Abstract
Background: Preterm labor (PTL) is one of the major causes of neonatal morbidity and mortality worldwide. It is commonly accepted that the act of giving birth is the final step in a proinflammatory signaling cascade, orchestrated by an intrauterine milieu coupled to hormonal cues. Consequently, the inflammatory process plays a pivotal role during the pathogenesis of human labor, both in term and preterm deliveries. The aim of this work was to analyze the abilities of innate lymphoid cells (ILCs), specifically ILC3 NCR- cells, to act as proinflammatory mediators and to elucidate their role in pregnancy. Accordingly, we hypothesize that altered ILC numbers may prompt preterm labor (PTL). Methods: We analyzed thirteen full term labor (FTL) and seven PTL pregnant women for the presence of ILCs. ILCs were isolated and characterized from maternal peripheral blood, maternal-fetal interface, and cord blood samples, using flow cytometry. For group analysis, two-way ANOVA was performed. Each data set was analyzed using student t-test with a confidence interval of 95%. Results: A tendency for decreased ILCs numbers in PTL samples compared to those in FTL samples was observed. Additionally, ILC3 NCR- cells were significantly increased in both PTL and FTL groups, when compared to ILC3NCR+. Conclusion: Our results support a potential inflammatory role of ILC3 NCR- in the instigation of labor. Moreover our work highlights the importance of ILCs actions in the regulation of labor.
Type 3 innate lymphoid cells induce proliferation of CD94+ natural killer cells
