CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.

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 expr...

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Main Authors: Shan Lang, Libing Li, Xuning Wang, Junping Sun, Xinying Xue, Yongjiu Xiao, Mingyue Zhang, Ting Ao, Jianxin Wang
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC5207674?pdf=render
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author Shan Lang
Libing Li
Xuning Wang
Junping Sun
Xinying Xue
Yongjiu Xiao
Mingyue Zhang
Ting Ao
Jianxin Wang
author_facet Shan Lang
Libing Li
Xuning Wang
Junping Sun
Xinying Xue
Yongjiu Xiao
Mingyue Zhang
Ting Ao
Jianxin Wang
author_sort Shan Lang
collection DOAJ
description 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.
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spelling doaj.art-8d5e1a59fec64dfdb741f8875899dddf2022-12-22T02:32:33ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01121e016910010.1371/journal.pone.0169100CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.Shan LangLibing LiXuning WangJunping SunXinying XueYongjiu XiaoMingyue ZhangTing AoJianxin WangThe 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.http://europepmc.org/articles/PMC5207674?pdf=render
spellingShingle Shan Lang
Libing Li
Xuning Wang
Junping Sun
Xinying Xue
Yongjiu Xiao
Mingyue Zhang
Ting Ao
Jianxin Wang
CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.
PLoS ONE
title CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.
title_full CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.
title_fullStr CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.
title_full_unstemmed CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.
title_short CXCL10/IP-10 Neutralization Can Ameliorate Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome in Rats.
title_sort cxcl10 ip 10 neutralization can ameliorate lipopolysaccharide induced acute respiratory distress syndrome in rats
url http://europepmc.org/articles/PMC5207674?pdf=render
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