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and MIP-1ß in Human Fetal Microglia1
Departments of
*
Pathology, and
Microbiology, Immunology, and
Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461
Leukocyte infiltration into the central nervous system (CNS) is a
key event in the inflammatory processes of neuroimmunologic diseases.
Microglia, resident macrophages of the CNS, may contribute to this
process by elaborating chemoattractants that are capable of recruiting
leukocytes across the blood-brain barrier. Such factors have been
detected in the CNS of animal models of multiple sclerosis and in the
brains of human and nonhuman primates with AIDS encephalitis. As the
expression of these chemoattractants may play an important role in the
initiation and progression of neuroimmunologic diseases, we analyzed
expression of the chemokines MIP-1
, MIP-1ß, MCP-1, and RANTES in
human fetal microglial cultures. Unstimulated microglia expressed
minimal levels of MIP-1, MIP-1ß, and MCP-1, while RANTES was
undetectable. In response to LPS, TNF-, or IL-1ß, both MIP-1
and MIP-1ß were induced at the mRNA and protein levels in a dose- and
time-dependent manner. IFN-
did not significantly induce chemokine
expression. MCP-1 was detectable in LPS- and cytokine-treated
microglia. TGF-ß, a cytokine with down-modulatory effects on other
cell types, had little effect on chemokine expression in microglia when
used concomitantly before or during treatment with LPS. These results
illustrate the ability of certain inflammatory stimuli to induce
expression of MIP-1, MIP-1ß, and MCP-1 by human fetal microglia.
The expression of these chemoattractants may function to recruit
inflammatory cells into the CNS during the course of neuroimmunologic
diseases and may modulate the ability of HIV to infect the CNS.
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