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 Raquel Guillamat-Prats
A1 Ferranda Puig
A1 Marta Camprubí-Rimblas
A1 Thomas Lebouvier
A1 Antonio Artigas
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.