PMC5251288_01
Endothelial phenotype with respect to barrier function. Fluorescence immunocytochemistry staining for vascular endothelial (VE)-cadherin (green), F-actin (red), was performed on confluent human umbilical vein endothelial cells (HUVECs) as described before. Cells were treated for 30 min with media supplemented with 5% serum from an individual with septic shock before (2nd row) and after cytokine removal (3rd row); 5% healthy human serum served as a control (1st row). Scale bar 10 mum
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PMC5251288_01_40560_2017_208_Fig1_HTML.jpg
Fig1
These contraction forces from the cytoskeletal architecture then contribute to the formation of visible gaps between adjacent cells, the cellular correlate for the clinical "vascular leakage syndrome" (Fig. 1, middle panel). When ECs were challenged with serum from the same patient after cytokine removal, the cells showed slightly less formation of stress fibers and were protected from the development of intracellular gaps (Fig. 1, right panel). All together, the endothelial phenotype after cytokine removal was comparable to cells that were stimulated with serum from a healthy control person (Fig. 1, left panel). 
Transendothelial resistance (TER) of HUVECs treated with septic serum. Normalized transendothelial electrical resistance (TER) was longitudinally measured in real time in human umbilical vein endothelial cells (HUVECs) with an electric cell-substrate impedance sensing (ECIS) device. HUVECs were then challenged with either septic serum before cytokine removal (bold line) or with serum from the same patient 24 h after cytokine removal (dotted line). TER normalization refers to the start point of the experiment for each condition (i.e., 5 min before septic serum incubation)
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Fig2
ECs challenged with serum before cytokine removal showed a rapid drop in mean resistance (consistent with an increase in permeability) (Fig. 2, bold line) whereas serum from the same patient after cytokine removal evidently blunted the permeability response (Fig. 2, dotted line).