Anti-lysophosphatidic acid antibodies improve traumatic brain injury outcomes
Affiliation
Department of Pharmacology, the University of Melbourne, Parkville, AustraliaDepartment of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia
Barrow Neurological Institute, Department of Child Health, Phoenix Children’s Hospital, University of Arizona, Phoenix, AZ, USA
Division of Cardiovascular Medicine, University of Kentucky College of Medicine, Lexington, KY, USA
Department of Biology, San Diego State University and Lpath Inc, 4025 Sorrento Valley Blvd, San Diego, CA, USA
Florey Institute of Neuroscience and Mental Health, Parkville, Australia
Department of Anatomy and Neuroscience, the University of Melbourne, Parkville, Australia
Australian Centre for Blood Diseases, Monash University, Melbourne, Australia
Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital & Department of Ophthalmology, the University of Melbourne, East Melbourne, Australia
Australian Regenerative Medicine Institute, Monash University, Clayton, AustraliaNational Trauma Research Institute, Alfred Hospital & Monash University, Melbourne, AustraliaNeuroengineering Laboratory, Department of Electrical and Electronic Engineering, the University of Melbourne, Parkville, Australia
Issue Date
2014Keywords
Lysophosphatidic acidTraumatic brain injury
Human cerebrospinal fluid
Control cortical impact
Magnetic resonance imaging
Anti-LPA antibody
IL-6
Metadata
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BioMed CentralCitation
Crack et al. Journal of Neuroinflammation 2014, 11:37 http://www.jneuroinflammation.com/content/11/1/37Journal
Journal of NeuroinflammationRights
© 2014 Crack et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).Collection Information
This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.Abstract
BACKGROUND:Lysophosphatidic acid (LPA) is a bioactive phospholipid with a potentially causative role in neurotrauma. Blocking LPA signaling with the LPA-directed monoclonal antibody B3/Lpathomab is neuroprotective in the mouse spinal cord following injury.FINDINGS:Here we investigated the use of this agent in treatment of secondary brain damage consequent to traumatic brain injury (TBI). LPA was elevated in cerebrospinal fluid (CSF) of patients with TBI compared to controls. LPA levels were also elevated in a mouse controlled cortical impact (CCI) model of TBI and B3 significantly reduced lesion volume by both histological and MRI assessments. Diminished tissue damage coincided with lower brain IL-6 levels and improvement in functional outcomes.CONCLUSIONS:This study presents a novel therapeutic approach for the treatment of TBI by blocking extracellular LPA signaling to minimize secondary brain damage and neurological dysfunction.EISSN
1742-2094Version
Final published versionAdditional Links
http://www.jneuroinflammation.com/content/11/1/37Scopus Count
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Except where otherwise noted, this item's license is described as © 2014 Crack et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).