Aryl hydrocarbon receptor negatively regulates NLRP3 inflammasome activity by inhibiting NLRP3 transcription

Wanwan Huai, Rui Zhao, Hui Song, Jing Zhao, Lei Zhang, Lining Zhang, Chengjiang Gao, Lihui Han () and Wei Zhao ()
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Wanwan Huai: Shandong University School of Medicine
Rui Zhao: Changhai Hospital, Second Military Medical University
Hui Song: Shandong University School of Medicine
Jing Zhao: Shandong University School of Medicine
Lei Zhang: Shandong University School of Medicine
Lining Zhang: Shandong University School of Medicine
Chengjiang Gao: Shandong University School of Medicine
Lihui Han: Shandong University School of Medicine
Wei Zhao: Shandong University School of Medicine

Nature Communications, 2014, vol. 5, issue 1, 1-9

Abstract: Abstract NLRP3 inflammasome is a multi-protein complex, which plays crucial roles in host defense against pathogens. The NLRP3 protein level is considered rate limiting for the activation of the inflammasome, thus its expression must be tightly controlled to maintain immune homeostasis. However, the molecular mechanisms that modulate NLRP3 expression, especially at the transcriptional level, remain largely unknown. In the present study, we show that aryl hydrocarbon receptor (AhR) activation inhibits NLRP3 expression, caspase-1 activation and subsequent IL-1β secretion in peritoneal macrophages, whereas siRNA knockdown of AhR has opposite effects. AhR could bind to the xenobiotic response element (XRE) in the NLRP3 promoter and inhibit NLRP3 transcription. Furthermore, AhR activation suppresses Alum-induced peritonitis in vivo. Therefore, we identified AhR as a negative regulator of NLRP3 inflammasome activity by inhibiting the transcription of NLRP3 and suggested AhR as a potential target for the intervention of diseases with uncontrolled inflammasome activation.

Date: 2014
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DOI: 10.1038/ncomms5738

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