RT Journal Article SR Electronic T1 Effect of antithrombin in an in vitro model of acute respiratory distress syndrome JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP OA3027 DO 10.1183/13993003.congress-2016.OA3027 VO 48 IS suppl 60 A1 Guillamat-Prats, Raquel A1 Puig, Ferranda A1 Camprubí-Rimblas, Marta A1 Lebouvier, Thomas A1 Artigas, Antonio YR 2016 UL http://erj.ersjournals.com/content/48/suppl_60/OA3027.abstract AB Acute Respiratory Distress Syndrome(ARDS) is an acute failure that develops in all ages patients with diverse clinical disorders and high mortality. ARDS pathogenesis involves inflammatory and procoagulant mechanisms. There is an increased inflammatory pulmonary edema with a great number of neutrophils and platelets,and endothelial and epithelial injury. The equilibrium between coagulation and fibrinolysis is disrupted and replaced by a procoagulant state.Antihombin III(ATIII) neutralizes several enzymes in the coagulation cascade,including thrombin,one of the most important procoagulant proteins found in ARDS patients.The aim of the study was to test the antinflammatory effect of ATIII in an invitro model of acute injury.We isolated human alveolar typeII cells from surgical resections. Acute damage was induced with Lipopolysaccharide of E. coli(100ng/ml) and 2h later we administered ATIII(5IU/ml) to one cell group. After 24h the expression of iNOS, TNFα, IL1ß and IL12p40 was evaluated by qRT-PCR. Data are expressed as mean±SEM; one-way ANOVA and Bonferroni post-hoc test was performed(n=6). Statistical differences are considered with p≤0.05.The expression of iNOS,TNFα,IL1ß and IL12p40 were increased in our invitro acute injury model. ATIII was able to reverse significantly the increase of all the proinflammatory markers. In conclusion ATIII reduces proinflammatory activation of Alveolar typeII cells and could help to recover ARDS.