Ventilator-induced lung injury (VILI) is one of the most common complications of mechanical ventilation (MV), which strongly impacts the outcome of ventilated patients. Current evidences indicated that inflammation is a major contributor to the pathogenesis of VILI. Our results showed that MV induced excessive proinflammatory cytokine productions together with decreased CXCL14 and increased PKM2 expressions in injured lungs. In addition, CXCL14 overexpression downregulated PKM2 expression and attenuated VILI with reduced inflammation. Moreover, the overexpression of PKM2 markedly diminished the protective effects of CXCL14 against VILI as reflected by worsened morphology and increased cytokine production, whereas PKM2 knockdown decreased cytokine production and attenuated VILI. Collectively, these results suggested that CXCL14 overexpression attenuates VILI through the downregulation of PKM2-mediated proinflammatory cytokine production.

中文翻译：

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CXCL14的过表达通过下调PKM2介导的细胞因子生产来缓解呼吸机诱发的肺损伤。

呼吸机诱发的肺损伤（VILI）是机械通气（MV）的最常见并发症之一，它会严重影响通气患者的预后。当前证据表明炎症是VILI发病机理的主要诱因。我们的研究结果表明，MV诱导过量的促炎性细胞因子产生，同时在受伤的肺中降低了CXCL14并增加了PKM2表达。此外，CXCL14的过表达下调了PKM2的表达并减弱了VILI，从而减轻了炎症。此外，PKM2的过表达显着减弱了CXCL14对VILI的保护作用，这由形态恶化和细胞因子生成增加所反映，而PKM2的基因敲低则降低了细胞因子生成并减弱了VILI。总的来说，