Microglia, which constitute the resident macrophages of the central nervous 
system (CNS), are generally considered as the primary immune cells in the brain 
and spinal cord. Microglial cells respond to various factors which are produced 
following nerve injury of multiple aetiologies and contribute to the development 
of neuronal disease. Chemokine (C-C motif) ligand 1 (CCL-1), a 
well-characterized chemokine secreted by activated T cells, has been shown to 
play an important role in neuropathic pain induced by nerve injury and is also 
produced in various cell types in the CNS, especially in dorsal root ganglia 
(DRG). However, the role of CCL-1 in the CNS and the effects on microglia 
remains unclear. Here we showed the multiple effects of CCL-1 on microglia. We 
first showed that CCR-8, a specific receptor for CCL-1, was expressed on primary 
cultured microglia, as well as on astrocytes and neurons, and was upregulated in 
the presence of CCL-1. CCL-1 at concentration of 1 ng/ml induced chemotaxis, 
increased motility at a higher concentration (100 ng/ml), and increased 
proliferation and phagocytosis of cultured microglia. CCL-1 also activated 
microglia morphologically, promoted mRNA levels for brain-derived neurotrophic 
factor (BDNF) and IL-6, and increased the release of nitrite from microglia. 
These indicate that CCL-1 has a role as a mediator in neuron-glia interaction, 
which may contribute to the development of neurological diseases, especially in 
neuropathic pain.