Neural-respiratory inflammasome axis in traumatic brain injury

Research output: Contribution to journalReview article

Abstract

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality. Approximately 20–25% of TBI subjects develop Acute Lung Injury (ALI), but the pathomechanisms of TBI-induced ALI remain poorly defined. Currently, mechanical ventilation is the only therapeutic intervention for TBI-induced lung injury. Our recent studies have shown that the inflammasome plays an important role in the systemic inflammatory response leading to lung injury-post TBI. Here, we outline the role of the extracellular vesicle (EV)-mediated inflammasome signaling in the etiology of TBI-induced ALI. Furthermore, we evaluate the efficacy of a low molecular weight heparin (Enoxaparin, a blocker of EV uptake) and a monoclonal antibody against apoptosis speck-like staining protein containing a caspase recruitment domain (anti-ASC) as therapeutics for TBI-induced lung injury. We demonstate that activation of an EV-mediated Neural-Respiratory Inflammasome Axis plays an essential role in TBI-induced lung injury and disruption of this axis has therapeutic potential as a treatment strategy.

Original languageEnglish (US)
Article number113080
JournalExperimental Neurology
Volume323
DOIs
StatePublished - Jan 2020

Fingerprint

Inflammasomes
Lung Injury
Acute Lung Injury
Enoxaparin
Traumatic Brain Injury
Low Molecular Weight Heparin
Therapeutics
Artificial Respiration
Monoclonal Antibodies
Apoptosis
Staining and Labeling
Morbidity
Mortality

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience

Cite this

Neural-respiratory inflammasome axis in traumatic brain injury. / Kerr, Nadine; de Rivero Vaccari, Juan Pablo; Dietrich, W. Dalton; Keane, Robert W.

In: Experimental Neurology, Vol. 323, 113080, 01.2020.

Research output: Contribution to journalReview article

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