ArticleJournal of neurotrauma2018
Microglial Inflammasome Activation in Penetrating Ballistic-Like Brain Injury.
Article in Journal of neurotrauma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 90 citations in OpenAlex.
- Exosomes from LPS-stimulated macrophages alleviate neuroinflammatory responses by reducing pyroptosis in systemic lipopolysaccharide-induced mice.Journal of applied biomedicine · 2025Article
- The NOX2-ROS-NLRP3 inflammasome axis in traumatic brain injury.Journal of neuroinflammation · 2025Article
- Review
- Detection of NLRP3, ASC, and Caspase-1 in serum and cerebrospinal fluid of traumatic brain injury patients: implications for short-term prognosis.Acta neurologica Belgica · 2025Article
- Revisiting the critical roles of reactive microglia in traumatic brain injury.International journal of surgery (London, England) · 2025Review
- Role of damage-associated molecular patterns in the pathogenesis and therapeutics of traumatic brain injury.Burns & trauma · 2025Review
- Microglial Mayhem NLRP3 Inflammasome's Role in Multiple Sclerosis Pathology.CNS neuroscience & therapeutics · 2024Review
- Beneficial Effects of Human Schwann Cell-Derived Exosomes in Mitigating Secondary Damage After Penetrating Ballistic-Like Brain Injury.Journal of neurotrauma · 2024Article
- Increased inflammasome protein expression identified in microglia from postmortem brains with schizophrenia.Journal of neuropathology and experimental neurology · 2024Article
- Multiple sclerosis: the NLRP3 inflammasome, gasdermin D, and therapeutics.Annals of translational medicine · 2024Review
- Modulation of Inflammatory Response by Electromagnetic Field Stimulation in Traumatic Brain Injury in Yucatan Swine.Journal of surgery and research · 2024Article
- An overview of preclinical models of traumatic brain injury (TBI): relevance to pathophysiological mechanisms.Frontiers in cellular neuroscience · 2024Review
- Interleukin-1 Receptor Antagonist as Therapy for Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Genetic predisposition to Alzheimer's disease alters inflammasome activity after traumatic brain injury.Translational research : the journal of laboratory and clinical medicine · 2023Article
- Activation of inflammasomes and their effects on neuroinflammation at the microelectrode-tissue interface in intracortical implants.Biomaterials · 2023Article
- Inflammasome activation in traumatic brain injury and Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Antidepressant and Neuroprotective Effects of 3-Hydroxy Paroxetine, an Analog of Paroxetine in Rats.The international journal of neuropsychopharmacology · 2023Article
- Regulation of microglial responses after pediatric traumatic brain injury: exploring the role of SHIP-1.Frontiers in neuroscience · 2023Article
- Methods to Study Inflammasome Activation in the Central Nervous System: Immunoblotting and Immunohistochemistry.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Penetrating traumatic brain injury (PTBI) is a significant cause of death and disability in the United States. Inflammasomes are one of the key regulators of the interleukin (IL)-1β mediated inflammatory responses after traumatic brain injury. However, the contribution of inflammasome signaling after PTBI has not been determined. In this study, adult male Sprague-Dawley rats were subjected to sham procedures or penetrating ballistic-like brain injury (PBBI) and sacrificed at various time-points. Tissues were assessed by immunoblot analysis for expression of IL-1β, IL-18, and components of the inflammasome: apoptosis-associated speck-like protein containing a caspase-activation and recruitment domain (ASC), caspase-1, X-linked inhibitor of apoptosis protein (XIAP), nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3), and gasdermin-D (GSDMD). Specific cell types expressing inflammasome proteins also were evaluated immunohistochemically and assessed quantitatively. After PBBI, expression of IL-1β, IL-18, caspase-1, ASC, XIAP, and NLRP3 peaked around 48 h. Brain protein lysates from PTBI animals showed pyroptosome formation evidenced by ASC laddering, and also contained increased expression of GSDMD at 48 h after injury. ASC-positive immunoreactive neurons within the perilesional cortex were observed at 24 h. At 48 h, ASC expression was concentrated in morphologically activated cortical microglia. This expression of ASC in activated microglia persisted until 12 weeks following PBBI. This is the first report of inflammasome activation after PBBI. Our results demonstrate cell-specific patterns of inflammasome activation and pyroptosis predominantly in microglia, suggesting a sustained pro-inflammatory state following PBBI, thus offering a therapeutic target for this type of brain injury.
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Registered trials
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