Neural-respiratory inflammasome axis in traumatic brain injury
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 l...
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| Published in | Experimental neurology Vol. 323; p. 113080 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.01.2020
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0014-4886 1090-2430 1090-2430 |
| DOI | 10.1016/j.expneurol.2019.113080 |
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| 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. |
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| AbstractList | 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. 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.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. Traumatic brain injury (TBI) is a leading cause of morbidity and mortality. Approximately 20-25 percent 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. |
| ArticleNumber | 113080 |
| Author | Kerr, Nadine Dietrich, W. Dalton de Rivero Vaccari, Juan Pablo Keane, Robert W. |
| AuthorAffiliation | 1 Department of Neurological Surgery, University of Miami Miller School of Medicine 3 Department of Physiology and Biophysics, University of Miami Miller School fo Medicine, 1600 NW10th Avenue, Miami, FL 33136 2 Miami Project to Cure Paralysis |
| AuthorAffiliation_xml | – name: 2 Miami Project to Cure Paralysis – name: 1 Department of Neurological Surgery, University of Miami Miller School of Medicine – name: 3 Department of Physiology and Biophysics, University of Miami Miller School fo Medicine, 1600 NW10th Avenue, Miami, FL 33136 |
| Author_xml | – sequence: 1 givenname: Nadine surname: Kerr fullname: Kerr, Nadine organization: Department of Neurological Surgery, University of Miami Miller School of Medicine, United States of America – sequence: 2 givenname: Juan Pablo surname: de Rivero Vaccari fullname: de Rivero Vaccari, Juan Pablo organization: Department of Neurological Surgery, University of Miami Miller School of Medicine, United States of America – sequence: 3 givenname: W. Dalton surname: Dietrich fullname: Dietrich, W. Dalton organization: Department of Neurological Surgery, University of Miami Miller School of Medicine, United States of America – sequence: 4 givenname: Robert W. orcidid: 0000-0003-4068-9511 surname: Keane fullname: Keane, Robert W. email: rkeane@miami.edu organization: Department of Neurological Surgery, University of Miami Miller School of Medicine, United States of America |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31626746$$D View this record in MEDLINE/PubMed |
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| Snippet | 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... 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... Traumatic brain injury (TBI) is a leading cause of morbidity and mortality. Approximately 20-25 percent of TBI subjects develop Acute Lung Injury (ALI), but... |
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| SubjectTerms | Acute Lung Injury - etiology Acute Lung Injury - immunology Acute Lung Injury - physiopathology Animals Brain Injuries, Traumatic - complications Brain Injuries, Traumatic - immunology Brain Injuries, Traumatic - physiopathology Extracellular Vesicles - immunology Humans Inflammasomes - immunology Inflammation - etiology Inflammation - immunology Inflammation - physiopathology |
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| Title | Neural-respiratory inflammasome axis in traumatic brain injury |
| URI | https://dx.doi.org/10.1016/j.expneurol.2019.113080 https://www.ncbi.nlm.nih.gov/pubmed/31626746 https://www.proquest.com/docview/2307127748 https://pubmed.ncbi.nlm.nih.gov/PMC6981270 https://www.ncbi.nlm.nih.gov/pmc/articles/6981270 |
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