PT  - JOURNAL ARTICLE
AU  - Raquel Guillamat-Prats
AU  - Ferranda Puig
AU  - Marta Camprubí-Rimblas
AU  - Thomas Lebouvier
AU  - Antonio Artigas
TI  - Effect of antithrombin in an in vitro model of acute respiratory distress syndrome
AID  - 10.1183/13993003.congress-2016.OA3027
DP  - 2016 Sep 01
TA  - European Respiratory Journal
PG  - OA3027
VI  - 48
IP  - suppl 60
4099  - http://erj.ersjournals.com/content/48/suppl_60/OA3027.short
4100  - http://erj.ersjournals.com/content/48/suppl_60/OA3027.full
SO  - Eur Respir J2016 Sep 01; 48
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.