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Updated: Jun 6, 2026

Analyzing the Permeability of the Blood-Brain Barrier by Microbial Traversal through Microvascular Endothelial Cells
Published on: February 14, 2020
Septic-associated encephalopathy--everything starts at a microlevel
Tarek Sharshar1, Andrea Polito, Anthony Checinski
1Department of Intensive Care Medicine, Raymond Poincaré teaching Hospital and University of Versailles Saint-Quentin en Yvelines, 104 Boulevard Raymond Poincaré, 92380 Garches, France. tarek.sharshar@rpc.aphp.fr
Abstract:
Sepsis-associated encephalopathy is associated with increased mortality and morbidity. Its pathophysiology remains insufficiently elucidated, although there is evidence for a neuroinflammatory process sequentially involving endothelial activation, blood-brain barrier alteration and cellular dysfunction and alteration in neurotransmission. Experimental studies have shown that microcirculatory dysfunction, a consequence of endothelial activation, is an early pathogenic step. To date, we do not know whether it is present in septic patients, whether it accounts for clinical features and whether it is treatable.
Insights
Sepsis-associated encephalopathy involves brain inflammation, potentially starting with blood vessel issues. Further research is needed to confirm its presence in patients and explore treatment options.
Area of Science:
- Neuroscience
- Critical Care Medicine
- Pathophysiology
Background:
- Sepsis-associated encephalopathy (SAE) significantly increases patient mortality and morbidity.
- The exact mechanisms of SAE are not fully understood, but neuroinflammation is implicated.
- Evidence suggests a sequence involving endothelial activation, blood-brain barrier changes, and neuronal dysfunction.
Discussion:
- Microcirculatory dysfunction, stemming from endothelial activation, is a proposed early pathogenic event in SAE.
- It remains unclear if microcirculatory dysfunction occurs in septic patients.
- The link between microcirculatory dysfunction and SAE's clinical manifestations requires investigation.
Key Insights:
- SAE pathophysiology involves neuroinflammation and endothelial activation.
- Microcirculatory dysfunction is a potential early step in SAE.
- Clinical relevance and treatability of microcirculatory dysfunction in SAE are unknown.
Outlook:
- Investigate the presence of microcirculatory dysfunction in septic patients.
- Determine if microcirculatory dysfunction correlates with SAE clinical features.
- Explore therapeutic strategies targeting microcirculatory dysfunction for SAE treatment.
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