CLICs-dependent chloride efflux is an essential and proximal upstream event for NLRP3 inflammasome activation

Tiantian Tang, Xueting Lang, Congfei Xu, Xiaqiong Wang, Tao Gong, Yanqing Yang, Jun Cui, Li Bai, Jun Wang, Wei Jiang () and Rongbin Zhou ()
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Tiantian Tang: University of Science and Technology of China
Xueting Lang: University of Science and Technology of China
Congfei Xu: University of Science and Technology of China
Xiaqiong Wang: University of Science and Technology of China
Tao Gong: University of Science and Technology of China
Yanqing Yang: University of Science and Technology of China
Jun Cui: Sun Yat-sen University
Li Bai: University of Science and Technology of China
Jun Wang: University of Science and Technology of China
Wei Jiang: University of Science and Technology of China
Rongbin Zhou: University of Science and Technology of China

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: Abstract The NLRP3 inflammasome can sense different pathogens or danger signals, and has been reported to be involved in the development of many human diseases. Potassium efflux and mitochondrial damage are both reported to mediate NLRP3 inflammasome activation, but the underlying, orchestrating signaling events are still unclear. Here we show that chloride intracellular channels (CLIC) act downstream of the potassium efflux-mitochondrial reactive oxygen species (ROS) axis to promote NLRP3 inflammasome activation. NLRP3 agonists induce potassium efflux, which causes mitochondrial damage and ROS production. Mitochondrial ROS then induces the translocation of CLICs to the plasma membrane for the induction of chloride efflux to promote NEK7–NLRP3 interaction, inflammasome assembly, caspase-1 activation, and IL-1β secretion. Thus, our results identify CLICs-dependent chloride efflux as an essential and proximal upstream event for NLRP3 activation.

Date: 2017
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DOI: 10.1038/s41467-017-00227-x

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