Background: The uncontrolled inflammatory response following infection is closely related to the morbidity and mortality of neonates. Interleukin 6 (IL-6) plays an important role in the pathogenesis and prognosis of this process. To better elucidate the secretion of IL-6 following infection in neonates, we investigated the IL-6 level and mechanism of IL-6/TLR4 signaling pathways.
Methods: We compared the IL-6, procalcitonin (PCT), and CRP levels between septic neonates and toddlers. In vitro cord blood samples from healthy term neonates and peripheral venous blood from healthy adult volunteers were collected. Protein expression was analyzed by Western blotting, mRNA expression by real-time PCR and membrane molecule expression by flow cytometry.
Results: The IL-6 concentrations were significantly higher in the neonate group than in the toddler group (p < 0.05). In the toddler group, the IL-6 concentrations were correlated positively with both PCT and CRP (PCT: r = 0.451, p = 0.001; CRP: r = 0.243, p = 0.023). In vitro, the secretion of IL-6 increased with the rising concentrations of LPS; at 1000 ng/ml LPS, IL-6 secretion from the monocytes of neonates was significantly higher than that of adults. There was a marked decreased level of MyD88 in neonate monocytes compared with that in adult monocytes. Additionally, the mRNA levels of Zc3h12a in neonate monocytes were significantly lower than those in adult monocytes following LPS stimulation.
Conclusion: Neonates displayed enhanced IL-6 production after infection. Our study, for the first time, reported a significant decrease in the expression of Zc3h12a in neonates. Thus, Zc3h12a may be a key factor for the aberrant increase in IL-6 after neonate infection.
Keywords: IL-6; MyD88; Zc3h12a; neonatal sepsis.
Copyright © 2017. Published by Elsevier B.V.