Microglial inflammatory reactions regulated by oxidative stress.

Abstract

Microglia are immune cells in the brain that can respond to endogenous and exogenous substrates to elicit inflammatory reactions. The transcription factor nuclear factor kappa-light-chain-enhancer of activated B induces proinflammatory gene expression in response to foreign matter via pattern recognition receptors; thus, nuclear factor kappa-light-chain-enhancer of activated B is a master regulator of inflammation. During the inflammatory process, very large amounts of reactive oxygen species are generated and promote the onset and progression of inflammation. Interestingly, nuclear factor kappa-light-chain-enhancer of activated B drives the transcription of superoxide dismutase 2 in many types of cells, including microglia. Superoxide dismutase 2 is an antioxidative enzyme that catalyzes the dismutation of superoxide anions into molecular oxygen and hydrogen peroxide. Of note, nuclear factor kappa-light-chain-enhancer of activated B can initiate inflammation to elicit proinflammatory gene expression, while its transcription product superoxide dismutase 2 can suppress inflammation. In this review, we use recent knowledge to describe the interaction between oxidative stress and nuclear factor kappa-light-chain-enhancer of activated B and discuss the complicated role of microglial superoxide dismutase 2 in inflammation.