Neuroinflammation in Sepsis: Molecular Pathways of Microglia Activation

Pharmaceuticals

Tarek Sharshar¹  CarolinaAraújo Moraes²  Joana d’Avila²  FernandoAugusto Bozza³  Camila Zaverucha-do-Valle³  Renaud Fleurance⁴ 

[1] Experimental Neuropathology, Infection, and Epidemiology Department, Institut Pasteur, 75015 Paris, France;Immunopharmacology Lab, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro 21045-900, Brazil;National Institute of Infectious Disease Evandro Chagas, Oswaldo Cruz Foundation, Ministry of Health, Rio de Janeiro 21040-360, Brazil;UCB Biopharma SRL, 1420 Braine L’Alleud, Belgium;

关键词: brain;    sepsis-associated encephalopathy;    neuroinflammation;    microglia;    inflammasome;    oxidative stress;   

DOI  :  10.3390/ph14050416

来源: DOAJ

【 摘 要 】

Frequently underestimated, encephalopathy or delirium are common neurological manifestations associated with sepsis. Brain dysfunction occurs in up to 80% of cases and is directly associated with increased mortality and long-term neurocognitive consequences. Although the central nervous system (CNS) has been classically viewed as an immune-privileged system, neuroinflammation is emerging as a central mechanism of brain dysfunction in sepsis. Microglial cells are major players in this setting. Here, we aimed to discuss the current knowledge on how the brain is affected by peripheral immune activation in sepsis and the role of microglia in these processes. This review focused on the molecular pathways of microglial activity in sepsis, its regulatory mechanisms, and their interaction with other CNS cells, especially with neuronal cells and circuits.

【 授权许可】

Unknown