Interleukin-1 as a pharmacological target in acute brain injury

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Interleukin-1 as a pharmacological target in acute brain injury

Interleukin-1 as a pharmacological target in acute brain injury

1. David Brough,
2. Nancy J Rothwell^* and
3. Stuart M Allan

DOI: 10.1113/EP085135

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Experimental Physiology

Accepted Article (Accepted, unedited articles published online and citable. The final edited and typeset version of record will appear in future.)

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1. This is an Accepted Article that has been peer-reviewed and approved for publication in the Experimental Physiology, but has yet to undergo copy-editing and proof correction. Please cite this article as an ‘Accepted Article’; doi: 10.1113/EP085135.

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Acute brain injury is one of the leading causes of mortality and disability worldwide. Despite this, treatments for acute brain injuries are limited and there remains a massive unmet clinical need. Inflammation has emerged as a major contributor to non-communicable diseases and there is now substantial and growing evidence that inflammation, driven by the cytokine interleukin-1 (IL-1), worsens acute brain injury. IL-1 is regulated by large multi-molecular complexes called inflammasomes. Here we discuss the latest research on the regulation of inflammasomes and IL-1 in the brain, pre-clinical efforts to establish the IL-1 system as a therapeutic target, and the promise of recent and future clinical studies of blocking IL-1 action for the treatment of brain injury.