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Journal of Mucosal Immunology Research
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  • Review Article   
  • J Mucosal Immunol Res,

Does Sepsis-Associated Encephalopathy Begin and End with T Cells?

Masafumi Saito*
Department of Disaster and Emergency and Critical Care Medicine, Kobe University Graduate School of Medicine, Kobe, Japan
*Corresponding Author : Dr. Masafumi Saito, Department of Disaster and Emergency and Critical Care Medicine, Kobe University Graduate School of Medicine, Kusunoki-Cho 7-5-2, Chuo-Ward, Kobe, Japan, Tel: +81-78-382-6521, Fax: +81-78-341-5254;, Email: msaito@med.kobe-u.ac.jp

Received Date: Oct 12, 2021 / Accepted Date: Oct 26, 2021 / Published Date: Nov 02, 2021

Abstract

A recent study revealed that 20%-40% of sepsis survivors suffer from mental disorders, more than a year after being discharged from the hospital. Although sepsis-associated encephalopathy (SAE) is complicated by septic conditions and is critically associated with increased mortality, it also leads to neurological dysfunction, which includes mental impairments. Therefore, finding a suitable treatment for neurological dysfunction is of vital importance for the survival and long-term prognosis of patients who contracted sepsis. Neuro-inflammation is the major pathogenesis of SAE, which is caused by the infiltration of inflammatory monocytes into the brain and by the activation of glial cells. However, the mechanism by which T cells are involved in the pathogenesis of SAE remains unclear. This review attempts to understand the underlying mechanisms associated with glial cells and T cells in the development and recovery of SAE and mental impairment following sepsis.

Keywords: Sepsis-associated encephalopathy; T cell; Mental impairment; Microglia; Astrocyte

Citation: Saito M (2021) Does Sepsis-Associated Encephalopathy Begin and End with T Cells? J Mucosal Immunol Res 5:130.

Copyright: © 2021 Saito M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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