Figure 5.

MiR‐148 down‐regulated the expression of ATG16L1 and genes related to VAP. A, MiR‐148 was overexpressed in primary PBMCs genotyped as GG transfected with miR‐148 mimics and inhibited in primary PBMCs genotyped as GG transfected with miR‐148 inhibitors (*P value < 0.05 compared with NC). B, ATG16L1 mRNA was inhibited in primary PBMCs genotyped as GG transfected with miR‐148 mimics and up‐regulated by miR‐148 inhibitors (*P value < 0.05 compared with NC). C, ATG16L1, Beclin‐I and LC3‐II proteins were down‐regulated in primary PBMCs genotyped as GG transfected with miR‐148 mimics and were up‐regulated by miR‐148 inhibitors. D, MiR‐148 mimics inhibited the luciferase activity of ATG16L1 3′ UTR, while miR‐148 inhibitors increased the luciferase activity of ATG16L1 3′ UTR in primary PBMCs genotyped as GG (*P value < 0.05 compared with miR‐control; **P value < 0.05 compared with anti‐miR‐control). E, MiR‐148 was overexpressed in primary PBMCs genotyped as AA transfected with miR‐148 mimics and inhibited by miR‐148 inhibitors (*P value < 0.05 compared with NC). F, ATG16L1 mRNA was inhibited in primary PBMCs genotyped as AA transfected with miR‐148 mimics and up‐regulated by miR‐148 inhibitors (*P value < 0.05 compared with NC). G, ATG16L1, Beclin‐I and LC3‐II proteins were down‐regulated in primary PBMCs genotyped as AA transfected with miR‐148 mimics and were up‐regulated by miR‐148 inhibitors. H, MiR‐148 mimics inhibited the luciferase activity of ATG16L1 3′ UTR, while miR‐148 inhibitors increased the luciferase activity of ATG16L1 3′ UTR in primary PBMCs genotyped as AA (*P value < 0.05 compared with miR‐control; **P value < 0.05 compared with anti‐miR‐control). PBMCs, peripheral blood mononuclear cells; VAP, ventilator‐associated pneumonia