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

Figure 9

Formoterol induces claudin-5 protein expression and prevents virus-induced endothelial permeability.

(A) Whole cell lysates were probed for claudin-5 after incubation with pCPT-cAMP (pCPT, both 24 hours before and during infection with UV-influenza, MOI 8). Blots and quantitation are representative of 5 experiments. (B) Whole cell lysates were probed for claudin-5 after 24 hours of incubation with formoterol. GAPDH is the loading control. Quantitation of claudin-5 protein levels in whole cell lysates, normalized to control (mean and SE); blot is representative of 3 experiments, *p<0.05. (C–D) Formoterol attenuates the loss of claudin-5 induced by replication-deficient influenza. Lung endothelium was infected with replication-deficient influenza (UV-flu, MOI 8) with or without 0.1 µM formoterol. Cells were probed by Western blot for claudin-5 in C and by immunofluorescence in D. In D, note the paucity of claudin-5 at cell-cell junctions of infected cells compared to uninfected controls and the induction of the protein by formoterol. The quantitation in C (mean, SD) is normalized to control, and is representative of 3 experiments; *p<0.05. (E) Formoterol attenuates the endothelial permeability caused by replication-deficient influenza (UV-flu). Cells were infected with UV-flu (MOI 8) with or without 0.1 µM formoterol for 24 hours and permeability was assessed by TEER. Results (mean, SE) are normalized to uninfected cells and are from 5 experiments; *p<0.05.

Figure 9