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Influenza Infects Lung Microvascular Endothelium Leading to Microvascular Leak: Role of Apoptosis and Claudin-5

Figure 2

Human influenza induces lung endothelial permeability.

(A) Influenza induces an increase in permeability to dextran in a dose-dependent fashion. Cells were infected at the indicated multiplicity of infection (MOI) for 24 hours before permeability to dextran was analyzed. Results (mean, SD) are experiments and are normalized to control, *p<0.05 versus control. (B) A clinical H3N2 influenza isolate was used to infect lung microvascular endothelium for 24 hours. Permeability to dextran was measured as in A. Results (mean, SD) are from 3 experiments and are normalized to control, *p<0.05. (C) Similar to A, except the transendothelial electrical resistance (TEER) was measured before and after infection. Results (mean, SE) are from 3 experiments and are normalized to control, *p<0.05. (D) Influenza induces endothelial permeability even after infection from the basal aspect. Human lung microvascular endothelium seeded on transwells was infected from the basal aspect of the transwell (MOI 8) and the change in TEER was measured 24 hours later. Results (mean, SD) are from 2 experiments and are normalized to control, *p<0.05.

Figure 2

doi: https://doi.org/10.1371/journal.pone.0047323.g002