PMID- 12111820
OWN - NLM
STAT- MEDLINE
DCOM- 20020904
LR  - 20061115
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 69
IP  - 1
DP  - 2002 Jul 1
TI  - Cytokines, chemokines, and cytokine receptors in human microglia.
PG  - 94-103
AB  - Enriched populations of human microglial cells were isolated from mixed cell 
      cultures prepared from embryonic human telencephalon tissues. Human microglial 
      cells exhibited cell type-specific antigens for macrophage-microglia lineage 
      cells including CD11b (Mac-1), CD68, B7-2 (CD86), HLA-ABC, HLA-DR and ricinus 
      communis aggulutinin lectin-1 (RCA-1), and actively phagocytosed latex beads. 
      Gene expression and protein production of cytokines, chemokines and 
      cytokine/chemokine receptors were investigated in the purified populations of 
      human microglia. Normal unstimulated human microglia expressed constitutively 
      mRNA transcripts for interleukin- 1beta (IL-1beta) -6, -8, -10, -12, -15, tumor 
      necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein-1alpha 
      (MIP-1alpha), MIP-1beta, and monocyte chemoattractant protein-1 (MCP-1), while 
      treatment with lipopolysaccharide (LPS) or amyloid beta peptides (Abeta) led to 
      increased expression of mRNA levels of IL-8, IL-10, IL-12, TNF-alpha, MIP-1alpha, 
      MIP-1beta, and MCP-1. Human microglia, in addition, expressed mRNA transcripts 
      for IL-1RI, IL-1RII, IL-5R, IL-6R, IL-8R, IL-9R, IL-10R, IL-12R, IL-13R, and 
      IL-15R. Enzyme-linked immunosorbent assays (ELISA) showed increased protein 
      levels in culture media of IL-1beta, IL-8, TNF-alpha, and MIP-1alpha in human 
      microglia following treatment with LPS or Abeta. Increased TNF-alpha release from 
      human microglia following LPS treatment was completely inhibited with IL-10 
      pretreatment, but not with IL-6, IL-9, IL-12, IL-13, or transforming growth 
      factor-beta (TGF-beta). Present results should help in understanding the basic 
      microglial biology, but also the pathophysiology of activated microglia in 
      neurological diseases such as Alzheimer disease, Parkinson disease, Huntington 
      disease, amyotrophic lateral sclerosis, stroke, and neurotrauma.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Lee, Yong B
AU  - Lee YB
AD  - Division of Neurology, Department of Medicine, University of British Columbia, 
      Vancouver, Canada.
FAU - Nagai, Atsushi
AU  - Nagai A
FAU - Kim, Seung U
AU  - Kim SU
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Receptors, Cytokine)
SB  - IM
MH  - Brain/cytology/embryology
MH  - Cells, Cultured
MH  - Chemokines/*analysis/biosynthesis/genetics
MH  - Cytokines/*analysis/biosynthesis/genetics
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Gene Expression Regulation, Developmental
MH  - Humans
MH  - Microglia/cytology/*metabolism
MH  - Receptors, Cytokine/*analysis/biosynthesis/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2002/07/12 10:00
MHDA- 2002/09/06 10:01
CRDT- 2002/07/12 10:00
PHST- 2002/07/12 10:00 [pubmed]
PHST- 2002/09/06 10:01 [medline]
PHST- 2002/07/12 10:00 [entrez]
AID - 10.1002/jnr.10253 [doi]
PST - ppublish
SO  - J Neurosci Res. 2002 Jul 1;69(1):94-103. doi: 10.1002/jnr.10253.