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. 2022 Aug 10;78(6):617–630. doi: 10.1136/thoraxjnl-2021-218194

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© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/.

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MSC EVs transfer miR-181a which modulates macrophage intracellular signalling through PTEN-pSTAT5-SOCS1 axis. Left: Stimulation of macrophage with inflammatory stimuli (LPS or ARDS plasma) results in the upregulation of secretion levels of pro-inflammatory cytokines TNF-α and IL-8. Right: miR181a packaged in MSC-EVs reprogrammes macrophage towards anti-inflammatory state through downregulation of PTEN and enhancement of pSTAT5/SOCS1 expression resulting in reduced levels of TNF-α and IL-8 production. ARDS, acute respiratory distress syndrome; EVs, extracellular vesicles; IL, interleukin; MSCs, mesenchymal stromal cells; PTEN, phosphatase and tensin homolog; pSTAT, phosphorylated STAT; SOCS1, suppressor of cytokine signalling 1; STAT, signal transducers and activators of transcription; TNF, tumour necrosis factor.