Neutrophils from acute respiratory distress syndrome patients induce greater endothelial barrier dysfunction. Change in monolayer resistance at 30 minutes, 60 minutes, and 180 minutes. Groups were analyzed using two-way analysis of variance with Holm–Sidak post-hoc analysis. Values presented as mean ± standard error of the mean. Neutrophils from septic patients with acute respiratory distress syndrome (ARDS) produced greater loss of barrier function than those obtained from septic patients without ARDS. *P <0.05.