Irstly stratified based on culture results (culture-positive and culture-negative), then subsequently divided into survivors and nonsurvivors. Venous blood samples were obtained from each patient within 6 hours of hospital/ICU admission (T-0) and at the end of first week of hospital/ICU stay (T-1). Serum samples were collected and used for simultaneous determination of IL-10 and sCD25, using a cytokine biochip array on the Evidence Investigator analyser (Randox Laboratories Ltd, Crumlin, UK), while PCT was assayed by an enzyme-linked fluorescent assay (VIDAS BRAHMS PCT; bioMerieux, PX105684 price France). Statistically significant differences between groups were established by the Mann-Whitney U test. The receiver-operating characteristic (ROC) curve was used to evaluate the diagnostic accuracy (defined by the area under the ROC curve (AUROCC)) of the analyzed cytokines and to determine the sensitivity and specificity at selected cutoff values. The statistical analyses were performed using SPSS 14.0 software (SPSS, Chicago, IL, USA). Results: PCT, IL-10 and sCD25 were significantly (P < 0.05) increased in infectious versus non-infectious SIRS patients at hospital admission (T-0) and after 1 week of hospital stay (T-1). Diagnostic accuracy of PCT, IL-10 and sCD25 was evaluated by AUROCC and exhibited a significance index of 0.0001, 0.0021 and 0.0095 respectively at T-0, while at T-1 the P values were 0.0011, 0.0016 and 0.0201 respectively. Regarding prognosticmarkers, PCT showed a prognostic significance only at T-1 (P = 0.04). However when IL-10 and sCD25 values from survivors were compared with those from nonsurvivors, significant differences were found for the former and the latter marker with P = 0.0014 and P = 0.014 respectively at PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/29069523 T-0, as well as with P = 0.0002 and P = 0.014 respectively at T-1. Conclusion: In our study, well-known PCT and IL-10 markers and novel sCD25 significantly contributed to diagnosis and prognosis of SIRS and septic patients.P44 Ninjurin 1 contributes to TLR-induced inflammation in endothelial cells C Jennewein*, K Zacharowski Hospital of the Goethe-University Frankfurt, Clinic of Anaesthesiology, Intensive Care and Pain Therapy, Frankfurt, Germany Critical Care 2012, 16(Suppl 3):P44 Background: Nerve injury induced protein 1 (Ninjurin 1 (Ninj1)) was first identified in Schwann cells and neurons contributing to cell adhesion and nerve regeneration. Recently, the role of Ninj1 has been linked to inflammatory processes in the central nervous system where functional repression reduced leukocyte infiltration and clinical disease activity during experimental autoimmune encephalomyelitis in mice [1]. But Ninj1 is also expressed outside the nervous system in various organs such as the liver and kidney as well as on leukocytes [2,3]. Therefore, we hypothesized that Ninj1 contributes to inflammation in general; that is, also outside the nervous system, with special interest in the pathogenesis of sepsis. Methods: Ninj1 was repressed by transfecting HMEC-1 cells, a human dermal microvascular endothelial cell line with siRNA targeting Ninj1 (siNinj1) or a negative control (siC). Subsequently, cells were stimulated with 100 ng/ml LPS (TLR4 agonist), 3 g/ml LTA (TLR2 agonist) or 100 n/ml poly(I: C) (TLR3 agonist) for 3 hours. The inflammatory response was analyzed by real-time PCR. In addition, transmigration of neutrophils across a HMEC-1 monolayer was measured using transwell plates (pore size 3 m). Results: Repression of Ninj1 by s.