Figure 6

Pharmacological inhibition of Integrin/Rac1 and acting polymerization partially blocked miR-155 and miR-23a induced K. pneumoniae adhesion.

K. pneumoniae adhesion was measured on A549 cells transfected with miRNA mimics and then treated with RGD (50 nM, 24 hours) or NSC23766 (NSC, 50 μM, 2 hours) (A) or cytochalasin (B) (CytoB, 10 μM, 2 hours) (C) prior to K. pneumoniae exposure (MOI = 100 for 2 hours). Untreated miR-NC was defined as 100% of relative adhesion. (B) Western blot analysis showing the expressions of F-actin in A549 cells treated with RGD or NSC23766 under the same condition as (A). (Data are the mean ± SD and represent three individual experiments. **p < 0.01). (D) The schematic diagram depicting miR-155 and miR23a pathway: miRNAs promote intergrin α5β1 and Rac1 activities by targeting negative transcriptional regulators of integrin -HMGN2 and NFI and result in actin polymerization (black solid lines). The exposure of K. pneumoniae causes the active reduction of these two miRNAs, which subsequently de-represses HMGN2 and NFI to inhibit integrin/Rac1 function and slows actin polymerization (green and red arrows).