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In order to investigate the neuropathological effects on the developing rat brain after intrauterine infection, identification of glail fibrillary acidic protein (GFAP), 2′, 3′-cyclic nucleotide phosphodiesterase (CNPase), and neurofilament (NF) was observed.  Escherichia coli  ( E. coli ) was inoculated into uterine horn of pregnant rats when gestation was 70% complete (15 days) and the control group was inoculated with normal saline. Immunohistochemistry was used for evaluation of GFAP, CNPase, and NF expression in pup brains at postnatal day 7 (P7) and reverse transcriptase-PCR (RT-PCR) to analyze macrophage inflammatory protein-1 α mRNA (MIP-1 α mRNA), macrophage inflammatory protein-1 β mRNA (MIP-1β mRNA), the regulated upon activation normal T expressed and secreted chemokine mRNA (RANTES mRNA) and Eotaxin mRNA expression in pup brains at P1, P3 and P7. The numbers of GFAP-positive cells of the  E. coli -treated group pups were marked increased in periventricular white matter and hippocampus at P7 compared with the control group but no significant different levels of GFAP expression in corpus callosum were found between two groups. The integrate density (ID) of CNPase-positive staining of the  Escherichia coli -treated group pups were marked decreased in periventricular white matter and corpus callosum at P7 compared with the control group. The ID of NF-positive staining of the  Escherichia coli -treated group pups were marked decreased in periventricular white matter at P7 compared with the control group and no significant different levels of NF expression in corpus callosum were found between two groups. The expression of MIP-1 α mRNA and MIP-1 β mRNA in brain of the  E. coli -treated pup rat were higher than the control at P1, but the expression of MIP-1 α mRNA and MIP-1 β mRNA in brain of the pup rat at P3 and P7 had no significant difference between two groups. The alteration of expression of GFAP, CNPase, and NF in the brain of neonatal rats after intrauterine infection suggested that intrauterine infection could cause neonatal white matter damage. Moreover, the transient increase in expression of chemokine such as MIP-1 α, MIP-1 β in neonatal brain after intrauterine infection indicated that MIP-1 α, MIP-1 β may be a mechanism mediating between the neonatal white matter damage and the intrauterine infection.

White matter damage and chemokine induction in developing rat brain after intrauterine infection