The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Exosomal miR-30d-5p of neutrophils induces M1 macrophage polarization and primes macrophage pyroptosis in sepsis-related acute lung injury
Open accessAbstract
Background: Polymorphonuclear neutrophils (PMNs) play an important role in sepsis-related acute lung injury (ALI). Accumulating evidence suggests PMN-derived exosomes as a new subcellular entity acting as a fundamental link between PMN-driven inflammation and tissue damage. However, the role of PMN-derived exosomes in sepsis-related ALI and the underlying mechanisms remains unclear. Methods: Tumor necrosis factor-α (TNF-α), a key regulator of innate immunity in sepsis-related ALI, was used to stimulate PMNs from healthy C57BL/6J mice in vitro. Exosomes isolated from the supernatant were injected to C57BL/6J wild-type mice intraperitoneally (i.p.) and then examined for lung inflammation, macrophage (Mϕ) polarization and pyroptosis. In vitro co-culture system was applied where the mouse Raw264.7 macrophages or bone marrow-derived macrophages (BMDMs) were co-cultured with PMN-derived exosomes to further confirm the results of in vivo animal study and explore the potential mechanisms involved. Results: Exosomes released by TNF-α-stimulated PMNs (TNF-Exo) promoted M1 macrophage activation after in vivo i.p. injection or in vitro co-culture. In addition, TNF-Exo primed macrophage for pyroptosis by upregulating NOD-like receptor 3 (NLRP3) inflammasome expression through nuclear factor κB (NF-κB) signaling pathway. Mechanistic studies demonstrated that miR-30d-5p mediated the function of TNF-Exo by targeting suppressor of cytokine signaling (SOCS-1) and sirtuin 1 (SIRT1) in macrophages. Furthermore, intravenous administration of miR-30d-5p inhibitors significantly decreased TNF-Exo or cecal ligation and puncture (CLP)-induced M1 macrophage activation and macrophage death in the lung, as well as the histological lesions. Conclusions: The present study demonstrated that exosomal miR-30d-5p from PMNs contributed to sepsis-related ALI by inducing M1 macrophage polarization and priming macrophage pyroptosis through activating NF-κB signaling. These findings suggest a novel mechanism of PMN-Mϕ interaction in sepsis-related ALI, which may provide new therapeutic strategies in sepsis patients.
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Cites
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Cited by
Savin, I. A., Zenkova, M. A., & Sen’kova, A. V. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232314959 · Cited by 279
Tu, Y., Liu, J., Kong, D., Guo, X., Li, J., Long, Z., Peng, J., Wang, Z., Wu, H., Liu, P., et al. (2023) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2023.03.014 · Cited by 89
Metadata
- Authors
- Jiao, Y., Zhang, T., Zhang, C., Ji, H., Tong, X., Xia, R., Wang, W., Ma, Z., & Shi, X.
- Venue
- Critical Care
- Published
- 2021-10-12
- Volume
- 25
- Issue
- 1
- Pages
- 356-356
- ISSN
- 1364-8535 (ISSN-L)
- OpenAlex
- W3206257957
- Cited by
- 558
- References
- 42
- FWCI
- 21.33
- Type
- journal article
- Language
- en
- Open access
- gold
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- Jiao, Y., Zhang, T., Zhang, C., Ji, H., Tong, X., Xia, R., Wang, W., Ma, Z., & Shi, X. (2021). Exosomal miR-30d-5p of neutrophils induces M1 macrophage polarization and primes macrophage pyroptosis in sepsis-related acute lung injury. Critical Care. https://doi.org/10.1186/s13054-021-03775-3
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