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Cutibacterium acnes Infection Induces Type I Interferon Synthesis Through the cGAS-STING Pathway

Katrin Fischer1, Roland Tschismarov2, Andreas Pilz1

  • 1Max Perutz Labs, Department of Microbiology, Immunobiology and Genetics, University of Vienna, Vienna Biocenter, Vienna, Austria.

Frontiers in Immunology
|November 12, 2020
PubMed

Insights

Cutibacterium acnes triggers type I interferon signaling in macrophages via the cGAS-STING pathway. This discovery offers new insights into inflammatory diseases linked to C. acnes accumulation.

Area of Science:

  • Immunology
  • Microbiology
  • Cellular Biology

Background:

  • Cutibacterium acnes (C. acnes), a common human commensal, is linked to inflammatory diseases like acne and prostate cancer.
  • C. acnes accumulation correlates with increased inflammation, involving known pathways like NF-κB and inflammasomes.
  • The role of C. acnes in activating the type I interferon (IFN-I) pathway remains unexplored.

Purpose of the Study:

  • To investigate if C. acnes can induce the type I interferon (IFN-I) signaling pathway in human macrophages.
  • To elucidate the specific intracellular mechanisms involved in C. acnes-mediated IFN-I induction.

Main Methods:

  • Human macrophages were exposed to C. acnes.
  • Activation of the cGAS-STING pathway and IFN-I signaling was assessed.
  • The role of the adapter protein TRIF in the signaling cascade was evaluated.
  • Bacterial intracellular replication was monitored.

Main Results:

  • C. acnes successfully induced the IFN-I signaling axis in human macrophages.
  • The cGAS-STING pathway was identified as the trigger for IFN-I induction by C. acnes.
  • IFN-I signaling was dependent on the adapter protein TRIF in a non-canonical manner.
  • These events occurred without detectable intracellular C. acnes replication.

Conclusions:

  • C. acnes activates the type I interferon (IFN-I) signaling pathway in macrophages through the cGAS-STING pathway.
  • TRIF plays a crucial role in this non-canonical IFN-I induction.
  • IFN-I signaling may contribute to the pathogenesis of C. acnes-associated inflammatory diseases.
  • Findings suggest potential therapeutic targets for C. acnes-related inflammatory conditions.
Keywords:
Cutibacterium acnesListeria (L.) monocytogenesNFkB = nuclear factor kappa bSTAT (signal transducer and activator of transcription)TIR-domain-containing adapter-inducing interferon-βcyclic GMP-AMP synthaseinterferonstimulator of interferon genes

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