Upregulation of miR-223 by SIRT1 attenuates the inflammatory response in neonatal sepsis.

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.