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

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- kappa B. Tissue injury releases a danger-associated molecular pattern that provides positive feedback for NF-kappa B 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 beta-catenin in the cytoplasm, which subsequently reaches the nucleus to inhibit the transcription factor NF-kappa B. The inhibition of NF-kappa B by beta-catenin is a mechanism that reduces inflammation.