Abstract
Several mechanisms are associated with brain dysfunction during sepsis; one of the most important are activation of microglia and astrocytes. Activation of glial cells induces changes in permeability of the blood-brain barrier, secretion of inflammatory cytokines, and these alterations could induce neuronal dysfunction. Furthermore, blood-borne leukocytes can also reach the brain and participate in inflammatory response. Mechanisms involved in sepsis-associated brain dysfunction were revised here, focusing in neuroinflammation and involvement of blood-borne leukocytes and glial cells in this process.
Highlights
Sepsis is referred as a systemic inflammatory response due to an infection [1] and presents a wide spectrum of severity: from severe sepsis to septic shock and multi-organ dysfunction syndrome [2]
The blood-brain barrier (BBB) is understood as a complex regulated system. Terms such as neuro- or gliavascular unit (NVU, GVU) describe the strong influence of the microenvironment on the brain endothelium [120]. Neighboring cell types such as astrocytes, pericytes, microglia, or even neurons are known to influence the functionality of BBB in health as well as in disease, which is supported by their physical proximity and consequent small diffusion distances for signaling molecules [120, 121]
The results presented by Hernandes et al, 2014 [127] provide evidence that Nox2 is the main source of reactive oxygen species (ROS) involved in the oxidative damage to the hippocampus in Sepsis-associated encephalopathy (SAE) and that Nox2-derived ROS are determining factors for cognitive impairments after sepsis
Summary
Sepsis is referred as a systemic inflammatory response due to an infection [1] and presents a wide spectrum of severity: from severe sepsis to septic shock and multi-organ dysfunction syndrome [2]. Mechanisms that link SAE and long-term cognitive dysfunction are not well understood, evidences that link neuroinflammation and both acute and longterm sepsis-associated brain dysfunction were here reviewed. Microglia activation has a major role in the generation of oxidative damage and inflammation in the brain during several different CNS diseases.
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