Sensing of cytosolic LPS through caspy2 pyrin domain mediates noncanonical inflammasome activation in zebrafish

Dahai Yang, Xin Zheng, Shouwen Chen, Zhuang Wang, Wenting Xu, Jinchao Tan, Tianjian Hu, Mingyu Hou, Wenhui Wang, Zhaoyan Gu, Qiyao Wang, Ruilin Zhang, Yuanxing Zhang and Qin Liu ()
Additional contact information
Dahai Yang: East China University of Science and Technology
Xin Zheng: East China University of Science and Technology
Shouwen Chen: East China University of Science and Technology
Zhuang Wang: East China University of Science and Technology
Wenting Xu: East China University of Science and Technology
Jinchao Tan: East China University of Science and Technology
Tianjian Hu: East China University of Science and Technology
Mingyu Hou: East China University of Science and Technology
Wenhui Wang: East China University of Science and Technology
Zhaoyan Gu: East China University of Science and Technology
Qiyao Wang: East China University of Science and Technology
Ruilin Zhang: Shanghai Collaborative Innovation Center for Biomanufacturing
Yuanxing Zhang: East China University of Science and Technology
Qin Liu: East China University of Science and Technology

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract The noncanonical inflammasome is critical for cytosolic sensing of Gram-negative pathogens. Here, we show that bacterial infection induces caspy2 activation in zebrafish fibroblasts, which mediates pyroptosis via a caspase-5-like activity. Zebrafish caspy2 binds directly to lipopolysaccharide via the N-terminal pyrin death domain, resulting in caspy2 oligomerization, which is critical for pyroptosis. Furthermore, we show that caspy2 is highly expressed in the zebrafish gut and is activated during infection. Knockdown of caspy2 expression impairs the ability of zebrafish to restrict bacterial invasion in vivo, and protects larvae from lethal sepsis. Collectively, our results identify a crucial event in the evolution of pattern recognition into the death domain superfamily-mediated intracellular lipopolysaccharide-sensing pathway in innate immunity.

Date: 2018
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/s41467-018-04984-1 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04984-1

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-018-04984-1

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().