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Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
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Human Lung Cell Pyroptosis Following Traumatic Brain Injury.
Nadine A Kerr1, Juan Pablo de Rivero Vaccari2, Oliver Umland3
1Department of Neurological Surgery, University of Miami, Miami, FL 33136, USA. N.Kerr@med.miami.edu.
Cells
|January 24, 2019
Summary
Serum extracellular vesicles (EVs) carrying inflammasome proteins like ASC are elevated in traumatic brain injury (TBI) patients with lung injury. These EVs promote lung endothelial cell pyroptosis, highlighting a key mechanism in TBI-induced lung injury.
Area of Science:
- Biomedical research
- Trauma science
- Cellular biology
Background:
- Traumatic brain injury (TBI) frequently leads to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS).
- Extracellular vesicle (EV)-mediated inflammasome signaling is implicated in TBI-induced lung injury.
- The role of serum-derived EVs and inflammasome components in TBI patients with lung injury requires further elucidation.
Purpose of the Study:
- To analyze serum-derived EVs in severe TBI patients, focusing on particle characteristics and inflammasome component levels.
- To investigate the association between serum and EV-bound inflammasome components (specifically ASC) and the presence of lung injury post-TBI.
- To determine the functional impact of serum-derived EVs from TBI patients on lung microvascular endothelial cells (HMVEC-L) in vitro.
Main Methods:
- Serum-derived EVs from TBI patients were characterized for size, concentration, and origin.
- Levels of the inflammasome component ASC were quantified in serum and serum-derived EVs.
- EVs were co-cultured with HMVEC-L to assess inflammasome activation and endothelial cell pyroptosis.
- Comparison of ASC levels between TBI patients with and without lung injury.
Main Results:
- TBI patients exhibited increased serum-derived EV concentration and ASC levels.
- Severe TBI patients with lung injury showed significantly higher ASC levels in serum and EVs compared to those without lung injury.
- EVs from TBI patients induced inflammasome activation and pyroptosis in HMVEC-L.
- Neural origin of EVs was observed only in TBI patients with gunshot wounds.
Conclusions:
- Serum-derived EVs and inflammasome proteins play a critical role in TBI-induced lung injury pathogenesis.
- An EV-mediated neural-respiratory inflammasome axis is implicated in TBI-induced lung injury.
- Elevated ASC in serum EVs may serve as a biomarker for lung injury following TBI.
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