CLINICAL, MOLECULAR, AND EXOSOMAL MECHANISMS OF CARDIAC AND BRAIN DYSFUNCTION IN SEPSIS

Sepsis is a complex disease resulting from a dysregulated inflammatory response to an infection. Initiation of sepsis occurs from a localized infection that disseminates to the bloodstream placing all organ systems at risk. Septic shock is classically observed to manifest itself as systemic hypotension with hyporesponsiveness to vasopressor agents. Myocardial dysfunction occurs resulting in an inability to perfuse major organ systems throughout the body. Most importantly, the brain is hypoperfused creating an ischemic and inflammatory state resulting in the clinical observation of acute mental status changes and cognitive dysfunction commonly known as sepsis-associated encephalopathy. This short review describes the inflammatory molecular mechanisms of myocardial dysfunction, discusses the evidence of the dual roles of the microglia resulting in blood-brain barrier disruption, and suggests that septic-derived exosomes, endosome-derived lipid bilayer spheroids released from living cells, influence cardiac and neurological cellular function.

Automated summary

Sepsis is a complex disease caused by an uncontrolled inflammatory response to infection. It originates from a localized infection and spreads throughout the bloodstream, putting all organs at risk. Septic shock is characterized by systemic hypotension and poor response to vasopressor agents. Myocardial dysfunction leads to inadequate perfusion of major organ systems, with the brain being particularly affected, resulting in acute mental status changes and cognitive dysfunction known as sepsis-associated encephalopathy. This review discusses the inflammatory mechanisms of myocardial dysfunction, the dual roles of microglia in blood-brain barrier disruption, and the impact of septic-derived exosomes on cardiac and neurological cellular function.