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Exposure to air pollution interacts with obesogenic nutrition to induce tissue-specific response patterns

机译：暴露于空气污染与致肥胖营养相互作用，诱导组织特异性反应模式

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Obesity and exposure to particular matter (PM) have become two leading global threats to public health. However, the exact mechanisms and tissue-specificity of their health effects are largely unknown. Here we investigate whether a metabolic challenge (early nutritional obesity) synergistically interacts with an environmental challenge (PM exposure) to alter genes representing key response pathways, in a tissue specific manner. Mice subjected to 7 weeks obesogenic nutrition were exposed every other day during the final week and a half to aqueous extracts of PM collected in the city of London (UK). The expression of 61 selected genes representing key response pathways were investigated in lung, liver, white and brown adipose tissues. Principal component analysis (PCA) revealed distinct patterns of expression changes between the 4 tissues, particularly in the lungs and the liver. Surprisingly, the lung responded to the nutrition challenge. The response of these organs to the PM challenge displayed opposite patterns for some key genes, in particular, those related to the Nrf2 pathway. While the contribution to the variance in gene expression changes in mice exposed to the combined challenge were largely similar among the tissues in PCA1, PCA2 exhibited predominant contribution of inflammatory and oxidative stress responses to the variance in the lungs, and a greater contribution of autophagy genes and MAP kinases in adipose tissues. Possible involvement of alterations in DNA methylation was demonstrated by cell-type-specific responses to a methylation inhibitor. Correspondingly, the DNA methyltransferase Dnmt3a2 increased in the lungs but decreased in the liver, demonstrating potential tissue-differential synergism between nutritional and PM exposure. The results suggest that urban PM, containing dissolved metals, interacts with obesogenic nutrition to regulate diverse response pathways including inflammation and oxidative stress, in a tissue-specific manner. Tissue-differential effects on DNA methylation may underlie tissue-specific responses to key stress-response genes such as catalase and Nrf2. (C) 2018 Elsevier Ltd. All rights reserved.
机译：肥胖和特定物质暴露已成为全球范围内对公共健康的两大主要威胁。但是，其健康影响的确切机制和组织特异性在很大程度上尚不清楚。在这里，我们调查了代谢挑战（早期营养性肥胖）是否与环境挑战（PM暴露）协同相互作用，以组织特异性方式改变代表关键反应途径的基因。在最后一周内，隔两天每天对遭受7周致肥胖营养作用的小鼠进行一次暴露于伦敦市（英国）收集的PM的水提取物的暴露。在肺，肝，白色和棕色脂肪组织中研究了代表关键反应途径的61个选定基因的表达。主成分分析（PCA）显示了4种组织之间表达变化的明显模式，尤其是在肺和肝中。令人惊讶的是，肺对营养挑战作出了反应。这些器官对PM挑战的反应显示出某些关键基因的相反模式，特别是与Nrf2途径相关的那些关键基因。虽然暴露于联合攻击的小鼠对基因表达变化的变化的贡献在PCA1的组织之间非常相似，但PCA2表现出炎症和氧化应激反应对肺部变化的主要贡献，而自噬基因的贡献更大和脂肪组织中的MAP激酶。通过对甲基化抑制剂的细胞类型特异性反应证明了DNA甲基化变化的可能参与。相应地，DNA甲基转移酶Dnmt3a2在肺中增加，但在肝中减少，表明营养暴露和PM暴露之间潜在的组织差异协同作用。结果表明，含有溶解金属的城市PM与致肥胖营养相互作用，以组织特异性方式调节包括炎症和氧化应激在内的多种反应途径。组织对DNA甲基化的差异作用可能是针对关键应激反应基因（例如过氧化氢酶和Nrf2）的组织特异性反应的基础。 （C）2018 Elsevier Ltd.保留所有权利。

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