The blood-brain barrier dysfunction in sepsis.
Tatiana BarichelloJaqueline S GenerosoAllan CollodelFabricia PetronilhoFelipe Dal-PizzolPublished in: Tissue barriers (2020)
Sepsis is a life-threatening organ dysfunction triggered by a dysregulated host immune response attempting to eliminate the infection. After hospital discharge, half of the sepsis survivors recover, one-third of the patients die the following year, and one-sixth have a long-term cognitive impairment, including memory dysfunction, anxiety, depression, and post-traumatic stress disorder. The infection triggers the host immune response, and both can cause vascular endothelial damage, interrupting tight junctions proteins; consequently, the blood-brain barrier (BBB) breaks down, allowing and facilitating the entry of peripheral immune cells into the brain, which triggers or exacerbates the activation of glial cells and neuroinflammation. The focus of this review is to identify biochemical abnormalities induced by sepsis, which is associated with BBB dysfunction; provide evidence of biomarkers involved in the tight junction disruption and BBB damage, and draw attention to the role of the BBB as a bridge between systemic infection and brain inflammation.
Keyphrases
- blood brain barrier
- oxidative stress
- immune response
- cerebral ischemia
- septic shock
- acute kidney injury
- intensive care unit
- cognitive impairment
- induced apoptosis
- end stage renal disease
- working memory
- newly diagnosed
- traumatic brain injury
- ejection fraction
- depressive symptoms
- chronic kidney disease
- toll like receptor
- prognostic factors
- peritoneal dialysis
- resting state
- dendritic cells
- endothelial cells
- young adults
- sleep quality
- lipopolysaccharide induced
- inflammatory response
- single molecule
- signaling pathway
- multiple sclerosis
- cell death
- spinal cord injury
- spinal cord
- endoplasmic reticulum stress
- lps induced
- chemotherapy induced