Neurochemical effects of sepsis on the brain

Author:

Barichello Tatiana12,Giridharan Vijayasree V1,Catalão Carlos Henrique R13,Ritter Cristiane2,Dal-Pizzol Felipe2ORCID

Affiliation:

1. 1Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, U.S.A.

2. 2Graduate Program in Health Sciences, Department of Medicine, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil

3. 3Department of Neurosciences and Behavioral Sciences, Ribeirao Preto Medical School, University of São Paulo (USP), Ribeirao Preto, SP, Brazil

Abstract

Abstract Sepsis is a life-threatening organ dysfunction triggered by a dysregulated host immune response to eliminate an infection. After the host immune response is activated, a complex, dynamic, and time-dependent process is triggered. This process promotes the production of inflammatory mediators, including acute-phase proteins, complement system proteins, cytokines, chemokines, and antimicrobial peptides, which are required to initiate an inflammatory environment for eliminating the invading pathogen. The physiological response of this sepsis-induced systemic inflammation can affect blood–brain barrier (BBB) function; subsequently, endothelial cells produce inflammatory mediators, including cytokines, chemokines, and matrix metalloproteinases (MMPs) that degrade tight junction (TJ) proteins and decrease BBB function. The resulting BBB permeability allows peripheral immune cells from the bloodstream to enter the brain, which then release a range of inflammatory mediators and activate glial cells. The activated microglia and astrocytes release reactive oxygen species (ROS), cytokines, chemokines, and neurochemicals, initiate mitochondrial dysfunction and neuronal damage, and exacerbate the inflammatory milieu in the brain. These changes trigger sepsis-associated encephalopathy (SAE), which has the potential to increase cognitive deterioration and susceptibility to cognitive decline later in life.

Publisher

Portland Press Ltd.

Subject

General Medicine

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