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Streptococcus pneumoniae , a leading cause of invasive pneumococcal disease, is responsible for high mortality and morbidity worldwide. A previous study showed that the NLR family pyrin domain containing 3 (NLRP3) and absent in melanoma 2 (AIM2) inflammasomes are essential for caspase-1 activation and IL-1β production in the host response to  S. pneumoniae  infection. The function of NLRP3 in host innate immunity to  S. pneumoniae  was studied  in vivo  and  in vitro . However, the role of AIM2 in host defence against  S. pneumoniae  remains unclear. Here, we show that AIM2-deficient (AIM2 –/– ) mice display increased susceptibility to intra-nasal infection with  S. pneumoniae  in comparison to wild type mice and that this susceptibility was associated with defective IL-1β production. Macrophages from AIM2 –/–  mice infected with  S. pneumoniae  showed impaired secretion of IL-1β as well as activation of the inflammasome, as determined by the oligomerisation of apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1 activation. Taken together, these results indicate that the AIM2 inflammasome is essential for caspase-1-dependent cytokine IL-1β production and eventual protection from pneumococcal infection in mice.

Absent in melanoma 2 inflammasome is required for host defence against Streptococcus pneumoniae infection