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Echinococcus granulosus cyst fluid inhibits the type I interferon response by promoting ROS in macrophages

Chunxue Fu1, Chun Yang1, Caiya Ni1

  • 1NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, the First Affiliated Hospital/Shihezi University School of Medicine, Shihezi, Xinjiang, China; Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, Shihezi, Xinjiang, China.

Acta Tropica
|December 15, 2023
PubMed

Insights

Cystic echinococcosis fluid (EgCF) impairs macrophage immunity by increasing reactive oxygen species (ROS), which blocks the cGAS-STING-IRF3 pathway and reduces the type I interferon response. Restoring ROS levels with NAC treatment reactivates this pathway.

Area of Science:

  • Immunology
  • Parasitology
  • Cellular Biology

Background:

  • Cystic echinococcosis (CE) is a parasitic infection where Echinococcus granulosus cystic fluid (EgCF) may suppress macrophage immunity.
  • The impact of EgCF on the crucial type I interferon (IFN-I) response is not well understood.

Purpose of the Study:

  • To investigate whether EgCF affects the type I interferon response in macrophages.
  • To elucidate the underlying molecular mechanisms, focusing on the cGAS-STING-IRF3 signaling pathway and reactive oxygen species (ROS).

Main Methods:

  • Macrophages were treated with EgCF and stimulated with 2'3'-cGAMP.
  • Interferon-beta (IFN-β) production, cGAS-STING-IRF3 signaling activation, and intracellular ROS levels were measured.
  • The effect of the ROS inhibitor N-acetylcysteine (NAC) was assessed.

Main Results:

  • EgCF significantly reduced 2'3'-cGAMP-induced IFN-β production in macrophages.
  • EgCF inhibited the cGAS-STING-IRF3 signaling pathway.
  • EgCF treatment led to increased intracellular ROS levels.
  • NAC administration restored cGAS-STING-IRF3 signaling and IFN-β expression.

Conclusions:

  • EgCF impairs macrophage-mediated type I interferon responses.
  • This impairment is mediated by EgCF-induced increases in ROS, which inhibit the cGAS-STING-IRF3 signaling pathway.

Keywords:
Echinococcus granulosusMacrophagesROSType I interferoncGAS-STING

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