ArticleBrain : a journal of neurology2026
P2X7 receptor-mediated IL-1β release by human brain tissue: the impact of CNS-penetrant potential therapeutics.
Article in Brain : a journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Traumatic brain injury is a major cause of death throughout the world, and currently there are no approved drugs to treat this debilitating condition, emphasizing the clear unmet substantial clinical need. It is well recognized that microglial activation and the hostile neuroinflammatory response arising after the initial insult provide a therapeutic window for pharmacological intervention. The purinergic P2X7 receptor (P2X7R) is a key driver of neuroinflammation in a range of animal models of traumatic brain injury. To generate translational evidence for the role of the P2X7R, we optimized two human inflammatory models, human cells (monocyte-derived microglia) in vitro and human brain tissue ex vivo, to test the impact of clinical-stage brain-penetrant P2X7R antagonists. Using lipopolysaccharide-primed human monocyte-derived microglia, the P2X7R agonist 2'(3')-O-(4-benzoylbenzoyl) ATP (BzATP), evoked a concentration-dependent increase in pro-inflammatory interleukin (IL)-1β and IL-18 release, which was antagonized in a concentration-dependent manner by selective P2X7R antagonists and also by inhibitors of either the NLRP3 complex or caspase-1, implicating a role for the inflammasome in P2X7R-mediated cytokine release. Using slices of human brain tissue, BzATP similarly evoked cytokine release in a concentration-dependent manner that was also antagonized by selective P2X7R antagonists at pharmacologically relevant concentrations. The present study demonstrates the ability of P2X7R antagonists to suppress the neuroinflammatory response from primed human monocyte-derived microglia and human brain slices to offer direct translational data that central P2X7R antagonism might limit pathology-driven pro-inflammatory responses in the brain. This is predicted to improve the clinical outcomes for patients with traumatic brain injury and other neuroinflammatory pathologies.
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