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 language | English |
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Article number | 7299 |
Journal | International Journal of Molecular Sciences |
Volume | 24 |
Issue number | 8 |
DOIs | |
Publication status | Published - Apr 2023 |
Keywords
- NF-κB
- PGE2
- acute respiratory distress syndrome
- infectious disease
- influenza virus
- mesenchymal stem cell
- β-catenin