ArticleMediators of inflammation2016
Nonessential Role for the NLRP1 Inflammasome Complex in a Murine Model of Traumatic Brain Injury.
Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Inflammasome adaptor ASC promotes sustained neuroinflammation and mild cognitive impairment in a closed-head injury model.The Journal of clinical investigation · 2026Article
- Mesenchymal stem cell exosomes therapy for the treatment of traumatic brain injury: mechanism, progress, challenges and prospects.Journal of translational medicine · 2025Review
- Skull bone marrow-derived immune cells infiltrate the injured cerebral cortex and exhibit anti-inflammatory properties.Brain, behavior, and immunity · 2025Article
- Inflammasomes at the crossroads of traumatic brain injury and post-traumatic epilepsy.Journal of neuroinflammation · 2024Review
- Detrimental Roles of Hypoxia-Inducible Factor-1α in Severe Hypoxic Brain Diseases.International journal of molecular sciences · 2024Review
- Role of pyroptosis in the pathogenesis of various neurological diseases.Brain, behavior, and immunity · 2024Review
- Immunoregulatory and neutrophil-like monocyte subsets with distinct single-cell transcriptomic signatures emerge following brain injury.Journal of neuroinflammation · 2024Article
- Efferocytosis is restricted by axon guidance molecule EphA4 via ERK/Stat6/MERTK signaling following brain injury.Journal of neuroinflammation · 2023Article
- Do astrocytes act as immune cells after pediatric TBI?Neurobiology of disease · 2023Review
- Non-coding RNAs and Exosomal Non-coding RNAs in Traumatic Brain Injury: the Small Player with Big Actions.Molecular neurobiology · 2023Review
- Article
- The Relationship between the Serum NLRP1 Level and Coronary Lesions in Patients with Coronary Artery Disease.International journal of clinical practice · 2023Article
- Ligustroflavone exerts neuroprotective activity through suppression of NLRP1 inflammasome in ischaemic stroke mice.Experimental and therapeutic medicine · 2023Article
- Inflammasomes as biomarkers and therapeutic targets in traumatic brain injury and related-neurodegenerative diseases: A comprehensive overview.Neuroscience and biobehavioral reviews · 2023Review
- Monocyte proinflammatory phenotypic control by ephrin type A receptor 4 mediates neural tissue damage.JCI insight · 2022Article
- Type I Interferon Response Is Mediated by NLRX1-cGAS-STING Signaling in Brain Injury.Frontiers in molecular neuroscience · 2022Article
- Glial Cells and Brain Diseases: Inflammasomes as Relevant Pathological Entities.Frontiers in cellular neuroscience · 2022Review
- NLRP1 Inflammasomes: A Potential Target for the Treatment of Several Types of Brain Injury.Frontiers in immunology · 2022Review
- Ablation of GSDMD Attenuates Neurological Deficits and Neuropathological Alterations After Traumatic Brain Injury.Frontiers in cellular neuroscience · 2022Article
- Neuroinflammation Following Traumatic Brain Injury: Take It Seriously or Not.Frontiers in immunology · 2022Review
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8 authors.
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Abstract
Traumatic brain injury (TBI) elicits the immediate production of proinflammatory cytokines which participate in regulating the immune response. While the mechanisms of adaptive immunity in secondary injury are well characterized, the role of the innate response is unclear. Recently, the NLR inflammasome has been shown to become activated following TBI, causing processing and release of interleukin-1β (IL-1β). The inflammasome is a multiprotein complex consisting of nucleotide-binding domain and leucine-rich repeat containing proteins (NLR), caspase-1, and apoptosis-associated speck-like protein (ASC). ASC is upregulated after TBI and is critical in coupling the proteins during complex formation resulting in IL-1β cleavage. To directly test whether inflammasome activation contributes to acute TBI-induced damage, we assessed IL-1β, IL-18, and IL-6 expression, contusion volume, hippocampal cell death, and motor behavior recovery in Nlrp1(-/-), Asc(-/-), and wild type mice after moderate controlled cortical impact (CCI) injury. Although IL-1β expression is significantly attenuated in the cortex of Nlrp1(-/-) and Asc(-/-) mice following CCI injury, no difference in motor recovery, cell death, or contusion volume is observed compared to wild type. These findings indicate that inflammasome activation does not significantly contribute to acute neural injury in the murine model of moderate CCI injury.
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