Exposure to airborne organic dust (OD), rich in microbial pathogen-associated molecular patterns (PAMPs), is shown to induce lung inflammation. A common manifestation in lung inflammation is altered mitochondrial structure and bioenergetics that regulate mitochondrial ROS (mROS) and feed a vicious cycle of mitochondrial dysfunction. The role of mitochondrial dysfunction in other airway diseases is well known. However, whether OD exposure induces mitochondrial dysfunction remains elusive. Therefore, we tested a hypothesis that organic dust extract (ODE) exposure induces mitochondrial stress using a human monocytic cell line (THP1). We examined whether co-exposure to ethyl pyruvate (EP) or mitoapocynin (MA) could rescue ODE exposure induced mitochondrial changes. Transmission electron micrographs showed significant differences in cellular and organelle morphology upon ODE exposure. ODE exposure with and without EP co-treatment increased the mtDNA leakage into the cytosol. Next, ODE exposure increased PINK1, Parkin, cytoplasmic cytochrome c levels, and reduced mitochondrial mass and cell viability, indicating mitophagy. MA treatment was partially protective by decreasing Parkin expression, mtDNA and cytochrome c release and increasing cell viability.

暴露于富含微生物病原体相关分子模式 (PAMP) 的空气中的有机粉尘 (OD) 会诱发肺部炎症。肺部炎症的一个常见表现是改变线粒体结构和调节线粒体活性氧 (mROS) 并导致线粒体功能障碍的恶性循环的生物能量学。线粒体功能障碍在其他气道疾病中的作用是众所周知的。然而，OD 暴露是否会导致线粒体功能障碍仍然难以捉摸。因此，我们测试了一个假设，即有机粉尘提取物 (ODE) 暴露会使用人类单核细胞系 (THP1) 诱导线粒体应激。我们检查了共同暴露于丙酮酸乙酯 (EP) 或线粒体夹竹桃麻素 (MA) 是否可以挽救 ODE 暴露引起的线粒体变化。透射电子显微照片显示 ODE 暴露后细胞和细胞器形态存在显着差异。有和没有 EP 共处理的 ODE 暴露增加了 mtDNA 泄漏到细胞质中。接下来，ODE 暴露增加了 PINK1、Parkin、细胞质细胞色素 c 水平，并降低了线粒体质量和细胞活力，表明线粒体自噬。MA 治疗通过降低 Parkin 表达、mtDNA 和细胞色素 c 释放和增加细胞活力来部分保护。