title: Autotransplantation of circulating endothelial progenitor cells protects against lipopolysaccharide-induced acute lung injury in rabbit.
abstract: Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) are leading causes of morbidity and mortality in critically ill patients. Recent studies suggest that endothelial progenitor cells (EPCs) transplantation could become a novel cell-based therapeutic strategy for ALI/ARDS, but the exact therapeutic effect and possible mechanisms still need to be elucidated. In the present study, autologous circulating EPCs were obtained from rabbits using Ficoll centrifugation and cultured in vitro for 7 days. ALI was induced in rabbits by lipopolysaccharide (LPS), and EPCs were administered systemically. Fluorescence microscopy showed that CM-DiI labelled EPCs could migrate to the injured lung tissues. Reduced pulmonary edema level, inflammation, hemorrhage and hyaline membrane formation were present in rabbit treated with EPCs. EPCs autotransplantation significantly decreased the expression of adhesion molecules of sICAM-1 and P-selectin. Furthermore, EPCs administration mediated a down-regulation of proinflammatory responses (reducing IL-1β and TNF-α) while increasing the anti-inflammatory cytokine IL-10. Apoptosis of endothelial and epithelial cells was substantially reduced in EPCs-treated rabbit. Those findings suggest that autotransplantation of circulating EPCs can reduce the severity of LPS-induced ALI. Possible mechanisms include EPCs engraftment and reendothelization, down-regulation of adhesion molecules, alleviation of inflammatory response and apoptosis prevention.
authors.affiliation: Department of Respiratory Medicine, Chinese People's Liberation Army General Hospital, 28 Fuxing Road, Beijing 100853, PR China.
authors.forename: Xiaofang
authors.initials: X
authors.lastname: Gao
authors.forename: Weizhen
authors.initials: W
authors.lastname: Chen
authors.forename: Zhixin
authors.initials: Z
authors.lastname: Liang
authors.forename: Liangan
authors.initials: L
authors.lastname: Chen
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D017209:Apoptosis; D001773:Blood Cells / Q000166:cytology / Q000378:metabolism* / Q000637:transplantation; D002465:Cell Movement; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000008:administration & dosage; D045164:Mesenchymal Stem Cell Transplantation; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000378:metabolism*; D019007:P-Selectin / Q000235:genetics / Q000378:metabolism; D011014:Pneumonia; D011654:Pulmonary Edema; D011817:Rabbits; D014182:Transplantation, Autologous
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D019007:P-Selectin; D018799:Intercellular Adhesion Molecule-1