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“Background Sepsis-induced encephalopathy is caused by systemic inflammation in the absence of direct brain infection and clinically characterized

by slowing of mental processes, impaired attention, disorientation, delirium, or coma. Importantly, septic encephalopathy (SE) is an early sign of sepsis and associated with an increased rate of morbidity and Rucaparib cell line mortality. The pathogenesis of SE is unlikely to be directly induced by a pathogenic toxin, because similar encephalopathy can develop as a result of a number of systemic inflammatory response syndromes that lack an infectious etiology (e.g., acute pancreatitis and burns). Clinical and experimental data suggested that a number of factors including the local generation of pro-inflammatory cytokines and impaired cerebral microcirculation. The imbalance of neurotransmitters or the negative impacts of peripheral organ failure contribute to the development of SE [1–3]. Microglia, innate immune cells of the CNS, become activated in response to injury and appear to have important role in the defense against invading microbes and in wound repair [4].

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