Prohibitin and the extracellular matrix are upregulated in murine alveolar epithelial cells with LPS-induced acute injury

Inflammation of epithelial and endothelial cells accelerates the progress of acute lung injury (ALI), and pulmonary fibrosis is the leading cause of mortality in patients with acute respiratory distress syndrome. Interleukin-6 (IL-6) is a pleiotropic cytokine implicated in the pathogenesis of a number of immune-mediated disorders, and is involved in pulmonary fibrosis. Prohibitin (PHB) is a highly conserved protein implicated in various cellular functions, including proliferation, apoptosis, tumor suppression, transcription and mitochondrial protein folding. PHB was identified to be associated with a variety of pulmonary diseases, including pulmonary fibrosis. Based on the lipopolysaccharide (LPS)-induced cell model of ALI, the present study examined the expression of PHB and the extracellular matrix (ECM) in the process of pulmonary inflammation. MLE-12 cells were divided into 2 groups: The control group was administered sterile PBS; the treatment group was administered 500 ng/ml LPS for 12 h. The mRNA expression of IL-6 in the treatment group was significantly upregulated compared with the control group (P<0.05). The protein expression of IL-6 in the treatment group was markedly increased compared with the control group (P<0.05). ECM components, including collagen-IV and fibronectin, in the treatment group were markedly increased when compared with the control group (P<0.05). The mRNA and protein expression levels of PHB1 and PHB2 were significantly upregulated following treatment with LPS (both P<0.05). The present study identified that PHB and ECM component levels increased in the LPS-induced ALI cell model, and further investigations may be performed to verify the detailed mechanism.