长期接触二次有机气溶胶会导致肺组织损伤,Environmental Science & Technology

当前位置： X-MOL 学术 › Environ. Sci. Technol. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

长期接触二次有机气溶胶会导致肺组织损伤
Environmental Science & Technology ( IF 10.8 ) Pub Date : 2023-04-04 , DOI: 10.1021/acs.est.2c08753
Tanguy Déméautis ₁ , Alexandra Bouyssi ₁ , Annelise Chapalain ₂ , Johann Guillemot ₂ , Patricia Doublet ₂ , Alain Geloen ₃ , Christian George ₄ , Jean Menotti ₁ , Olivier Glehen _{1,

5} , Gilles Devouassoux _{1,

6} , Abderrazzak Bentaher ₁

Affiliation

最近，二次有机气溶胶（SOA）成为细颗粒物的主要成分。然而，SOA 的致病机制仍然知之甚少。在此，我们证明小鼠长期暴露于 SOA 会导致肺部炎症和组织破坏。组织学分析发现肺空腔扩大与以巨噬细胞为主的大量炎症细胞募集相关。伴随着这种细胞的流入，我们的结果发现一系列炎症介质的水平发生了变化以响应 SOA。有趣的是，我们观察到，接触 SOA 一个月后，编码 TNF-α 和 IL-6 的基因表达显着增加；已被大量记录在慢性肺部炎症病理中发挥作用的介质。细胞培养研究证实了这些体内发现。同样重要的是，我们的研究表明基质金属蛋白酶蛋白水解活性增加，表明其对肺组织炎症和降解有贡献。我们的工作代表了第一项体内研究，该研究报告称，长期接触 SOA 会导致肺部炎症和组织损伤。因此，我们希望这些数据能够促进新的研究，以增强我们对 SOA 潜在致病机制的理解，并可能有助于设计针对 SOA 介导的肺损伤的治疗策略。

"点击查看英文标题和摘要"

Chronic Exposure to Secondary Organic Aerosols Causes Lung Tissue Damage

Recently, secondary organic aerosols (SOAs) emerged as a predominant component of fine particulate matter. However, the pathogenic mechanism(s) of SOAs are still poorly understood. Herein, we show that chronic exposure of mice to SOAs resulted in lung inflammation and tissue destruction. Histological analyses found lung airspace enlargement associated with massive inflammatory cell recruitment predominated by macrophages. Concomitant with such cell influx, our results found changes in the levels of a series of inflammatory mediators in response to SOA. Interestingly, we observed that the expression of the genes encoding for TNF-α and IL-6 increased significantly after one month of exposure to SOAs; mediators that have been largely documented to play a role in chronic pulmonary inflammatory pathologies. Cell culture studies confirmed these in vivo findings. Of importance as well, our study indicates increased matrix metalloproteinase proteolytic activity suggesting its contribution to lung tissue inflammation and degradation. Our work represents the first in vivo study, which reports that chronic exposure to SOAs leads to lung inflammation and tissue injury. Thus, we hope that these data will foster new studies to enhance our understanding of the underlying pathogenic mechanisms of SOAs and perhaps help in the design of therapeutic strategies against SOA-mediated lung injury.

更新日期：2023-04-04

点击分享查看原文

点击收藏

阅读更多本刊新发论文本刊介绍/投稿指南