Fig. 1

Time course of pulmonary microvascular endothelial cell (PMVEC) albumin-permeability barrier dysfunction, death and apoptosis following cecal ligation/perforation (CLP)-sepsis in mice in vivo. a The leak of Evans blue (EB) dye-labeled albumin into lung tissue increased 2 and 4 h after CLP-induced sepsis, compared to sham control mice. n = 14 (Sham) and n = 3–10 /time point (CLP). b PMVEC death, as assessed through nuclear propidium iodide (PI+) staining visualized by fluorescence intravital videomicroscopy, was observed 2 and 4 h after CLP-induced sepsis, compared to sham control mice. n = 6 (Sham; combined 0.5 and 4 h time points) and n = 3–9 /time point (CLP). c PMVEC apoptosis was quantified by 3 complementary molecular markers: phosphatidyl serine expression (Annexin V+ staining), caspase activation (FLIVO+ staining), and DNA fragmentation (TUNEL+ labeling). Compared to low-level PMVEC apoptosis in sham control mice, enhanced septic PMVEC apoptosis was observed 0.5 – 1 h after CLP-induced sepsis and increased in time-dependent manner until 4 h. n = 6 (Sham; combined 0.5 and 4 h time points) and n = 3–9 /time point (CLP). *p < 0.05 and **p < 0.01 for CLP vs. sham group