Inflammatory cell infiltration is a characteristic feature of COPD and correlates directly with the severity of the disease. Interleukin‐23 (IL‐23) is a pro‐inflammatory cytokine that regulates Th‐17 inflammation, which mediates many pathophysiological events in COPD. The primary goal of this study was to determine the role of IL‐23 as a mediator of key pathologic processes in cigarette smoke‐induced COPD. In this study, we report an increase in IL23 gene expression in the lung biopsies of COPD patients compared to controls and identified a positive correlation between IL23 gene expression and disease severity. In a cigarette smoke‐induced murine emphysema model, the suppression of IL‐23 with a monoclonal blocking antibody reduced the severity of cigarette smoke‐induced murine emphysema. Mechanistically, the suppression of IL‐23 was associated with a reduction in immune cell infiltration, oxidative stress injury, and apoptosis, suggesting a role for IL‐23 as an essential immune mediator of the inflammatory processes in the pathogenesis of CS‐induced emphysema.

中文翻译：

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阻断 IL-23 信号转导可减轻香烟烟雾诱导的小鼠肺气肿


炎性细胞浸润是 COPD 的一个特征，与疾病的严重程度直接相关。白细胞介素-23 （IL-23） 是一种促炎细胞因子，可调节 Th-17 炎症，介导 COPD 中的许多病理生理事件。本研究的主要目标是确定 IL-23 在香烟烟雾诱导的 COPD 中作为关键病理过程介质的作用。在这项研究中，我们报告了与对照组相比，COPD 患者肺活检中 IL23 基因表达的增加，并确定了 IL23 基因表达与疾病严重程度之间的正相关。在香烟烟雾诱导的小鼠肺气肿模型中，用单克隆阻断抗体抑制 IL-23 降低了香烟烟雾诱导的小鼠肺气肿的严重程度。从机制上讲，IL-23 的抑制与免疫细胞浸润、氧化应激损伤和细胞凋亡的减少有关，这表明 IL-23 在 CS 诱导的肺气肿发病机制中作为炎症过程的重要免疫介质发挥作用。