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