Journal
NATURE COMMUNICATIONS
Volume 11, Issue 1, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-020-14534-3
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Funding
- Australian Government Research Training Program (RTP) Scholarship
- John Curtin School of Medical Research Gordon Ada Scholarship
- John Curtin School of Medical Research International Ph.D. scholarship
- Terrell International Undergraduate Scholarship from the Australian National University
- National Collaborative Research Infrastructure Strategy (NCRIS) via the Australian Phenomics Network
- National Health and Medical Research Council of Australia [APP1143008, APP1084283, APP1126599, APP1104329, APP1141504, APP1146864, APP1162103, APP1163358]
- Australian Research Council [DP180101494, FT150100452, DP190101325]
- National Natural Science Foundation of China [81772214]
- Cancer Institute NSW [15/CDF/1-11]
- UNSW Scientia Fellowship
- Intramural Program of the National Institute of Allergy and Infectious Diseases, NIH, USA
- Australian National University
- R.D. Wright Career Development Fellowship [APP1162025]
- Gretel and Gordon Bootes Medical Research Foundation
- Australian Research Council [FT150100452] Funding Source: Australian Research Council
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZIAAI001032] Funding Source: NIH RePORTER
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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.
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