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 (IL-16) 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 cytokine levels. A
luciferase reporter assay was used to confirm the interaction between miR-96 and IL-16.
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 noninvasive
biomarker for NS diagnosis. In addition, miR-96 inhibits LPS-induced inflammatory
responses by targeting IL-16 in monocytes. The miR-96/IL-16 axis may provide novel therapeutic
targets for NS treatment.