Effect of Phospholipid Transfer Protein on Cigarette Smoke Extract-Induced IL-8 Production in Human Pulmonary Epithelial Cells.
To investigate the effect of phospholipid transfer protein (PLTP) on the cigarette smoke extract (CSE)-induced production of interleukin-8 (IL-8) in human pulmonary epithelial cells, male Wistar rats were exposed to air and cigarette smoke (n = 10/exposure) for 6 h/day on three consecutive days. Their lungs were sectioned and bronchoalveolar lavage fluid (BALF) examined. The expression of PLTP and IL-8 in the lung was detected immunohistochemically. Lung injury was accompanied by the upregulation of PLTP and IL-8 in the CSE-exposed rat model, and the number of white blood cells in the BALF was significantly increased compared with those of the controls. Both neutrophils and macrophages were clearly increased. Human alveolar epithelial cells (A549) and human bronchial epithelial cells (HBECs) were treated with different concentrations of CSE for various times. The cells were also transfected with small interfering RNA directed against PLTP, and U0126, an inhibitor of the ERK1/2 pathway, was administered before CSE exposure. The expression of PLTP and IL-8 mRNAs and PLTP, IL-8, total ERK, and phosphorylated ERK proteins was analyzed. The expression of IL-8 and phosphorylated ERK was significantly increased in A549 cells and HBECs after CSE stimulation, and CSE upregulated the expression of PLTP in A549 cells. In contrast, CSE inhibited the expression of PLTP in HBECs. The CSE-induced expression of IL-8 and p-ERK was significantly increased by the knockdown of PLTP. Therefore, PLTP may regulate CSE-induced IL-8 expression via the ERK1/2 signaling pathway in human pulmonary epithelial cells.
Respiratory Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Youlun
Y
Li
Respiratory Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.|Respiratory Department, Yubei District People's Hospital, Chongqing, 400016, China.
Xiuying
X
Yu
Respiratory Department, Yubei District People's Hospital, Chongqing, 400016, China.
Xiaofeng
X
Fu
Respiratory Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Fengping
F
Wu
Respiratory Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Linlin
L
Zou
Respiratory Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yuhan
Y
Chen
Respiratory Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. yajuanchencqmu@sina.com.
Yajuan
Y
Chen
D000072283:A549 Cells; D000818:Animals; D001980:Bronchi / Q000473:pathology; D004847:Epithelial Cells / Q000378:metabolism*; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis*; D020935:MAP Kinase Signaling System; D008297:Male; D049294:Phospholipid Transfer Proteins / Q000502:physiology*; D010766:Phosphorylation; D051381:Rats; D017208:Rats, Wistar; D012906:Smoke
C508606:CXCL8 protein, human; D016209:Interleukin-8; D049294:Phospholipid Transfer Proteins; D012906:Smoke
A549 cells; HBECs; cigarette smoke extract; p-ERK; phospholipid transfer protein