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ESCRT-dependent membrane repair negatively regulates pyroptosis downstream of GSDMD activation

Sebastian Rühl1,2, Kateryna Shkarina3, Benjamin Demarco3

  • 1Focal Area Infection Biology, Biozentrum, University of Basel, Klingelbergstrasse 50/70, 4056 Basel, Switzerland.

Science (New York, N.Y.)
|November 24, 2018
PubMed

Insights

Cellular membrane repair, involving the ESCRT-III machinery, limits pyroptosis and inflammation. This process is triggered by calcium influx through gasdermin D pores, offering insights into cell survival.

Area of Science:

  • Cellular Biology
  • Immunology
  • Molecular Mechanisms of Cell Death

Background:

  • Pyroptosis is an inflammatory programmed cell death pathway activated by inflammasomes.
  • Inflammatory caspases cleave gasdermin D (GSDMD), forming pores that execute pyroptosis.

Purpose of the Study:

  • To investigate the role of cellular repair mechanisms in pyroptosis.
  • To determine if membrane repair influences pyroptosis extent and associated inflammation.

Main Methods:

  • Activation of canonical and noncanonical inflammasome pathways in human and murine cells.
  • Analysis of calcium influx through GSDMD pores.
  • Assessment of ESCRT-III machinery recruitment and function.
  • Inhibition of ESCRT-III to evaluate effects on pyroptosis and IL-1β release.

Main Results:

  • Calcium influx via GSDMD pores signals for ESCRT-mediated membrane repair.
  • ESCRT-III machinery is recruited to GSDMD-induced membrane damage.
  • Inhibition of ESCRT-III significantly potentiates pyroptosis and IL-1β release.

Conclusions:

  • The ESCRT-III system plays a critical anti-inflammatory role by repairing pyroptotic membrane pores.
  • Cellular membrane repair mechanisms are crucial for limiting pyroptosis and its inflammatory consequences.
  • Findings provide insights into cellular survival strategies during pyroptosis.

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