In recent years, airborne fine particulate matter (PM_2.5) is drawing more public attention due to its various physicochemical features and causing pathological harm, as proven by epidemiological and clinical studies. However, the mechanism of PM_2.5-exposure-induced lung injury has not been fully characterized. Here, we established a PM_2.5-induced rat injury model for both short-term and long-term exposures at different concentrations. We employed the Fast-seq technique to profile 6316 proteins and the catTFRE approach to profile 387 transcription factors (TFs) in the lung tissue. In short-term exposure, we elucidated gradually upregulated proteins enriched in response to oxidative stress, phagosome, and the extracellular matrix (ECM)–receptor interaction pathway. Long-term exposure mainly showed the immune response pathway to be consisting of increased lymphocytes and cytokines. Intriguingly, we found that immune-related proteins were recoverable during short-term exposure. During the process of PM_2.5 exposure, upregulated proteins presented dose-dependence in the lung, including stress response at low dose, minor immune response at middle dose, and severe inflammatory response at high dose. This data set provides a rich resource to facilitate the understanding of PM_2.5-induced lung damage and repair mechanism.

中文翻译：

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PM2.5暴露诱导的大鼠肺损伤和修复的时间和剂量分辨蛋白质组。

近年来，由于流行病学和临床研究证明，由于空气中的细颗粒物（PM _2.5）的各种理化特性和引起病理性损害，因此引起了更多公众的关注。但是，PM _2.5暴露引起的肺损伤的机制尚未完全阐明。在这里，我们建立了PM _2.5浓度不同的短期和长期暴露所致的大鼠损伤模型。我们采用Fast-seq技术分析了6316种蛋白质，采用catTFRE方法分析了肺组织中的387个转录因子（TF）。在短期暴露中，我们阐明了在氧化应激，吞噬体和细胞外基质（ECM）-受体相互作用途径中逐渐富集的蛋白质。长期接触主要显示免疫反应途径由增加的淋巴细胞和细胞因子组成。有趣的是，我们发现免疫相关蛋白在短期暴露过程中是可恢复的。在PM _2.5的过程中暴露后，上调的蛋白质在肺中呈剂量依赖性，包括低剂量时的应激反应，中剂量时的轻微免疫反应和高剂量时的严重炎症反应。该数据集提供了丰富的资源，以促进对PM _2.5诱导的肺损伤和修复机制的理解。