PPARα activation has been shown to suppress glial inflammatory responses to lipopolysaccharide (LPS), an endotoxin which is expressed on the outer membrane of bacteria. LPS-induced innate immune response in the brain is mediated through Toll-like receptor 4 (Rivest, 2009). In vitro studies using dissociated glial cultures have provided a substantial amount of data concerning the effects of PPARα activation on the glial response to LPS (Lee et al., 2005; Paintlia et al., 2008a,b; Xu et al., 2005, 2006, 2007); however, in vitro studies often lack other crucial cellular components, such as endothelial cells and peripheral blood cells, for inflammation. One study recently reported that maternal LPS exposure depleted developing oligodendrocyte in the fetal brain, which was prevented by Wy-14643, a PPARα-specific agonist (Paintlia et al., 2008b). Less is known about the in vivo effects of PPARα activation on LPS-induced neuroinflammation in adult brain.
