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首页> 外文期刊>Mediators of inflammation >CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine Production
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CXCL14 Overexpression Attenuates Sepsis-Associated Acute Kidney Injury by Inhibiting Proinflammatory Cytokine Production

机译:CXCL14过表达通过抑制促血液炎症细胞因子生产衰减败血症相关的急性肾损伤

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CXCL14 is a relatively novel chemokine with a wide spectrum of biological activities. The present study was designed to investigate whether CXCL14 overexpression attenuates sepsis-associated acute kidney injury (AKI) in mice. Sepsis model has been established by cecal ligation and puncture (CLP). CLP induced AKI in mice as assessed by increased renal neutrophil gelatinase-associated lipocalin (NGAL) expression and serum creatinine levels. We found that renal CXCL14 expression in the kidney was significantly decreased at 12 hours after CLP. Correlation analysis demonstrated a negative association between renal CXCL14 expression and AKI markers including serum creatinine and renal NGAL. Moreover, CXCL14 overexpression reduced cytokine (TNF-α, IL-6, and IL-1β) production and NGAL expression in the kidney and decreased serum creatinine levels. In vivo and in vitro experiments found that CXCL14 overexpression inhibited M1 macrophage polarization but increased M2 polarization. Together, these results suggest that CXCL14 overexpression attenuates sepsis-associated AKI probably through the downregulation of macrophages-derived cytokine production. However, further studies are required to elucidate the underlying mechanism.
机译:CXCL14是一种相对新的趋化因子,具有广泛的生物活性。设计本研究旨在研究CXCL14过表达是否衰减小鼠中的脓毒症相关的急性肾损伤(AKI)。通过CECAL连接和穿刺(CLP)建立了SEPSIS模型。 CLP诱导小鼠中的Aki,如肾中性粒细胞凝胶酶相关的脂素(NGAL)表达和血清肌酐水平评估。我们发现CLP后12小时内肾脏中肾CXCL14的表达显着降低。相关性分析证明了肾CXCL14表达与炎症标记物之间的阴性关联,包括血清肌酐和肾NGAL。此外,CXCL14过表达减少细胞因子(TNF-α,IL-6和IL-1β)的产生和NGAL表达在肾脏中并降低血清肌酐水平。体内和体外实验发现CXCL14过表达抑制M1巨噬细胞偏振,但是增加了M2极化。这些结果表明,CXCL14过表达可能通过巨噬细胞衍生的细胞因子产生的下调衰减败血症相关的AKI。然而,需要进一步的研究来阐明潜在机制。

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