[Activation of platelet activating factor receptor by Acinetobacter baumannii results in oxidative stress and apoptosis in human bronchial epithelial cells].

ABSTRACT

Objective To investigate the effect of platelet activating factor receptor (PAFR) on human bronchial epithelial (HBE) cells infected by Acinetobacter baumannii (A. baumannii). Methods HBE cells were divided into control group, ginkgolide B (GB) group, A. baumannii infected group, A. baumannii infection and inhibitor group. HBE cells were infected with low dose (1×103 CFU/mL), medium dose (1×105 CFU/mL) and high dose (1×107 CFU/mL) A. baumannii separated from clinical samples. The PAFR activity was blocked by the 10 µmol/L GB. The expression of PAFR was detected using Western blotting in HBE cells. The proliferation ability of HBE cells was detected using CCK-8 assay. The oxidative stress level was evaluated by superoxide dismutase (SOD) and malondialdehyde(MDA) kits. Apoptosis of HBE cells was observed by annexin V-FITC-V/PI staining. The phosphorylation level of PAFR and its downstream molecule JAK1/STAT1 in HBE cells were examined by Western blot analysis. Results Compared with the control group, the expression of PAFR increased significantly in A. baumannii infected group. A. baumannii infection could decrease cell vitality, but increase intracellular oxidative stress, apoptosis, and JAK1/STAT1 phosphorylation. Conclusion PAFR is an important mediator molecule for A. baumannii infection in HBE cells, and PAFR/JAK1/STAT1 signaling pathway plays an important role in the pulmonary infection of A. baumannii.