Next Article in Journal
Possible Mechanisms by which Stefin B could Regulate Proteostasis and Oxidative Stress
Next Article in Special Issue
Circulating Cell-Free mtDNA Contributes to AIM2 Inflammasome-Mediated Chronic Inflammation in Patients with Type 2 Diabetes
Previous Article in Journal
Retinal Neuron Is More Sensitive to Blue Light-Induced Damage than Glia Cell Due to DNA Double-Strand Breaks
Article Menu
Issue 1 (January) cover image

Export Article

Open AccessArticle

Human Lung Cell Pyroptosis Following Traumatic Brain Injury

Department of Neurological Surgery, University of Miami, Miami, FL 33136, USA
Diabetes Research Institute, University of Miami; Miami, FL 33136, USA
Department of Cell Biology, University of Miami, Miami, FL 33136, USA
Department of Physiology and Biophysics, University of Miami School of Medicine, 1600 NW 10th Ave. RMSB 5054, Miami, FL 33136, USA
Author to whom correspondence should be addressed.
Cells 2019, 8(1), 69;
Received: 12 December 2018 / Revised: 9 January 2019 / Accepted: 15 January 2019 / Published: 18 January 2019
(This article belongs to the Special Issue Mechanisms of Inflammasome Activation)
PDF [2259 KB, uploaded 18 January 2019]
  |     |  


Approximately 30% of traumatic brain injured patients suffer from acute lung injury or acute respiratory distress syndrome. Our previous work revealed that extracellular vesicle (EV)-mediated inflammasome signaling plays a crucial role in the pathophysiology of traumatic brain injury (TBI)-induced lung injury. Here, serum-derived EVs from severe TBI patients were analyzed for particle size, concentration, origin, and levels of the inflammasome component, an apoptosis-associated speck-like protein containing a caspase-recruiting domain (ASC). Serum ASC levels were analyzed from EV obtained from patients that presented lung injury after TBI and compared them to EV obtained from patients that did not show any signs of lung injury. EVs were co-cultured with lung human microvascular endothelial cells (HMVEC-L) to evaluate inflammasome activation and endothelial cell pyroptosis. TBI patients had a significant increase in the number of serum-derived EVs and levels of ASC. Severe TBI patients with lung injury had a significantly higher level of ASC in serum and serum-derived EVs compared to individuals without lung injury. Only EVs isolated from head trauma patients with gunshot wounds were of neural origin. Delivery of serum-derived EVs to HMVEC-L activated the inflammasome and resulted in endothelial cell pyroptosis. Thus, serum-derived EVs and inflammasome proteins play a critical role in the pathogenesis of TBI-induced lung injury, supporting activation of an EV-mediated neural-respiratory inflammasome axis in TBI-induced lung injury. View Full-Text
Keywords: pyroptosis; inflammasome; caspase-1; inflammation; brain injury; extracellular vesicles pyroptosis; inflammasome; caspase-1; inflammation; brain injury; extracellular vesicles

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

Kerr, N.A.; de Rivero Vaccari, J.P.; Umland, O.; Bullock, M.R.; Conner, G.E.; Dietrich, W.D.; Keane, R.W. Human Lung Cell Pyroptosis Following Traumatic Brain Injury. Cells 2019, 8, 69.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Cells EISSN 2073-4409 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top