Background: Neonatal sepsis (NS) remains one of the leading causes of mortality among newborns. This study
found the deregulated microRNA-96 (miR-96) in NS neonates, and aimed to evaluate the clinical significance of miR-96, as
well as its effect on LPS-induced inflammatory response in monocytes. In addition, the relationship of interleukin-16 (IL16) and miR-96 was investigated to understand the underlying mechanisms.
Methods: Expression of miR-96 was examined using real-time quantitative PCR. Monocytes stimulated by LPS was used to
mimic excessive inflammation in the pathogenesis of NS. The enzyme-linked immunosorbent assay was applied to evaluate
pro-inflammatory cytokines levels. A luciferase reporter assay was used to confirm the interaction between miR-96 and IL16.
Results: Serum miR-96 expression was decreased in NS newborns and had considerable diagnostic value for NS screening.
LPS inhibited miR-96 expression in monocytes, and the overexpression of miR-96 could reverse the effects of LPS on the
inflammation of monocytes. IL-16 was a target gene of miR-96 and negatively correlated with miR-96 levels in NS
neonates. The inhibited inflammatory responses induced by miR-96 overexpression was abolished by the elevated IL-16 in
Conclusion: All the data reveal that serum decreased miR-96 may serve as a candidate non-invasive biomarker for NS
diagnosis. In addition, miR-96 inhibits LPS-induced inflammatory responses by targeting IL-16 in monocytes. The miR96/IL-16 axis may provide novel therapeutic targets for NS treatment.