AIM2 Inflammasome Is Critical for dsDNA-Induced IL-1β Secretion in Human Dental Pulp Cells

被引:7
作者
Huang, Shuheng [1 ,2 ]
Song, Zhi [1 ,2 ]
Huang, Qiting [1 ,2 ]
Jiang, Lan [1 ,2 ]
Chen, Lingling [1 ,2 ]
Wang, Runfu [1 ,2 ]
Lin, Zhengmei [1 ,2 ]
机构
[1] Sun Yat Sen Univ, Guanghua Sch Stomatol, Hosp Stomatol, Dept Operat Dent & Endodont, Guangzhou 510055, Guangdong, Peoples R China
[2] Guangdong Prov Key Lab Stomatol, Guangzhou 510055, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
absent in melanoma 2 (AIM2); inflammasome pathway; cytoplasmic DNA; IL-1; beta; human dental pulp; NLRP3; ACTIVATION; EXPRESSION; KERATINOCYTES; RECEPTORS; INFECTION; ROLES;
D O I
10.1007/s10753-017-0697-z
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The AIM2 inflammasome pathway has been determined to play an important role in cellular immune defense against bacterial and viral infections; however, its function and regulatory mechanism in human dental pulp cells (HDPCs) during pulpitis remains poorly understood. In this study, we explored whether the AIM2 inflammasome pathway was activated in HDPCs in response to dsDNA and defined its role in regulating IL-1 beta secretion. We demonstrated that stimulation with IFN-gamma and cytoplasmic DNA significantly activated the AIM2 inflammasome and increased IL-1 beta secretion in HDPCs. Moreover, AIM2 overexpression significantly up-regulated both cleaved Caspase-1 expression and IL-1 beta release in HDPCs, while suppression of ASC and Caspase-1 resulted in down-regulation of cleaved Caspase-1 and IL-1 beta secretion. These results suggest that Caspase-1-dependent IL-1 beta processing and secretion require the AIM2 inflammasome pathway in HDPCs and that the AIM2 inflammasome pathway is critical for regulation of the dental pulp immune response.
引用
收藏
页码:409 / 417
页数:9
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