重复暴露于桉木烟雾会改变雄性 Long-Evans 大鼠的肺部基因和新陈代谢特征。

IF 3.4 3区 医学 Q2 TOXICOLOGY
Samuel J Cochran, Katelyn Dunigan-Russell, Grace M Hutton, Helen Nguyen, Mette C Schladweiler, Dean P Jones, Wanda C Williams, Anna A Fisher, M Ian Gilmour, Janice A Dye, M Ryan Smith, Colette N Miller, Kymberly M Gowdy
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引用次数: 0

摘要

暴露于野火烟雾与急性和慢性心肺疾病都有关系,这一点对于反复暴露于木材烟雾的野地消防员来说尤为重要。有必要更好地了解木烟暴露会增加这一人群肺部疾病负担的潜在病理生理学。我们假设木烟暴露会导致肺功能障碍、肺部炎症以及与未来肺部并发症相关的基因表达谱。雄性 Long-Evans 大鼠间歇性暴露于低浓度(11.0 ± 1.89 毫克/立方米)和高浓度(23.7 ± 0.077 毫克/立方米)的烟熏桉木烟雾中,为期两周。在整个过程中,间歇性地测量全身胸透。在最终暴露 24 小时后收集肺组织和灌洗液,进行转录组学和代谢组学研究。烟雾暴露量的增加会上调支气管肺泡灌洗液中的中性粒细胞和某些细胞因子。在高烟雾暴露组大鼠的肺中,共有 3 446 个基因发生了差异表达,而在低烟雾暴露组中只有一个基因(Cd151)发生了差异表达。高浓度烟雾组的基因变化反映了真核启动因子 2(EIF2)应激和氧化应激反应的变化,这与代谢组学分析结果一致。xMWAS 整合分析显示,烟雾暴露显著改变了与氧化应激、肺形态发生和肿瘤增殖途径相关的通路。这些结果表明,间歇性暴露于桉木烟雾 2 周会导致肺部转录组学和代谢组学的变化,这些变化可能预示着未来肺部疾病的发展。总之,这些研究结果提供了对可能导致野外消防员慢性肺部疾病的细胞信号通路的深入了解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Repeated exposure to eucalyptus wood smoke alters pulmonary gene and metabolic profiles in male Long-Evans rats.

Exposure to wildfire smoke is associated with both acute and chronic cardiopulmonary illnesses, which are of special concern for wildland firefighters who experience repeated exposure to wood smoke. It is necessary to better understand the underlying pathophysiology by which wood smoke exposure increases pulmonary disease burdens in this population. We hypothesize that wood smoke exposure produces pulmonary dysfunction, lung inflammation, and gene expression profiles associated with future pulmonary complications. Male Long-Evans rats were intermittently exposed to smoldering eucalyptus wood smoke at 2 concentrations, low (11.0 ± 1.89 mg/m3) and high (23.7 ± 0.077 mg/m3), over a 2-week period. Whole-body plethysmography was measured intermittently throughout. Lung tissue and lavage fluid were collected 24 h after the final exposure for transcriptomics and metabolomics. Increasing smoke exposure upregulated neutrophils and select cytokines in the bronchoalveolar lavage fluid. In total, 3446 genes were differentially expressed in the lungs of rats in the high smoke exposure and only 1 gene in the low smoke exposure (Cd151). Genes altered in the high smoke group reflected changes to the Eukaryotic Initiation Factor 2 stress and oxidative stress responses, which mirrored metabolomics analyses. xMWAS-integrated analysis revealed that smoke exposure significantly altered pathways associated with oxidative stress, lung morphogenesis, and tumor proliferation pathways. These results indicate that intermittent, 2-week exposure to eucalyptus wood smoke leads to transcriptomic and metabolic changes in the lung that may predict future lung disease development. Collectively, these findings provide insight into cellular signaling pathways that may contribute to the chronic pulmonary conditions observed in wildland firefighters.

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来源期刊
Toxicological Sciences
Toxicological Sciences 医学-毒理学
CiteScore
7.70
自引率
7.90%
发文量
118
审稿时长
1.5 months
期刊介绍: The mission of Toxicological Sciences, the official journal of the Society of Toxicology, is to publish a broad spectrum of impactful research in the field of toxicology. The primary focus of Toxicological Sciences is on original research articles. The journal also provides expert insight via contemporary and systematic reviews, as well as forum articles and editorial content that addresses important topics in the field. The scope of Toxicological Sciences is focused on a broad spectrum of impactful toxicological research that will advance the multidisciplinary field of toxicology ranging from basic research to model development and application, and decision making. Submissions will include diverse technologies and approaches including, but not limited to: bioinformatics and computational biology, biochemistry, exposure science, histopathology, mass spectrometry, molecular biology, population-based sciences, tissue and cell-based systems, and whole-animal studies. Integrative approaches that combine realistic exposure scenarios with impactful analyses that move the field forward are encouraged.
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