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

Innate immunity

article

Siwei Feng¹  Rendong Fang¹  Tingting Chen¹  Guihua Lei¹  Fengqing Hou¹  Jiali Jiang¹  Qingyuan Huang¹  Yuanyi Peng¹  Chao Ye¹  Dong-Liang Hu² 

[1] College of Animal Science and Technology, Southwest University;Department of Zoonoses, Kitasato University School of Veterinary Medicine

关键词: Streptococcus pneumoniae;    AIM2;    inflammasome;    IL-1β;   

DOI  :  10.1177/1753425919860252

来源: Sage Journals

【 摘 要 】

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.

【 授权许可】

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