Background: Socioeconomic disparities negatively impact neonatal health. The influence of sociodemographic disparities on neonatal sepsis is understudied. We examined the association of insurance payer status, income, race and gender on neonatal sepsis mortality and healthcare resource utilization. Methods: We used the Kid’s Inpatient Database, a nationwide population-based survey from 2006, 2009 and 2012. Neonates diagnosed with sepsis were included in the study. Multivariable logistic regression (mortality) and multivariable linear regression (length of stay and total hospital costs) were constructed to determine the association of patient and hospital characteristics. Results: Our study cohort included a weighted sample of 160,677 septic neonates. Several sociodemographic disparities significantly increased mortality. Self-pay patients had increased mortality (odds ratio 3.26 [95% confidence interval: 2.60–4.08]), decreased length of stay (−2.49 ± 0.31 days, P < 0.0001) and total cost (−$5015.50 ± 783.15, P < 0.0001) compared with privately insured neonates. Additionally, low household income increased odds of death compared with the most affluent households (odds ratio 1.19 [95% confidence interval: 1.05–1.35]). Moreover, Black neonates had significantly decreased length of stay (−0.86 ± 0.25, P = 0.0005) compared with White neonates. Conclusions: This study identified specific socioeconomic disparities that increased odds of death and increased healthcare resource utilization. Moreover, this study provides specific societal targets to address to reduce neonatal sepsis mortality in the United States.

Hepatic stellate cell (HSC) activation is responsible for hepatic fibrogenesis and is associated with an overexpression of transcription 3 (STAT3). Luteolin, a common dietary flavonoid with potent anti-inflammatory properties, has previously demonstrated antifibrogenic properties in HSCs but the mechanism has not been fully elucidated. Activated human and rat hepatic stellate cell lines LX-2 and HSC-T6 were used to study the effects of luteolin on HSCs. Cellular proteins were determined by western blot and immunofluorescence. Cell proliferation was assessed with Alamar Blue assay. Luteolin significantly decreased LX-2 and HSC-T6 cell viability in a time-and-dose-dependent manner, as well as decreased HSC end-products α-smooth muscle actin (α-SMA), collagen I, and fibronectin. Luteolin decreased levels of total and phosphorylated STAT3, suppressed STAT3 nuclear translocation and transcriptional activity, and attenuated expression of STAT3-regulated proteins c-myc and cyclin D1. STAT3 specific inhibitors stattic and SH-4-54 demonstrated similar effects on HSC viability and α-SMA production. In LX-2 and HSC-T6 cells, luteolin demonstrates a potent ability to inhibit hepatic fibrogenesis via suppression of the STAT3 pathway. These results further elucidate the mechanism of luteolin as well as the effect of the STAT3 pathway on HSC activation.