title: CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.
abstract: The role of C-X-C motif chemokine 10 (CXCL10), a pro-inflammatory factor, in the development of acute respiratory distress syndrome (ARDS) remains unclear. In this study, we explored the role of CXCL10 and the effect of CXCL10 neutralization in lipopolysaccharide (LPS)-induced ARDS in rats. The expression of CXCL10 and its receptor chemokine receptor 3(CXCR3) increased after LPS induction. Moreover, neutralization of CXCL10 ameliorated the severity of ARDS by reducing pulmonary edema, inhibiting the release of inflammatory mediators (IFN-γ, IL-6 and ICAM-1) and limiting inflammatory cells (neutrophils, macrophages, CD8+ T cells) influx into the lung, with a reduction in CXCR3 expression in neutrophils and macrophages. Therefore, CXCL10 could be a potential therapeutic target in LPS-induced ARDS.
authors.affiliation: Department of Respiratory Diseases, Chinese PLA General Hospital, Beijing, China.
authors.forename: Shan
authors.initials: S
authors.lastname: Lang
authors.affiliation: Department of Cardiovascular Surgery, Chinese PLA General Hospital, Beijing, China.
authors.forename: Libing
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Surgical Oncology, Chinese PLA General Hospital, Beijing, China.
authors.forename: Xuning
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Respiratory Diseases, Chinese PLA General Hospital, Beijing, China.
authors.forename: Junping
authors.initials: J
authors.lastname: Sun
authors.affiliation: Department of Respiratory Diseases, Chinese PLA General Hospital, Beijing, China.
authors.forename: Xinying
authors.initials: X
authors.lastname: Xue
authors.affiliation: Department of Respiratory Diseases, Chinese PLA General Hospital, Beijing, China.
authors.forename: Yongjiu
authors.initials: Y
authors.lastname: Xiao
authors.affiliation: Department of Respiratory Diseases, Chinese PLA General Hospital, Beijing, China.
authors.forename: Mingyue
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Department of Respiratory Diseases, Chinese PLA General Hospital, Beijing, China.
authors.forename: Ting
authors.initials: T
authors.lastname: Ao
authors.affiliation: Department of Respiratory Diseases, Chinese PLA General Hospital, Beijing, China.
authors.forename: Jianxin
authors.initials: J
authors.lastname: Wang
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D001992:Bronchoalveolar Lavage Fluid; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D054357:Chemokine CXCL10 / Q000037:antagonists & inhibitors* / Q000737:chemistry*; D054371:Chemokine CXCL11 / Q000378:metabolism; D054370:Chemokine CXCL9 / Q000378:metabolism; D004195:Disease Models, Animal; D007249:Inflammation; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008024:Ligands; D008070:Lipopolysaccharides; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D054367:Receptors, CXCR3 / Q000378:metabolism; D012128:Respiratory Distress Syndrome / Q000139:chemically induced / Q000188:drug therapy*
chemical_list: C505723:CXCL9 protein, rat; D054357:Chemokine CXCL10; D054371:Chemokine CXCL11; D054370:Chemokine CXCL9; C091326:Cxcl10 protein, rat; C515205:Cxcl11 protein, rat; C515189:Cxcr3 protein, rat; C000609942:ICAM1 protein, rat; D015850:Interleukin-6; D008024:Ligands; D008070:Lipopolysaccharides; D054367:Receptors, CXCR3; D018799:Intercellular Adhesion Molecule-1; D007371:Interferon-gamma