Introduction

The pathogenesis of several neurological disorders, including Parkinson's disease,

Alzheimer's disease (Dickson et al., 1993; Liu and Hong, 2003), is now thought to be mediated by an inflammatory response by resident cells in the brain. Microglia, the resident immune cells of the brain, contribute to this inflammation by serving the role of immune surveillance and host defense (Kreutzberg, 1996). Activated microglia produce a variety of pro-inflammatory factors and reactive oxygen species (ROS), all of which serve immune surveillance functions by removing foreign microorganisms (Aloisi, 1999). Our previous results have shown that over-activation of microglia and overproduction of pro-inflammatory factors may lead to neuronal degeneration in the CNS (Liu et al., 2002).

Interleukin (IL)-10 is a cytokine produced by a variety of cell types including type 2 helper T cells, B cells, and macrophages. IL-10 has been shown to suppress inflammation in many experimental models of inflammatory disease. Mizuno et al. (1994) have found that cells in the CNS also produce IL-10. Microglia, which are cells in the CNS very similar both phenotypically and functionally to macrophages, express IL-10 receptor mRNA, and consequently they may be strongly regulated by IL-10. IL-10 produced in the CNS, therefore, may play an important role in the pathophysiology of CNS disorders by inhibiting the function of microglia.

The goal of the present study is to evaluate the effects of IL-10 on LPS-induced neurotoxicity in rat primary midbrain cultures. Here, we show that IL-10 attenuate microglial pro-inflammatory cytokine and ROS production and protect DA neurons from LPS-induced neurotoxicity.

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