BMC immunology · 2026
Upregulation of miR-223 by SIRT1 attenuates the inflammatory response in neonatal sepsis.
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Yan Anjian, Lu Chang, Wang Xuening
Аннотация
BACKGROUND: The diversity of clinical symptoms of neonatal sepsis leads to difficulties in diagnosis, and the treatment is limited. This study aims to investigate the role of the SIRT1/miR-223 signaling axis in neonatal sepsis.
METHODS: 100 neonates with sepsis and 100 healthy infants were included in this study. The RT-qPCR was used to detect RNA and inflammatory factor levels in serum. Peripheral blood neutrophils were isolated by gradient centrifugation. LPS-stimulated neutrophils were detected for MPO activity and inflammatory factor expression. Neutrophils were transfected with miR-223 oligonucleotide and SIRT1-related plasmid to detect changes in neutrophil-related parameters.
RESULTS: Neonates with sepsis had a significantly stronger inflammatory response than healthy infants, and the expression of miR-223 and SIRT1 in the serum was remarkably reduced. ROC curves showed that miR-223 had a diagnostic value for neonatal sepsis. The expression of miR-223 and SIRT1 was notably reduced in the model cells, and overexpression of miR-223 attenuated the inflammatory response in the LPS-induced neutrophil. Overexpression of SIRT1 could alleviate the enhanced inflammatory response due to inhibition of miR-223.
CONCLUSION: Overexpression of SIRT1 upregulated miR-223 expression, which attenuated the LPS-induced neutrophil activity and inflammatory response. The SIRT1/miR-223 signaling axis provides a potential therapeutic target for the clinical management of neonatal sepsis.
METHODS: 100 neonates with sepsis and 100 healthy infants were included in this study. The RT-qPCR was used to detect RNA and inflammatory factor levels in serum. Peripheral blood neutrophils were isolated by gradient centrifugation. LPS-stimulated neutrophils were detected for MPO activity and inflammatory factor expression. Neutrophils were transfected with miR-223 oligonucleotide and SIRT1-related plasmid to detect changes in neutrophil-related parameters.
RESULTS: Neonates with sepsis had a significantly stronger inflammatory response than healthy infants, and the expression of miR-223 and SIRT1 in the serum was remarkably reduced. ROC curves showed that miR-223 had a diagnostic value for neonatal sepsis. The expression of miR-223 and SIRT1 was notably reduced in the model cells, and overexpression of miR-223 attenuated the inflammatory response in the LPS-induced neutrophil. Overexpression of SIRT1 could alleviate the enhanced inflammatory response due to inhibition of miR-223.
CONCLUSION: Overexpression of SIRT1 upregulated miR-223 expression, which attenuated the LPS-induced neutrophil activity and inflammatory response. The SIRT1/miR-223 signaling axis provides a potential therapeutic target for the clinical management of neonatal sepsis.