell-mediated immunity in the brain, mechanisms which need to be further characterized.
Montero-Menei
C N
CN
INSERM U 298, CHU, Angers, France.
Sindji
L
L
Pouplard-Barthelaix
A
A
Jehan
F
F
Denechaud
L
L
Darcy
F
F
D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D015152:Blotting, Northern; D001921:Brain / Q000378:metabolism; D001930:Brain Injuries / Q000378:metabolism / Q000473:pathology; D019208:Brain-Derived Neurotrophic Factor; D004660:Encephalitis / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D007150:Immunohistochemistry; D007267:Injections; D008070:Lipopolysaccharides; D009414:Nerve Growth Factors / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014951:Wounds, Stab / Q000378:metabolism / Q000473:pathology
D015703:Antigens, CD; D019208:Brain-Derived Neurotrophic Factor; D005904:Glial Fibrillary Acidic Protein; D000949:Histocompatibility Antigens Class II; D008070:Lipopolysaccharides; D009414:Nerve Growth Factors; D009419:Nerve Tissue Proteins; D016212:Transforming Growth Factor beta