PMID- 8609424
OWN - NLM
STAT- MEDLINE
DCOM- 19960529
LR  - 20071114
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 156
IP  - 8
DP  - 1996 Apr 15
TI  - Localization of monocyte chemoattractant peptide-1 expression in the central 
      nervous system in experimental autoimmune encephalomyelitis and trauma in the 
      rat.
PG  - 3017-23
AB  - Monocyte chemoattractant protein-1 (MCP-1) is a member of the chemokine beta 
      family of chemoattractants that has been shown to play a major role in the 
      initiation of monocyte and T cell inflammation to sites of tissue injury. In this 
      study, we have examined the distribution of MCP-1 expression in inflammation in 
      the central nervous system (CNS) associated with the autoimmune disease 
      experimental autoimmune encephalomyelitis (EAE) and compared the results with 
      those detected in inflammation associated with trauma. In EAE, MCP-1 expression 
      was detected at the onset of inflammation, prior to clinical expression of 
      disease, in lymphocytes and endothelial cells in subarachnoid locations. Monocyte 
      infiltration into these areas appeared 24 h later. After the onset of clinical 
      signs, MCP-1 expression was widely distributed in the spinal cord with levels 
      increasing and decreasing in association with disease activity. Lymphocytes, 
      macrophages, astrocytes, and endothelial cells could be identified as sources of 
      MCP-1 by immunoreactivity and in situ hybridization. A similar close correlation 
      between macrophage infiltration and the levels of mRNA for MCP-1 was found in the 
      CNS of rats subjected to trauma, and in these animals MCP-1 was detected by 
      immunohistochemistry in macrophages and endothelial cells. The results support 
      the conclusion that MCP-1 is an important mediator of inflammation in the CNS.
FAU - Berman, J W
AU  - Berman JW
AD  - Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, 
      USA.
FAU - Guida, M P
AU  - Guida MP
FAU - Warren, J
AU  - Warren J
FAU - Amat, J
AU  - Amat J
FAU - Brosnan, C F
AU  - Brosnan CF
LA  - eng
GR  - HL48287/HL/NHLBI NIH HHS/United States
GR  - NS 07098/NS/NINDS NIH HHS/United States
GR  - NS 11920/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Animals
MH  - Brain Injuries/*etiology/metabolism/pathology
MH  - Chemokine CCL2/*metabolism
MH  - Encephalomyelitis, Autoimmune, Experimental/*etiology/metabolism/pathology
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Kinetics
MH  - Male
MH  - Organ Specificity
MH  - Rats
MH  - Rats, Inbred Lew
EDAT- 1996/04/15 00:00
MHDA- 1996/04/15 00:01
CRDT- 1996/04/15 00:00
PHST- 1996/04/15 00:00 [pubmed]
PHST- 1996/04/15 00:01 [medline]
PHST- 1996/04/15 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1996 Apr 15;156(8):3017-23.