Research progress of the mechanisms underlying transition of acute systemic inflammation to central inflammation

Background Systemic and central inflammation play important roles in surgery, trauma, and infection. It is still unclear how acute systemic inflammation develops into central inflammation. Objective To review the potential mechanisms and substrates for the transition from acute systemic inflammation to central inflammation in order to provide insights for preventing or alleviating postoperative neuroinflammation and cognitive dysfunction. Content Inflammation in the central nervous system is commonly seen in surgeries in non-nervous systems, septicemia, burn, and injury of organs, and might incur cognitive dysfunctions and neurodegenerative diseases. Inflammation factors and cytokines released during systemic inflammation increase permeability of blood-brain-brarrier (BBB), resulting in infiltration of inflammation factors, cytokines, and immune cells into the brain. The increase of permeability of blood-brain-brarrier is related to the damage of the integrity of endothelia glycocalyx layer following sepsis, inflammation, and dramatic hemodynamic perturbation, as well. Trend To improve integrity of endothelia glycocalyx layer, maintaining normal permeability of blood-brain-brarrier, may be a strategy to prevent the transition of systemic inflammation to central inflammation and neurodegenerative diseases. Key words: Systemic inflammation; Central inflammation; Lipopolysaccharide; Inflammatory factor; Endothelial surface layer