Zhu Rui, Lei Yan-Qing, Zhao Dong-Chi
Department of Pediatrics, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, Hubei 430071, China.
Department of Emergency, Xiangyang No.1 People's Hospital, Hubei University of Medicine, 15 Jiefang Road, Xiangyang, Hubei 441000, China.
Mediators Inflamm. 2020 Jul 23;2020:7650978. doi: 10.1155/2020/7650978. eCollection 2020.
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.
呼吸机诱导的肺损伤（VILI）是机械通气（MV）最常见的并发症之一，对接受通气治疗的患者的预后有重大影响。目前的证据表明，炎症是VILI发病机制的主要促成因素。我们的结果显示，MV诱导损伤肺组织中促炎细胞因子过度产生，同时CXCL14减少而PKM2表达增加。此外，CXCL14过表达下调PKM2表达，并减轻炎症，从而减轻VILI。而且，PKM2过表达显著削弱了CXCL14对VILI的保护作用，表现为形态学恶化和细胞因子产生增加，而敲低PKM2则减少细胞因子产生并减轻VILI。总体而言，这些结果表明，CXCL14过表达通过下调PKM2介导的促炎细胞因子产生来减轻VILI。
