Septic encephalopathy: when cytokines interact with acetylcholine in the brain

Qing-Hong Zhang, Zhi-Yong Sheng, Yong-Ming Yao, Qing-Hong Zhang, Zhi-Yong Sheng, Yong-Ming Yao

Abstract

Sepsis-associated encephalopathy (SAE) is a brain dysfunction that occurs secondary to infection in the body, characterized by alteration of consciousness, ranging from delirium to coma, seizure or focal neurological signs. SAE involves a number of mechanisms, including neuroinflammation, in which the interaction between cytokines and acetylcholine results in neuronal loss and alterations in cholinergic signaling. Moreover, the interaction also occurs in the periphery, accelerating a type of immunosuppressive state. Although its diagnosis is not specific in biochemistry and imaging tests, it could potentiate severe outcomes, including increased mortality, cognitive decline, progressive immunosuppression, cholinergic anti-inflammatory deficiency, and even metabolic and hydroelectrolyte imbalance. Therefore, the bilateral communication between SAE and the multiple peripheral organs and especially the immune system should be emphasized in sepsis management.

Keywords: Acetylcholine; Cholinergic anti-inflammatory pathway; Delirium; Immunosuppression; Neuroinflammation; Septic encephalopathy.

Figures

Figure 1
Figure 1
Interactions of cytokines with acetylcholine in the central nervous system that induces septic encephalopathy and its peripheral consequences.

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