Fig. 3.  Specific transforming growth factor-β1 (TGF-β1) inhibition attenuates Pseudomonas aeruginosa -induced increase in protein paracellular permeability across rat alveolar epithelial type II cell monolayers. (A ) Primary cultures of rat alveolar epithelial type II cell monolayers were treated with P. aeruginosa  or its vehicle for 3 h. Some cell monolayers were pretreated with a soluble chimeric TGF-β type II receptor (TGFβ-scRII, 10 ng/ml) or its vehicle before exposure to P. aeruginosa  or its vehicle. All experiments were performed at least in triplicate and repeated three times. Results are shown as mean ± SD; *P ≤ 0.05 from controls; **P ≤ 0.05 from cell monolayers treated with P. aeruginosa  and TGFβ-scRII vehicle. (B ) Primary cultures of rat alveolar epithelial type II cell monolayers were treated with P. aeruginosa  or its vehicle for 3 h with a specific RhoA inhibitor (CGX0287, 10 μg/ml) or its vehicle. All experiments were performed at least in triplicate and repeated three times. Data are shown as percent of controls; results are shown as mean ± SD; *P ≤ 0.05 from controls; **P ≤ 0.05 from cell monolayers treated with P. aeruginosa  and CGX0287 vehicle. PAK =Pseudomonas aeruginosa  strain K.

Fig. 3.  Specific transforming growth factor-β1 (TGF-β1) inhibition attenuates Pseudomonas aeruginosa -induced increase in protein paracellular permeability across rat alveolar epithelial type II cell monolayers. (A ) Primary cultures of rat alveolar epithelial type II cell monolayers were treated with P. aeruginosa  or its vehicle for 3 h. Some cell monolayers were pretreated with a soluble chimeric TGF-β type II receptor (TGFβ-scRII, 10 ng/ml) or its vehicle before exposure to P. aeruginosa  or its vehicle. All experiments were performed at least in triplicate and repeated three times. Results are shown as mean ± SD; *P ≤ 0.05 from controls; **P ≤ 0.05 from cell monolayers treated with P. aeruginosa  and TGFβ-scRII vehicle. (B ) Primary cultures of rat alveolar epithelial type II cell monolayers were treated with P. aeruginosa  or its vehicle for 3 h with a specific RhoA inhibitor (CGX0287, 10 μg/ml) or its vehicle. All experiments were performed at least in triplicate and repeated three times. Data are shown as percent of controls; results are shown as mean ± SD; *P ≤ 0.05 from controls; **P ≤ 0.05 from cell monolayers treated with P. aeruginosa  and CGX0287 vehicle. PAK =Pseudomonas aeruginosa  strain K.

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