Cited by 313Inflammasome and immune disordersTraumatic Brain Injury and Neurovascular DisturbancesInflammation biomarkers and pathways

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Therapeutic Neutralization of the NLRP1 Inflammasome Reduces the Innate Immune Response and Improves Histopathology after Traumatic Brain Injury

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de Rivero Vaccari, Juan Pablo, Lotocki, George, Alonso, Ofelia F, Bramlett, Helen M, Dietrich, W Dalton, Keane, Robert W·2009·Journal of Cerebral Blood Flow & Metabolism

DOI 10.1038/jcbfm.2009.46PMC PMC2846547

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Abstract

Traumatic brain injury elicits acute inflammation that in turn exacerbates primary brain damage. A crucial part of innate immunity in the immune privileged central nervous system involves production of proinflammatory cytokines mediated by inflammasome signaling. Here, we show that the nucleotide-binding, leucine-rich repeat pyrin domain containing protein 1 (NLRP1) inflammasome consisting of NLRP1, caspase-1, caspase-11, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), the X-linked inhibitor of apoptosis protein, and pannexin 1 is expressed in neurons of the cerebral cortex. Moderate parasagittal fluid-percussion injury (FPI) induced processing of interleukin-1β, activation of caspase-1, cleavage of X-linked inhibitor of apoptosis protein, and promoted assembly of the NLRP1 inflammasome complex. Anti-ASC neutralizing antibodies administered immediately after fluid-percussion injury to injured rats reduced caspase-1 activation, X-linked inhibitor of apoptosis protein cleavage, and processing of interleukin-1β, resulting in a significant decrease in contusion volume. These studies show that the NLRP1 inflammasome constitutes an important component of the innate central nervous system inflammatory response after traumatic brain injury and may be a novel therapeutic target for reducing the damaging effects of posttraumatic brain inflammation.

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Authors: de Rivero Vaccari, J. P., Lotocki, G., Alonso, O. F., Bramlett, H. M., Dietrich, W. D., & Keane, R. W.
Affiliations: Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA
University of Miami (US)
Corresponding author: Keane, Robert W
ORCID: Bramlett, Helen M
Dietrich, W Dalton
Keane, Robert W
Venue: Journal of Cerebral Blood Flow & Metabolism
Publisher: SAGE Publications
Published: 2009-04-29
Volume: 29
Issue: 7
Pages: 1251-1261
ISSN: 0271-678X (ISSN-L)
1559-7016
DOI: 10.1038/jcbfm.2009.46
PMC: PMC2846547
OpenAlex: W2012789061
Cited by: 312
References: 43
Citations by year: 2026: 10 · 2025: 12 · 2024: 15 · 2023: 16 · 2022: 27 · 2021: 17 · 2020: 32 · 2019: 17 · 2018: 24 · 2017: 21 · 2016: 18 · 2015: 26 · 2014: 27 · 2013: 20 · 2012: 14
FWCI: 4.03
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations: Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
U.S. Public Health Service (NN42133)
National Institute of Neurological Disorders and Stroke (NS-30291, R01NS042133, R01NS056072, P50NS030291)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords: NLRP1 inflammasome, traumatic brain injury, innate immunity, caspase-1, caspase-11, interleukin-1β processing, XIAP, ASC, pannexin 1, fluid percussion injury, neuroinflammation, cortical neurons, contusion volume, therapeutic target
MeSH terms: Animals, Antibodies, Monoclonal, Epitopes, Brain Injuries, Immunity, Innate, Inflammation, Male, Nerve Tissue Proteins, Rats, Sprague-Dawley, Caspase 1, Multiprotein Complexes, Rats, Interleukin-1beta

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Therapeutic Neutralization of the NLRP1 Inflammasome Reduces the Innate Immune Response and Improves Histopathology after Traumatic Brain Injury

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