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首页> 外文期刊>Scientific reports. >Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway
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Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway

机译：可溶性木材烟雾提取物通过MAPK信号通路促进肺泡上皮细胞中的屏障功能障碍

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Wildfire smoke induces acute pulmonary distress and is of particular concern to risk groups such as the sick and elderly. Wood smoke (WS) contains many of the same toxic compounds as those found in cigarette smoke (CS) including polycyclic aromatic hydrocarbons, carbon monoxide, and free radicals. CS is a well-established risk factor for respiratory diseases such as asthma and COPD. Limited studies investigating the biological effects of WS on the airway epithelium have been performed. Using a cell culture-based model, we assessed the effects of a WS-infused solution on alveolar epithelial barrier function, cell migration, and survival. The average geometric mean of particles in the WS was 178?nm. GC/MS analysis of the WS solution identified phenolic and cellulosic compounds. WS exposure resulted in a significant reduction in barrier function, which peaked after 24?hours of continuous exposure. The junctional protein E-cadherin showed a prominent reduction in response to increasing concentrations of WS. Furthermore, WS significantly repressed cell migration following injury to the cell monolayer. There was no difference in cell viability following WS exposure. Mechanistically, WS exposure induced activation of the p44/42, but not p38, MAPK signaling pathway, and inhibition of p44/42 phosphorylation prevented the disruption of barrier function and loss of E-cadherin staining. Thus, WS may contribute to the breakdown of alveolar structure and function through a p44/42 MAPK-dependent pathway and may lead to the development and/or exacerbation of respiratory pathologies with chronic exposure.
机译：野火烟雾诱导急性肺部痛苦，特别关注病患和病人等危险团体。木烟（WS）含有许多相同的毒性化合物，如香烟烟雾（CS）中发现的那些，包括多环芳烃，一氧化碳和自由基。 CS是一种良好的呼吸疾病危险因素，如哮喘和COPD。研究了研究WS对气道上皮的生物学效应的有限研究。使用基于细胞培养基的模型，我们评估了WS-Infused溶液对肺泡上皮阻挡功能，细胞迁移和存活的影响。 WS中颗粒的平均几何平均值为178μm。 GC / MS分析WS溶液鉴定酚类和纤维素化合物。 WS暴露导致屏障功能显着降低，其在24℃连续暴露后达到峰值。结蛋白E-钙粘蛋白表现出响应浓度的WS浓度的突出减少。此外，在细胞单层损伤后，WS显着压抑细胞迁移。 WS暴露后细胞活力没有差异。机械地，WS曝光诱导P44 / 42的激活，但不是P38，MAPK信号通路和P44 / 42磷酸化的抑制阻止了阻隔功能的破坏和E-Cadherin染色的丧失。因此，WS可以通过P44 / 42 MAPK依赖性途径有助于肺泡结构和功能的崩溃，并且可能导致慢性暴露的呼吸道病理的显影和/或加剧。

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