PMID- 8903849
OWN - NLM
STAT- MEDLINE
DCOM- 19970306
LR  - 20071115
IS  - 0889-1591 (Print)
IS  - 0889-1591 (Linking)
VI  - 9
IP  - 4
DP  - 1995 Dec
TI  - Central nervous system chemokine mRNA accumulation follows initial leukocyte 
      entry at the onset of acute murine experimental autoimmune encephalomyelitis.
PG  - 315-30
AB  - Central nervous system (CNS) expression of two chemokine mRNAs, encoding monocyte 
      chemoattractant protein-1 (MCP-1) and IFN-gamma-inducible protein (IP-10), was 
      previously shown to be closely related to the onset of clinical signs of murine 
      experimental autoimmune encephalomyelitis (EAE). Chemokine mRNAs accumulated in a 
      striking, transient burst within astrocytes, near inflammatory leukocyte 
      infiltrates. It remained unclear if chemokines functioned to initiate leukocyte 
      entry into CNS tissues, or to amplify the intrathecal inflammatory reaction. To 
      address this issue, we determined the expression of chemokine mRNAs at the 
      earliest evidence of CNS immune-mediated inflammation. For these experiments, 
      mice were sacrificed in pairs at varying times after immunization. Only one 
      member of each pair was symptomatic for EAE at the time of sacrifice. Symptom 
      presence correlated well with histological inflammation at the time of sacrifice. 
      RNA was prepared from two CNS sites, brain and spinal cord, and expression of 
      chemokine mRNAs was analyzed by a sensitive and quantitative reverse 
      transcriptase/polymerase chain reaction dot-blot hybridization assay. CNS 
      expressions of MCP-1 and IP-10 gene were correlated tightly with histological 
      inflammation; indeed, chemokine expression was never detected in the absence of 
      leukocyte infiltrates. In situ hybridizations showed that astrocytes expressed 
      chemokine transcripts. These findings provide new information about mechanisms 
      controlling chemokine mRNA expression during immune-mediated inflammation in EAE 
      and are consistent with a role for chemokines as amplifiers of CNS inflammatory 
      reactions.
FAU - Glabinski, A R
AU  - Glabinski AR
AD  - Research Institute, Cleveland Clinic Foundation, Ohio 44195, USA.
FAU - Tani, M
AU  - Tani M
FAU - Tuohy, V K
AU  - Tuohy VK
FAU - Tuthill, R J
AU  - Tuthill RJ
FAU - Ransohoff, R M
AU  - Ransohoff RM
LA  - eng
GR  - NS-29095/NS/NINDS NIH HHS/United States
GR  - R01-32151/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Behav Immun
JT  - Brain, behavior, and immunity
JID - 8800478
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cytokines)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Astrocytes/metabolism
MH  - Autoimmune Diseases/*genetics
MH  - Base Sequence
MH  - Central Nervous System/*metabolism
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Chemokine CXCL10
MH  - *Chemokines, CXC
MH  - *Chemotaxis, Leukocyte
MH  - Cytokines/*biosynthesis/genetics
MH  - Encephalomyelitis, Autoimmune, Experimental/*genetics
MH  - Female
MH  - *Gene Expression Regulation
MH  - Liver/metabolism
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Molecular Sequence Data
MH  - RNA, Messenger/*biosynthesis
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
AID - S0889-1591(85)71030-6 [pii]
AID - 10.1006/brbi.1995.1030 [doi]
PST - ppublish
SO  - Brain Behav Immun. 1995 Dec;9(4):315-30. doi: 10.1006/brbi.1995.1030.