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Adipose-derived stem cells therapy effectively attenuates PM(2.5)-induced lung injury
BACKGROUND: The adverse health effects of fine particulate matter (PM(2.5)) exposure are associated with marked inflammatory responses. Adipose-derived stem cells (ADSCs) have immunosuppressive effects, and ADSC transplantation could attenuate pulmonary fibrosis in different animal disease models. H...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8214780/ https://www.ncbi.nlm.nih.gov/pubmed/34147136 http://dx.doi.org/10.1186/s13287-021-02441-3 |
Sumario: | BACKGROUND: The adverse health effects of fine particulate matter (PM(2.5)) exposure are associated with marked inflammatory responses. Adipose-derived stem cells (ADSCs) have immunosuppressive effects, and ADSC transplantation could attenuate pulmonary fibrosis in different animal disease models. However, whether ADSCs affect PM(2.5)-induced lung injury has not been investigated. METHOD: C57BL/6 mice were exposed to PM(2.5) every other day via intratracheal instillation for 4 weeks. After that, the mice received tail vein injections of ADSCs every 2 weeks. RESULTS: ADSC transplantation significantly attenuated systemic and pulmonary inflammation, cardiac dysfunction, fibrosis, and cell death in PM(2.5)-exposed mice. RNA-sequencing results and bioinformatic analysis suggested that the downregulated differentially expressed genes (DEGs) were mainly enriched in inflammatory and immune pathways. Moreover, ADSC transplantation attenuated PM(2.5)-induced cell apoptosis and pyroptosis in the lungs and hearts. CONCLUSION: ADSCs protect against PM(2.5)-induced adverse health effects through attenuating pulmonary inflammation and cell death. Our findings suggest that ADSC transplantation may be a potential therapeutic approach for severe air pollution-associated diseases. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13287-021-02441-3. |
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