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RIPK1 Distinctly Regulates Yersinia-Induced Inflammatory Cell Death, PANoptosis

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Authors

Subbarao, Malireddi R.K.; Kesavardhana, Sannula; Karki, Rajendra; Kancharana, Balabhaskararao; Burton, Amanda R.; Kanneganti, Thirumala-Devi

Issue Date
2020-12
Publisher
American Association of Immunologists, Inc.
Citation
ImmunoHorizons, Vol.4 No.12, pp.789-796
Abstract
Bacterial pathogens from the genus Yersinia cause fatal sepsis and gastritis in humans. Innate immune signaling and inflammatory cell death (pyroptosis, apoptosis, and necroptosis [PANoptosis]) serve as a first line of antimicrobial host defense. The receptor-interacting protein kinase 1 (RIPK1) is essential for Yersinia-induced pyroptosis and apoptosis and an effective host response. However, it is not clear whether RIPK1 assembles a multifaceted cell death complex capable of regulating caspase-dependent pyroptosis and apoptosis or whether there is cross-talk with necroptosis under these conditions. In this study, we report that Yersinia activates PANoptosis, as evidenced by the concerted activation of proteins involved in PANoptosis. Genetic deletion of RIPK1 abrogated the Yersinia-induced activation of the inflammasome/pyroptosis and apoptosis but enhanced necroptosis. We also found that Yersinia induced assembly of a RIPK1 PANoptosome complex capable of regulating all three branches of PANoptosis. Overall, our results demonstrate a role for the RIPK1 PANoptosome in Yersinia-induced inflammatory cell death and host defense.
ISSN
2573-7732
URI
https://hdl.handle.net/10371/203007
DOI
https://doi.org/10.4049/immunohorizons.2000097
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  • College of Natural Sciences
  • School of Biological Sciences
Research Area Cytokine Storm, Host Defense, Innate Immunity in Metabolic and Inflammatory Diseases

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