Bacillus cereus non-haemolytic enterotoxin activates the NLRP3 inflammasome

Daniel Fox, Anukriti Mathur, Yansong Xue, Yunqi Liu, Wei Hong Tan, Shouya Feng, Abhimanu Pandey, Chinh Ngo, Jenni A. Hayward, Ines I. Atmosukarto, Jason D. Price, Matthew D. Johnson, Nadja Jessberger, Avril A. B. Robertson, Gaetan Burgio, David C. Tscharke, Edward M. Fox, Denisse L. Leyton, Nadeem O. Kaakoush, Erwin Märtlbauer, Stephen H. Leppla and Si Ming Man ()
Additional contact information
Daniel Fox: The Australian National University
Anukriti Mathur: The Australian National University
Yansong Xue: The Australian National University
Yunqi Liu: The Australian National University
Wei Hong Tan: The Australian National University
Shouya Feng: The Australian National University
Abhimanu Pandey: The Australian National University
Chinh Ngo: The Australian National University
Jenni A. Hayward: The Australian National University
Ines I. Atmosukarto: The Australian National University
Jason D. Price: The Australian National University
Matthew D. Johnson: The Australian National University
Nadja Jessberger: Faculty of Veterinary Medicine, Ludwig-Maximilians-Universität München
Avril A. B. Robertson: The University of Queensland
Gaetan Burgio: The Australian National University
David C. Tscharke: The Australian National University
Edward M. Fox: Northumbria University
Denisse L. Leyton: The Australian National University
Nadeem O. Kaakoush: UNSW Sydney
Erwin Märtlbauer: Faculty of Veterinary Medicine, Ludwig-Maximilians-Universität München
Stephen H. Leppla: Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Si Ming Man: The Australian National University

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract Inflammasomes are important for host defence against pathogens and homeostasis with commensal microbes. Here, we show non-haemolytic enterotoxin (NHE) from the neglected human foodborne pathogen Bacillus cereus is an activator of the NLRP3 inflammasome and pyroptosis. NHE is a non-redundant toxin to haemolysin BL (HBL) despite having a similar mechanism of action. Via a putative transmembrane region, subunit C of NHE initiates binding to the plasma membrane, leading to the recruitment of subunit B and subunit A, thus forming a tripartite lytic pore that is permissive to efflux of potassium. NHE mediates killing of cells from multiple lineages and hosts, highlighting a versatile functional repertoire in different host species. These data indicate that NHE and HBL operate synergistically to induce inflammation and show that multiple virulence factors from the same pathogen with conserved function and mechanism of action can be exploited for sensing by a single inflammasome.

Date: 2020
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DOI: 10.1038/s41467-020-14534-3

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