PMID- 7642742
OWN - NLM
STAT- MEDLINE
DCOM- 19950920
LR  - 20190825
IS  - 0165-5728 (Print)
IS  - 0165-5728 (Linking)
VI  - 60
IP  - 1-2
DP  - 1995 Jul
TI  - Production and function of monocyte chemoattractant protein-1 and other 
      beta-chemokines in murine glial cells.
PG  - 143-50
AB  - Monocyte chemoattractant protein-1 (MCP-1), formerly termed JE, is a member of 
      the beta-chemokine (C-C chemokine) family and has been shown to be produced by a 
      variety of cell types. Recently, mRNA of JE/MCP-1 was detected in astrocytes 
      during the acute phase of experimental allergic encephalomyelitis (EAE). In 
      addition, supernatants collected from human cultured astrocytes have recently 
      been found to be chemotactic for monocytes. However, chemokine production and 
      function in glial cells has not been fully examined. Using a sandwich ELISA 
      assay, we have now quantitated MCP-1 levels and assessed MCP-1 function on murine 
      glial cells. Lipopolysaccharide (LPS), interleukin (IL)-1 beta and tumor necrosis 
      factor (TNF)-alpha induced MCP-1 secretion by astrocytes, but not microglia. In 
      addition, pretreatment with interferon (IFN)-gamma significantly augmented MCP-1 
      production by either LPS or the above cytokines. In contrast, LPS preferentially 
      induced production of another beta-chemokine, macrophage inflammatory protein-1 
      alpha (MIP-1 alpha) from microglial cells. MCP-1 induced chemotaxis of microglial 
      cells and macrophages. Similarly, another beta-chemokine, TCA3, which is produced 
      by encephalitogenic T lymphocytes, also induced chemotaxis of microglia and 
      macrophages. These findings suggested that astrocytes and microglial cells 
      differentially produce chemokines in the central nervous system, and that both 
      astrocytes and T cells may facilitate recruitment and activation of microglial 
      cells via production of beta-chemokines.
FAU - Hayashi, M
AU  - Hayashi M
AD  - Department of Pathology, Harvard Medical School, Boston, MA, USA.
FAU - Luo, Y
AU  - Luo Y
FAU - Laning, J
AU  - Laning J
FAU - Strieter, R M
AU  - Strieter RM
FAU - Dorf, M E
AU  - Dorf ME
LA  - eng
GR  - NS-31152/NS/NINDS NIH 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  - J Neuroimmunol
JT  - Journal of neuroimmunology
JID - 8109498
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Cell Movement/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2
MH  - Chemotactic Factors/pharmacology/*physiology
MH  - Cytokines/*physiology
MH  - Female
MH  - Interleukin-1/pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred Strains
MH  - Neuroglia/drug effects/*physiology
MH  - Recombinant Proteins
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1995/07/01 00:00
MHDA- 2000/06/01 09:00
CRDT- 1995/07/01 00:00
PHST- 1995/07/01 00:00 [pubmed]
PHST- 2000/06/01 09:00 [medline]
PHST- 1995/07/01 00:00 [entrez]
AID - 0165-5728(95)00064-9 [pii]
AID - 10.1016/0165-5728(95)00064-9 [doi]
PST - ppublish
SO  - J Neuroimmunol. 1995 Jul;60(1-2):143-50. doi: 10.1016/0165-5728(95)00064-9.