The proliferation of fetal alveolar type II cells (FATIICs) was impaired in bronchopulmonary dysplasia (BPD), which is modulated by hyperoxia and inflammatory response. Interleukin 24 (IL-24), a cytokine produced by certain cell types, plays an essential role in inflammation and host protection against infection. However, the ability of FATIICs to produce IL-24 remains unclear, and the role of IL-24 in BPD progression is yet to be determined. With reverse transcription quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay, the authors evaluated whether FATIICs produce IL-24 in physiological conditions. The authors quantified IL-24 expression in the lungs of newborn rat pups exposed to hyperoxia (70% oxygen) and in FATIICs isolated on embryonic day 19 that were exposed to 95% oxygen or lipopolysaccharide (LPS). The role of IL-24 in FATIICs, cell proliferation, cell apoptosis, and cell cycle were further evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometric analysis. Also, they assessed caspase-3 and SOCS3 mRNA in IL-24 siRNA-treated cells by using RT-qPCR. During culture, IL-24 mRNA and protein levels in FATIICs gradually decreased with FATIIC differentiation. IL-24 expression increased significantly in rat lungs exposed to hyperoxia and FATIICs exposed to oxygen or LPS. Recombinant IL-24 enhanced cell proliferation by decreasing the proportion of apoptotic cells and increasing the proportion of cells in the S phase. The IL-24 siRNA-treated cells expressed more caspase-3 mRNA. Furthermore, suppressor of cytokine signaling 3 (SOCS3) mRNA was significantly decreased in rats and FATIICs exposed to oxygen, whereas it dramatically increased in FATIICs exposed to LPS. The IL-24 siRNA-treated cells expressed more SOCS3 mRNA. These studies suggest IL-24 is a pulmonary target cytokine in BPD, and may possibly regulate SOCS3 in oxidative stress and inflammation of the lung.

胎儿肺泡 II 型细胞 (FATIICs) 的增殖在支气管肺发育不良 (BPD) 中受损，其受高氧和炎症反应的调节。白细胞介素 24 (IL-24) 是一种由某些细胞类型产生的细胞因子，在炎症和宿主抵抗感染方面发挥着重要作用。然而，FATIICs 产生 IL-24 的能力仍不清楚，IL-24 在 BPD 进展中的作用尚待确定。通过逆转录定量聚合酶链反应 (RT-qPCR) 和酶联免疫吸附试验，作者评估了 FATIICs 是否在生理条件下产生 IL-24。作者量化了暴露于高氧（70% 氧气）的新生幼鼠肺中和暴露于 95% 氧气或脂多糖 (LPS) 的胚胎第 19 天分离的 FATIIC 中 IL-24 的表达。IL-24 在 FATIIC、细胞增殖、细胞凋亡和细胞周期中的作用通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物和流式细胞术分析进一步评估。此外，他们使用 RT-qPCR 评估了 IL-24 siRNA 处理的细胞中的 caspase-3 和 SOCS3 mRNA。在培养过程中，FATIICs 中 IL-24 mRNA 和蛋白质水平随着 FATIIC 分化而逐渐降低。IL-24 表达在暴露于高氧的大鼠肺和暴露于氧气或 LPS 的 FATIICs 中显着增加。重组IL-24通过降低凋亡细胞比例和增加S期细胞比例来增强细胞增殖。IL-24 siRNA 处理的细胞表达更多的 caspase-3 mRNA。此外，暴露于氧气的大鼠和 FATIICs 中细胞因子信号传导 3 (SOCS3) mRNA 的抑制因子显着降低，而在暴露于 LPS 的 FATIICs 中它急剧增加。IL-24 siRNA处理的细胞表达更多的SOCS3 mRNA。这些研究表明 IL-24 是 BPD 中的肺靶细胞因子，并且可能在氧化应激和肺部炎症中调节 SOCS3。