Systemic inflammation regulates microglial responses to tissue damage in vivo.

摘要: Microglia, the resident immune cells of central nervous system, exist in either a "resting" state associated with physiological tissue surveillance or an "activated" neuroinflammation. We recently showed that ATP is primary chemoattractor to damage vivo and elicits opposite effects on motility activated microglia vitro through activation adenosine A2A receptors. However, whether systemic inflammation affects microglial responses remains largely unknown. Using two-photon imaging mice, we show injection lipopolysaccharide (LPS) at levels can produce both clear neuroinflammation some features sepsis significantly reduced rate response laser-induced ablation injury vivo. Under proinflammatory conditions, processes initially retracted from site, but subsequently moved toward engulfed damaged area. Analyzing process dynamics 3D cultures indicated only , not A1 A3 receptors, mediate retraction LPS-activated microglia. The receptor antagonists caffeine preladenant adenosine-mediated vitro. Finally, administration before induction laser accelerated following inflammation. regulation rapid sites by receptors could have implications for their ability respond neuronal death occurring under conditions neurodegenerative disorders.