title: The role of aquaporin-1 (AQP1) expression in a murine model of lipopolysaccharide-induced acute lung injury.
abstract: A murine model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) was used to evaluate whether aquaporin-1 (AQP1) is involved in lung inflammation and lung edema formation. Swiss strain mice (n = 122) had LPS (5 mg/kg) instilled intratracheally (IT), and were then treated with either 0.9 % saline or dexamethasone (5 mg/kg/day). Mice were euthanized at 2 days and 7 days after treatment. Inflammatory cytokines (TNF-alpha, IL-6), protein concentration in bronchoalveolar lavage (BAL) fluid, lung wet-to-dry weight ratio, histology, immunohistochemistry, and AQP1 Western blot were performed. Lung wet-to-dry weight ratio and lung vascular permeability were also measured in the AQP1 knockout mice (n = 9) that received IT LPS (5 mg/kg) at 2 days. Intratracheal instillation of LPS produced a severe lung injury at 2 days, characterized by elevation of TNF-alpha, IL-6 in the BAL fluid, and by histological changes consistent with increased lung vascular permeability and neutrophil infiltration. AQP1-immunoreactivity in the pulmonary capillary endothelium was reduced at 2 days and 7 days. Administration of dexamethasone improved LPS-induced ALI and retained expression of AQP1. However, depletion of AQP1 did not affect lung edema formation, lung vascular permeability, or lung histology. The results suggest that although AQP1 expression is decreased after lung injury, depletion of AQP1 does not alter lung inflammation and lung edema induced by LPS.
authors.affiliation: Department of Pulmonary Medicine, Research Institute of Respiratory Diseases, Fudan University, Zhongshan Hospital, Shanghai 200032, PR China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Su
authors.forename: Yuanlin
authors.initials: Y
authors.lastname: Song
authors.forename: Jinjun
authors.initials: J
authors.lastname: Jiang
authors.forename: Chunxue
authors.initials: C
authors.lastname: Bai
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D051398:Aquaporin 1; D020346:Aquaporins / Q000235:genetics / Q000378:metabolism*; D015153:Blotting, Western / Q000379:methods; D018893:Bronchoalveolar Lavage / Q000379:methods; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000276:immunology; D002452:Cell Count / Q000379:methods; D016207:Cytokines / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology / Q000627:therapeutic use; D004195:Disease Models, Animal; D004347:Drug Interactions; D004487:Edema / Q000178:diet therapy / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology*; D006470:Hemorrhage / Q000188:drug therapy / Q000473:pathology; D007150:Immunohistochemistry / Q000379:methods; D008070:Lipopolysaccharides; D008168:Lung / Q000378:metabolism / Q000473:pathology; D051379:Mice; D009504:Neutrophils / Q000187:drug effects / Q000473:pathology; D009929:Organ Size; D011506:Proteins / Q000378:metabolism; D012128:Respiratory Distress Syndrome / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*; D013997:Time Factors
chemical_list: D000893:Anti-Inflammatory Agents; C496021:Aqp1 protein, mouse; D020346:Aquaporins; D016207:Cytokines; D008070:Lipopolysaccharides; D011506:Proteins; D051398:Aquaporin 1; D003907:Dexamethasone