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The Asthma Risk Gene, GSDMB, Promotes Mitochondrial DNA-induced ISGs Expression.

Tao Liu1, Julian Hecker1, Siqi Liu1

  • 1Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.

Journal of Respiratory Biology and Translational Medicine
|May 13, 2024
PubMed
Summary

Gasdermin B (GSDMB) promotes asthma-related inflammation by regulating the cGAS-STING pathway. GSDMB enhances mitochondrial DNA-induced interferon-stimulated gene (ISG) expression in airway cells.

Keywords:
Airway inflammationAsthmaGSDMBISGscGAS-STING pathway

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Area of Science:

  • Immunology
  • Genetics
  • Respiratory Medicine

Background:

  • Released mitochondrial DNA (mtDNA) activates the cGAS-STING pathway, inducing inflammation seen in asthma.
  • Gasdermin B (GSDMB) is a major asthma risk gene, but its role in this pathway is unknown.

Purpose of the Study:

  • To investigate how GSDMB regulates the mtDNA-activated cGAS-STING pathway and subsequent interferon-stimulated gene (ISG) induction in human airway epithelial cells.

Main Methods:

  • Utilized qPCR, ELISA, gel electrophoresis, co-immunoprecipitation, and immunofluorescence assays.
  • Examined GSDMB's role in BEAS-2B and primary normal human bronchial epithelial cells (nHBEs).
  • Analyzed mtDNA levels in asthmatic plasma and GSDMB association with RANTES expression.

Main Results:

  • GSDMB overexpression enhanced DNA-induced interferon (IFN) and ISG expression; GSDMB knockout weakened it.
  • GSDMB interacts with STING, promoting its Golgi translocation and IRF3 phosphorylation.
  • mtDNA copy number in asthmatics correlated with eosinophil counts, particularly in males.

Conclusions:

  • GSDMB promotes cGAS-STING pathway activation by mtDNA and poly(dA:dT) in airway epithelial cells.
  • This leads to enhanced ISG induction, contributing to asthma pathogenesis.
  • GSDMB is a key regulator linking innate immunity and genetic predisposition in asthma.