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- W72276968 abstract "Abstract The inflammasome constitutes one of the host's defenses against pathogens and deleterious stimuli by activating caspase-1. Inflammation with production of cytokines processed upon inflammasome activation is a crucial part of the secondary cascade of cell death induced after central nervous system (CNS) injury. The molecular mechanisms underlying trauma-induced inflammation in the CNS are poorly defined. In this study, the cellular distribution and protein association of inflammasome components were investigated in spinal cords and brains of rats subjected to moderate cervical injury and fluid-percussion brain injury, respectively. Coimmunoprecipitation experiments revealed that in the CNS, Apoptosis-Associated Speck-like protein containing a CARD (ASC) associates with caspase-1, caspase-11, NLR family, Pyrin domain containing 1 (NLRP1) and the inhibitor of apoptosis XIAP, forming the NLRP1 inflammasome. Injury to the CNS affects the composition of the inflammasome resulting in increased association of caspases-1 and -11 and NLRP1 with ASC and cleavage of XIAP. Immunohistochemistry revealed that motor neurons and cortical neurons express the NLRP1 inflammasome proteins. Therapeutic neutralization of ASC after injury inhibited inflammasome activation as shown by decreased caspase-1 activation and XIAP cleavage, resulting in reduced lesion volume and improved functional outcomes after spinal cord injury. Thus the inflammasome forms part of the innate immune response in the CNS and its inhibition may offer a novel therapeutic strategy to improve outcomes after injury and CNS inflammatory diseases. This research was supported by the NIH/NINDS and the US Army." @default.
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- W72276968 date "2009-04-01" @default.
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- W72276968 title "The inflammasome as a therapeutic target to improve outcomes after injury to the central nervous system (135.73)" @default.
- W72276968 doi "https://doi.org/10.4049/jimmunol.182.supp.135.73" @default.
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