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饮食调节肺脂质可影响吸入臭氧引起的炎症反应。

Dietary modulation of lung lipids influences inflammatory responses to inhaled ozone.

机构信息

Department of Pharmaceutical Sciences, University of New Mexico College of Pharmacy, Albuquerque, New Mexico, USA.

University of New Mexico Prevention Research Center, University of New Mexico, Albuquerque, New Mexico, USA.

出版信息

J Lipid Res. 2024 Sep;65(9):100630. doi: 10.1016/j.jlr.2024.100630. Epub 2024 Aug 30.

DOI:10.1016/j.jlr.2024.100630
PMID:39182607
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11417538/
Abstract

The pulmonary system represents a unique lipidomic environment as it contains cellular membrane-bound lipid species and a specialized reservoir of lipids in the airway epithelial lining fluid. As a major initial point of defense, airway lipids react to inhaled contaminants such as volatile organic compounds, oxides of nitrogen, or ozone (O), creating lipokine signaling that is crucial for both the initiation and resolution of inflammation within the lung. Dietary modulation of eicosanoids has gained increased attention in recent years for improvements to cardiovascular health. The current study sought to examine how dietary supplementation with eicosanoid precursors (i.e, oils rich in saturated or polyunsaturated fatty acids) might alter the lung lipid composition and subsequently modify the inflammatory response to ozone inhalation. Our study demonstrated that mice fed a diet high in saturated fatty acids resulted in diet-specific changes to lung lipid profiles and increased cellular recruitment to the lung following ozone inhalation. Bioinformatic analysis revealed an ozone-dependent upregulation of several lipid species, including phosphoserine 37:5. Pathway analysis of lipid species revealed the process of lateral diffusion of lipids within membranes to be significantly altered due to ozone exposure. These results show promising data for influencing pulmonary lipidomic profiles via diet, which may provide a pragmatic therapeutic approach to protect against lung inflammation and damage following pulmonary insult.

摘要

呼吸系统是一个独特的脂质组学环境,因为它包含细胞膜结合的脂质种类和气道上皮衬液中的特殊脂质储备。作为主要的初始防御点,气道脂质会对吸入的污染物(如挥发性有机化合物、氮氧化物或臭氧 (O))做出反应,产生脂激信号,这对于肺部炎症的启动和解决都至关重要。近年来,人们越来越关注饮食对类二十烷酸的调节,以改善心血管健康。本研究旨在探讨膳食中补充类二十烷酸前体(即富含饱和或多不饱和脂肪酸的油)如何改变肺脂质组成,并随后改变对臭氧吸入的炎症反应。我们的研究表明,喂食高脂肪饱和脂肪酸的小鼠的肺脂质谱发生了特定于饮食的变化,并在臭氧吸入后增加了细胞向肺部的募集。生物信息学分析显示,臭氧依赖性地上调了几种脂质种类,包括磷酸丝氨酸 37:5。脂质种类的途径分析显示,由于臭氧暴露,膜内脂质的侧向扩散过程发生了显著改变。这些结果为通过饮食影响肺脂质组学图谱提供了有希望的数据,这可能为保护肺部免受肺损伤后的炎症和损伤提供一种实用的治疗方法。

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