Research ArticleCELL DEATH

Noncanonical inflammasome signaling elicits gasdermin D–dependent neutrophil extracellular traps

See allHide authors and affiliations

Science Immunology  24 Aug 2018:
Vol. 3, Issue 26, eaar6676
DOI: 10.1126/sciimmunol.aar6676

eLetters is an online forum for ongoing peer review. Submission of eLetters are open to all. eLetters are not edited, proofread, or indexed.  Please read our Terms of Service before submitting your own eLetter.

Compose eLetter

Plain text

  • Plain text
    No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g.
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests

This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

Vertical Tabs

  • RE: Noncanonical inflammasome signaling elicits gasdermin D–dependent neutrophil extracellular traps
    • Dianne Sika-Paotonu, Associate Dean (Pacific)/Senior Lecturer Pathology & Molecular Medicine, Wellington School of Medicine & Health Sciences, University of Otago, New Zealand

    To the Editor,

    I read with interest the article published by Chen K. W., et al. (1) and entitled: “Non canonical inflammasome signalling elicits gasdermin D-dependent neutrophil extracellular traps.”

    This work explored a nonclassical host defense mechanism for neutralizing extracellular pathogens, involving neutrophil extrusion of neutrophil extracellular traps (NETs) and concomitant cell death (NETosis). NETs are DNA structures containing antimicrobial proteins that ensnare and neutralize microbes.

    Upon investigating neutrophil mediated host defense mechanisms against bacterial invasion, it was demonstrated that neutrophil cytosolic LPS or cytosolic Gram-negative bacteria could activate noncanonical (caspase-4/11) inflammasome signalling, and trigger gasdermin D (GSDMD)-dependent neutrophil death along with the extrusion of NETs.

    It was also reported that Caspase-11 and GSDMD were both required for neutrophil plasma membrane rupture during NET extrusion, and also for early NETosis within the context of host defense against extracellular pathogens.

    An unexpected discovery that was also described involved GSDMD (– also referred to as the executioner protein) as being a mediator for neutrophil extrusion of NETs and the concomitant NETosis against extracellular pathogens, in addition, to mediating macrophage death by pyroptosis for defense against intracellular pathogens.

    This work overall demonstrated the use of an inflammasome-a...

    Show More
    Competing Interests: None declared.

Stay Connected to Science Immunology

Navigate This Article