The role of perilipin 2 in Pseudomonas aeruginosa pulmonary infection

The aim of this study was to investigate the role and mechanism of perilipin 2 (PLIN2) in Pseudomonas aeruginosa pulmonary infection in vivo and in vitro. Twenty-eight-week-old male Balb/c mice were randomly divided into the control and PAO1 (P. aeruginosa standard strain) groups, which were administered phosphate-buffered saline (PBS) or PAO1 intratracheal instillation, respectively. RAW264.7 cells and BEAS-2B cells were stimulated with PBS or PAO1. The mRNA levels of PLIN2 and cytosolic phospholipase A2 (cPLA2) were detected by PCR. The protein expression of PLIN2 was detected by WB. BEAS-2B cells were transfected with shRNA against PLIN2, and cell proliferation was measured by CCK8. After 72 h, the expression of the PLIN2 gene in the PAO1 group was significantly higher than that in the control group. Compared with those in the control group, the protein levels of PLIN2, cyclooxygenase-2 (COX-2), and nuclear transcription factor-kappa B (NF-kappa B) in the PAO1 group were upregulated, while the expression of PLIN5 protein was downregulated. Furthermore, lung injury in the PAO1 group was more severe than that in the control group, and the lipid droplet (LD) level in lung tissue of PAO1 mice increased. After stimulation with P. aeruginosa, PLIN2 and cPLA2 genes in RAW264.7 and BEAS-2B cells were upregulated. CCK8 assay showed that proliferation decreased significantly in cells transfected with shRNA against PLIN2. In mice infected with P. aeruginosa, LDs accumulated in the lung tissue through an increase in PLIN2, which may result in increased COX-2-mediated anti-inflammatory cytokine release. This study provides a new understanding of the mechanism of lung infection and a new target for the treatment of clinical pulmonary injury.