Interleukin-1 beta does not induce reactive astrogliosis, neovascularization or scar formation in the immature rat brain.
The adult mammalian central nervous system (CNS) reacts to a penetrating injury with the formation of a glial scar consisting of a newly formed glia limitans accessoria, basement membrane and meningeal fibroblasts. By contrast, in fetal and perinatal mammals a similar injury evokes only a reduced reactive astrogliosis, and a typical astroglial scar begins to develop only when the lesion has been placed beyond a critical developmental period. In the present investigation we have tested the hypothesis that IL-1 beta plays a pivotal role in the process of cicatrization, by investigating whether immature animals develop a glial scar after IL-1 beta is injected into their CNS. Adult female rats were given injections of 2U recombinant IL-1 beta or PBS alone in the contralateral cortex in identical positions of the cerebral hemispheres. Postnatal day 2 (P2) rats received injections of either 1U IL-beta or PBS into the lateral aspect of the frontal cortex on each side. The animals were sacrificed 4 and 14 days post injection and the perilesional area was assessed for astrogliosis (expression of GFAP-immunoreactivity and the activity of glutamine synthetase), neovascularization (laminin-immunoreactivity on blood vessels at the lesion site), and the formation of a gliomeningeal scar (GFAP- and laminin-immunoreactivity at the lesion site). Using similar criteria for the evaluation, we found that in adult animals some of the processes associated with cicatrization are augmented. In the immature animals, however, the formation of the glio-meningeal scar is not altered by IL-1 beta, i.e. it remains absent. We conclude that IL-1 beta augments some responses of the cells involved in wound healing in the adult CNS, but does not alter key mechanisms operative in the reaction of the brain to a penetrating injury, as shown by its inability to alter the stage specific response of the immature brain.
Sievers
J
J
Anatomisches Institut der Universität Kiel, Germany.
Struckhoff
G
G
Puchner
M
M
D000818:Animals; D001253:Astrocytes / Q000502:physiology*; D001930:Brain Injuries / Q000473:pathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D002921:Cicatrix / Q000473:pathology*; D005260:Female; D005974:Glutamate-Ammonia Ligase / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000494:pharmacology*; D009389:Neovascularization, Pathologic / Q000139:chemically induced / Q000473:pathology*; D009457:Neuroglia / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins / Q000378:metabolism
D007375:Interleukin-1; D011994:Recombinant Proteins; D005974:Glutamate-Ammonia Ligase