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

被引：66

作者：

Lang, Shan ^{[1
]}

Li, Libing ^{[2
]}

Wang, Xuning ^{[3
]}

Sun, Junping ^{[1
]}

Xue, Xinying ^{[1
]}

Xiao, Yongjiu ^{[1
]}

Zhang, Mingyue ^{[1
]}

Ao, Ting ^{[1
]}

Wang, Jianxin ^{[1
]}

机构：

[1] Chinese Peoples Liberat Army Gen Hosp, Dept Resp Dis, Beijing, Peoples R China

[2] Chinese Peoples Liberat Army Gen Hosp, Dept Cardiovasc Surg, Beijing, Peoples R China

[3] Chinese Peoples Liberat Army Gen Hosp, Dept Surg Oncol, Beijing, Peoples R China

来源：

PLOS ONE | 2017年 / 12卷 / 01期

关键词：

ACUTE LUNG INJURY; NF-KAPPA-B; TNF-ALPHA; INFLAMMATION; CYTOKINE; BIOMARKERS; PATHOPHYSIOLOGY; PATHOGENESIS; ACTIVATION; EXPRESSION;

D O I：

10.1371/journal.pone.0169100

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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-gamma, IL-6 and ICAM-1) and limiting inflammatory cells (neutro-phils, 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.

引用

页数：16

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