CXCR3可能通过由CD8 + CD122 +调节性T细胞分泌的IL-10所调控的途径来帮助调节急性肺损伤中的炎症反应。
CXCR3 May Help Regulate the Inflammatory Response in Acute Lung Injury via a Pathway Modulated by IL-10 Secreted by CD8 + CD122+ Regulatory T Cells.
作者信息
Nie Li, Wu Wei, Lu Zhibing, Zhu Gangyan, Liu Juan
机构信息
Department of Geriatrics, Renmin Hospital of Wuhan University, 238, Jiefang Road, Wucang, Wuhan, 430060, China.
Clinical Laboratory Department, Renmin Hospital of Wuhan University, Wuhan, China.
出版信息
Inflammation. 2016 Apr;39(2):526-33. doi: 10.1007/s10753-015-0276-0.
The aim of this study is to investigate the role of CXCR3 and IL-10 in lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced by LPS injection (10 mg/kg) via the tail vein in C57BL/6 mice. Mice were sacrificed after 2 or 12 h to examine the levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and histopathologic assessments. At 12 h after LPS injection, mice exhibited more severe lung infiltration by CD8+ T cell and less infiltration by CD8+CD122+ regulatory T cells than at 2 h after LPS challenge or in the control (mice not exposed to LPS). At 12 h, IFN-γ, CXCR3, and CXCL10 were significantly higher in the lungs. IL-10 in the lungs was significantly lower. CXCR3 may help to recruit CD8+ T cells and promotes IFN-γ and CXCL10 release. Such effects could be inhibited by IL-10 secreted by CD8+CD122+ regulatory T cells.
本研究旨在探讨CXCR3和白细胞介素-10（IL-10）在脂多糖（LPS）诱导的急性肺损伤（ALI）中的作用。通过尾静脉注射LPS（10mg/kg）诱导C57BL/6小鼠发生ALI。在2小时或12小时后处死小鼠，以检测支气管肺泡灌洗液（BALF）中炎性细胞因子水平并进行组织病理学评估。LPS注射后12小时，与LPS攻击后2小时或对照组（未接触LPS的小鼠）相比，小鼠肺组织中CD8 + T细胞浸润更严重，而CD8 + CD122 +调节性T细胞浸润较少。在12小时时，肺组织中干扰素-γ（IFN-γ）、CXCR3和CXC趋化因子配体10（CXCL10）显著升高。肺组织中的IL-10显著降低。CXCR3可能有助于募集CD8 + T细胞，并促进IFN-γ和CXCL10释放。此类效应可被CD8 + CD122 +调节性T细胞分泌的IL-10抑制。
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