Hong-fu Gao1, Jian-cheng Yuan, Guang-xia Xiao. 1. State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Burn Research, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Abstract
OBJECTIVE: To investigate the protective effects of bactericidal/permeability increasing protein simulated peptide (bactericidal neutralizing endotoxin protein, BNEP) on murine acute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: A murine model of ALI was reproduced by lipopolysaccharide via intranasal instillation. The Balb/c mice were randomly divided into control (n = 20, with nasal instillation of isotonic saline), LPS instillation (n = 20, with nasal instillation of isotonic saline and LPS) and BNEP treatment (n = 20, with nasal instillation of isotonic saline plus LPS and BNEP) groups. The ratio of lung wet weight to dry weight, the permeability of pulmonary capillary vessels and the histopathology of pulmonary tissue were determined in all groups. The change in the expression of Toll-like receptor 2 and 4 (TLR2/4) in the pulmonary tissue was detected by immunohistochemistry. RESULTS: Compared with LPS instillation group, the ratio of lung wet weight to dry weight and the permeability of pulmonary capillary vessel was decreased significantly in the BNEP group, and the inflammatory infiltration in the pulmonary tissue induced by neutrophil influx was alleviated markedly with BNEP treatment. The expression of TLR2 and TLR4 in pulmonary vascular endothelial cells, macrophages and alveolar type II epithelial cells in BNEP group were lower than those in LPS group (TLR2: 128 +/- 10 vs 214 +/- 12, P < 0.01). CONCLUSION: BNEP, as a simulated peptide of BPI, exerted a remarkable protective effect on ALI induced by LPS.
OBJECTIVE: To investigate the protective effects of bactericidal/permeability increasing protein simulated peptide (bactericidal neutralizing endotoxin protein, BNEP) on murineacute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: A murine model of ALI was reproduced by lipopolysaccharide via intranasal instillation. The Balb/c mice were randomly divided into control (n = 20, with nasal instillation of isotonic saline), LPS instillation (n = 20, with nasal instillation of isotonic saline and LPS) and BNEP treatment (n = 20, with nasal instillation of isotonic saline plus LPS and BNEP) groups. The ratio of lung wet weight to dry weight, the permeability of pulmonary capillary vessels and the histopathology of pulmonary tissue were determined in all groups. The change in the expression of Toll-like receptor 2 and 4 (TLR2/4) in the pulmonary tissue was detected by immunohistochemistry. RESULTS: Compared with LPS instillation group, the ratio of lung wet weight to dry weight and the permeability of pulmonary capillary vessel was decreased significantly in the BNEP group, and the inflammatory infiltration in the pulmonary tissue induced by neutrophil influx was alleviated markedly with BNEP treatment. The expression of TLR2 and TLR4 in pulmonary vascular endothelial cells, macrophages and alveolar type II epithelial cells in BNEP group were lower than those in LPS group (TLR2: 128 +/- 10 vs 214 +/- 12, P < 0.01). CONCLUSION:BNEP, as a simulated peptide of BPI, exerted a remarkable protective effect on ALI induced by LPS.
Authors: Kirsten Neudoerffer Kangelaris; Arun Prakash; Kathleen D Liu; Bradley Aouizerat; Prescott G Woodruff; David J Erle; Angela Rogers; Eric J Seeley; Jeffrey Chu; Tom Liu; Thomas Osterberg-Deiss; Hanjing Zhuo; Michael A Matthay; Carolyn S Calfee Journal: Am J Physiol Lung Cell Mol Physiol Date: 2015-03-20 Impact factor: 5.464