Interleukin-1 and neuronal injury: mechanisms, modification, and therapeutic potential.
Interleukin-1 (IL-1) expression in the brain increases in response to acute and chronic insults, and IL-1 contributes directly to experimentally induced ischaemic, excitotoxic, and traumatic brain injury. Release and cleavage of active IL-1 beta may be achieved via purinergic P2X7 receptors and activation of caspase-1. The mechanisms of action of IL-1 are largely unknown, but may involve effects on glia, endothelia, and neurones, or on physical parameters within the brain such as temperature or acidity. The naturally occurring IL-1 receptor antagonist (IL-1ra) is currently being considered for treatment of stroke and other disorders.
Rothwell
Nancy
N
School of Biological Sciences, 1.124 Stopford Building, University of Manchester, Oxford Road, Manchester M13 9PT, UK. Nancy.Rothwell@man.ac.uk
D000818:Animals; D001930:Brain Injuries / Q000188:drug therapy / Q000378:metabolism*; D006801:Humans; D007375:Interleukin-1 / Q000009:adverse effects / Q000502:physiology* / Q000627:therapeutic use; D051379:Mice; D009474:Neurons / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D051381:Rats
D007375:Interleukin-1