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Richa Hanamsagar, Amy Aldrich and Tammy Kielian Critical role for the AIM2 inflammasome during acute CNS bacterial infection Journal of Neurochemistry 129

Version of Record online: 19 FEB 2014 | DOI: 10.1111/jnc.12669

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The AIM2 inflammasome is protective during acute CNS bacterial infection. A disconnect in phenotypes between the inflammasome sensor Nod-like receptor protein 3 (NLRP3) and its adaptor ASC (apoptosis-associated speck-like protein containing a caspase-1 recruitment domain) during acute CNS Staphylococcus aureus (S. aureus) infection led to the discovery of absent in melanoma 2 (AIM2) as a critical inflammasome sensor. The AIM2 inflammasome is potentially triggered by dsDNA in cells harboring intracellular S. aureus, leading to ASC and caspase 1 recruitment, resulting in pro-IL-1β processing and cytokine secretion. This cascade, in turn, is protective to the host during acute infection. The NLRP3 inflammasome is also activated in response to S. aureus challenge by α-hemolysin (hla); however, it is not critical for host survival. ASC also regulates the production of other inflammatory mediators, presumably via indirect effects mediated by IL-1β action.

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