PMID- 16238536
OWN - NLM
STAT- MEDLINE
DCOM- 20051212
LR  - 20071115
IS  - 0300-5577 (Print)
IS  - 0300-5577 (Linking)
VI  - 33
IP  - 5
DP  - 2005
TI  - White matter damage and chemokine induction in developing rat brain after 
      intrauterine infection.
PG  - 415-22
AB  - 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 alpha 
      mRNA (MIP-1 alpha mRNA), macrophage inflammatory protein-1 beta mRNA (MIP-1beta 
      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 alpha mRNA 
      and MIP-1 beta mRNA in brain of the E. coli-treated pup rat were higher than the 
      control at P1, but the expression of MIP-1 alpha mRNA and MIP-1 beta 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 alpha, MIP-1 beta in neonatal brain after 
      intrauterine infection indicated that MIP-1 alpha, MIP-1 beta may be a mechanism 
      mediating between the neonatal white matter damage and the intrauterine 
      infection.
FAU - Yuan, Tian-Ming
AU  - Yuan TM
AD  - Department of Neonatology, Laboratory, Children's Hospital, Zhejiang University 
      School of Medicine, Hangzhou, PR China.
FAU - Yu, Hui-Min
AU  - Yu HM
FAU - Gu, Wei-Zhong
AU  - Gu WZ
FAU - Li, Jian-Ping
AU  - Li JP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - J Perinat Med
JT  - Journal of perinatal medicine
JID - 0361031
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokines)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (RNA, Messenger)
RN  - EC 3.1.4.- (2',3'-Cyclic-Nucleotide Phosphodiesterases)
SB  - IM
MH  - 2',3'-Cyclic-Nucleotide Phosphodiesterases/metabolism
MH  - Animals
MH  - Animals, Newborn
MH  - Brain/*metabolism
MH  - Chemokine CCL4
MH  - Chemokines/*metabolism
MH  - Escherichia coli Infections/*metabolism/microbiology
MH  - Female
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Immunochemistry
MH  - Macrophage Inflammatory Proteins/metabolism
MH  - Pregnancy
MH  - Pregnancy Complications, Infectious/*metabolism/microbiology
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2005/10/22 09:00
MHDA- 2005/12/15 09:00
CRDT- 2005/10/22 09:00
PHST- 2005/10/22 09:00 [pubmed]
PHST- 2005/12/15 09:00 [medline]
PHST- 2005/10/22 09:00 [entrez]
AID - 10.1515/JPM.2005.074 [doi]
PST - ppublish
SO  - J Perinat Med. 2005;33(5):415-22. doi: 10.1515/JPM.2005.074.