PGE2 Produced by Exogenous MSCs Promotes Immunoregulation in ARDS Induced by Highly Pathogenic Influenza A through Activation of the Wnt-β-Catenin Signaling Pathway

Resti Yudhawati, Kazufumi Shimizu

Research output: Contribution to journalReview articlepeer-review

1 Citation (Scopus)

Abstract

Acute respiratory distress syndrome is an acute respiratory failure caused by cytokine storms; highly pathogenic influenza A virus infection can induce cytokine storms. The innate immune response is vital in this cytokine storm, acting by activating the transcription factor NF-κB. Tissue injury releases a danger-associated molecular pattern that provides positive feedback for NF-κB activation. Exogenous mesenchymal stem cells can also modulate immune responses by producing potent immunosuppressive substances, such as prostaglandin E2. Prostaglandin E2 is a critical mediator that regulates various physiological and pathological processes through autocrine or paracrine mechanisms. Activation of prostaglandin E2 results in the accumulation of unphosphorylated β-catenin in the cytoplasm, which subsequently reaches the nucleus to inhibit the transcription factor NF-κB. The inhibition of NF-κB by β-catenin is a mechanism that reduces inflammation.

Original languageEnglish
Article number7299
JournalInternational Journal of Molecular Sciences
Volume24
Issue number8
DOIs
Publication statusPublished - Apr 2023

Keywords

  • NF-κB
  • PGE2
  • acute respiratory distress syndrome
  • infectious disease
  • influenza virus
  • mesenchymal stem cell
  • β-catenin

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