BackgroundImmunosuppression is common even in the early stage of severe sepsis. Interleukin-10 (IL-10) secretion and lymphocyte exhaustion are the main features of sepsis-induced immunosuppression. However, the relationship between IL-10 and the lymphocyte is still unclear. We investigated if IL-10/lymphocyte ratio (IL10LCR) were associated with mortality in severe septic patients.MethodsAdult patients with severe sepsis admitted to ICU of the First Affiliated Hospital of Guangzhou Medical University were identified from October 2012 to August 2013. Within 24 hours of ICU admission, peripheral whole blood was collected for the measurement of IL-10 using commercial multiplex bead-based assay kits and determination of lymphocyte count from laboratory data. The primary outcome was 28-day mortality.ResultsA total of 63 severe sepsis patients were identified. There were 20 (32%) patients died within 28 days. IL10LCR in non-survival patients was significantly higher than survival patients (median (IQR) 36.78 (12.34–79.63) ng/ml2 versus 11.01(5.41–27.50) ng/ml2, P = 0.002). Correlation analysis showed that IL10LCR was significantly correlated with APACHE II score (Spearman’s rho = 0.424, P<0.001). The receiver operating characteristic (ROC) curves showed the area under the curve was 0.749 for IL10LCR level to predict 28-day mortality with sensitivity and specificity at 70.0% and 74.4%, respectively. At an optimal cutoff of 23.39ng/ml2, Kaplan-Meier curve showed survival in patients with IL10LCR level above 23.39ng/ml2 was significantly lower than in patients with IL10LCR level less than 23.39ng/ml2 (P = 0.001 by log-rank test).ConclusionIL10LCR level is significantly associated with the severity and outcome of severe septic patients. It may serve as a biomarker for sepsis-induced immunosuppression.

Acute respiratory distress syndrome (ARDS) remains a high morbidity and mortality disease entity in critically ill patients, despite decades of numerous investigations into its pathogenesis. To obtain global protein expression changes in acute lung injury (ALI) lung tissues, we employed a high-throughput proteomics method to identify key components which may be involved in the pathogenesis of ALI. In the present study, we analyzed lung tissue proteomes of Pseudomonas aeruginosa-induced ALI rats and identified eighteen proteins whose expression levels changed more than twofold as compared to normal controls. In particular, we found that PRDX1 expression in culture medium was elevated by a lipopolysaccharide (LPS) challenge in airway epithelial cells in vitro. Furthermore, overexpression of PRDX1 increased the expression of proinflammatory cytokines interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α), whereas knockdown of PRDX1 led to downregulated expression of cytokines induced by LPS. In conclusion, our findings provide a global alteration in the proteome of lung tissues in the ALI rat model and indicate that PRDX1 may play a critical role in the pathogenesis of ARDS by promoting inflammation and represent a novel strategy for the development of new therapies against ALI.

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