005 Endocan, a potential new endothelial marker in human sepsis

005 Endocan, a potential new endothelial marker in human sepsis

Infection - Inflammation - Réparation 004 PM induce TGF-B production by bronchial epithelium, suggesting an auto-inhibitory effect on cell renew 005...

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Infection - Inflammation - Réparation

004 PM induce TGF-B production by bronchial epithelium, suggesting an auto-inhibitory effect on cell renew

005 Endocan, a potential new endothelial marker in human sepsis

G. ~evouassoux',R. Naoui', A.L. ~ e b a r dN. ~ ,~ r e ~ m o n d ' , A. ~ i s l e r ' ,J. Bienvenu2, J.C. Bernengol, Y. Pacheco'

J. Pugin4, A.B. ~ o n n e l ' , ~P.,

'Respiratory Unit and EA 3091, Centre Hospitalier Lyon Sud 69495 Pierre-Bénite Cedex, France. Laboratoty oflmmunology, Centre Hospitalier Lyon Sud, 69495 Pierre-Bénite Cedex, France.

B. ~ r i ~ o r i u '~cherpereel',~, ,~. F. ~ e p o n t i e u ' ,M. ~ o u r d a i n ~ ,

ass salle'

INSERM 17416 Institut Pasteur de Lille, Lille, France. ~ewicede Pneumohgie, CHU Lille, France. Service de Réanimation mkdicale, CHU Lille, France. Service de véanimation, Hôpital de Genève, Suisse.

[email protected]

[email protected]

Introduction : Atmospheric pollutants act efficiently on immune response, facilitating ainvay inflammatory reaction to antigen and non-specific stimuli. Branchial epithelial ce11 is immediately implicated in this process. To gain new insights in the roles of this natural barrier in context of pollution, we investigated the effect of suspended particulate matter (SPM) on epithelium for cytokine, growth factor production and ce11 proliferation. Methods: SPMs were collected from Lyon city area, using TEOM collecter, filtered, then resuspended in distilled water. SV-40 transformed-foetal human bronchial epithelial ce11 line (WI26VA4) was cultured in MEM for at least 60% of confluence, then incubated for 48h at 37"C, in the absence, or in the presence of SPM (Pl < 0.2 pm, 0.2 < P2 d . 8 Pm, 0.8 < P3
Introduction : We previously reported that serum levels of endocan, an endothelial derived dermatan sulphate proteoglycan which regulates LFA-II ICAM-1 interactions i n vitro, are elevated in patients with sepsis. As the endothelium is an important player in sepsis, and endothelial activation parallel sepsis severity, we wonder if blood levels of endocan could be used as a diagnostic and prognostic marker in sepsis and how it compares with previously proposed markers as von Willebrand factor, IL6, ILIO, Procalcitonin or C reactive protein. We also studied kinetics of endocan secretion by endothelial cells in vitro after stimulation by soluble mediators involved in sepsis. Material and methods : Endocan values were quantified by an in house sandwich type ELISA. Commercial assays were used for procalcitonin, C reactive protein, IL10, IL6, von Willebrand Factor. Design : Prospective observational study. Setting : Intensive a r e unit (ICU) of the University Hospitals of Lille, France, and Geneva, Switzerland. Patients : Al1 patients admitted to the intensive care unit over a 6-month period with clinical evidence of sepsis. Interventions : None. Measurement~and main results : In vitro, we showed a sustained endocan secretion by endothelial cells after stimulation by LPS and TNFa. Circulating levels of endocan measured in 63 patients admitted in ICU with sepsis were significantly elevated compared to 20 healthy donors and 7 SIRS patients: 2.71 4.88 nglml vs 0.77 f 0.44 nglml vs 0.68 f 1.03 nglml (median f interquartile range) (p < 0.001). Endocan levels were higher in patients with septic shock (6.1 1 f 12.99 nglml, n = 22) than in patients with severe sepsis (1.97 f 7.8 nglml, n = 12) or sepsis (1.95 + 1.63 nglml, n = 29). Measurement of endocan at ICU admission revealed higher levels in non survivors (n = 12) than in patients still alive 10 days later (n = 51) (6.98 k 13.8 us 2.45 f 4.09, p < 0.01) and was the only marker which had a prognostic significance. Conclusions : These results suggest that in septic patients, endocan blood level is related to the severity and to the outcome of the patients, and may represent a novel endothelial ce11 dysfunction marker.

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