■鉴于全球野火的流行,了解野火空气污染物对人体健康的影响-特别是在特定的免疫途径中-至关重要。暴露于空气污染物与心肺疾病有关;然而,免疫和上皮屏障改变需要进一步研究。
■我们试图通过使用蛋白质组学和免疫细胞表型来确定野火烟雾暴露对免疫系统和上皮屏障的影响。
■旧金山湾地区的一个队列(n=15;年龄30±10岁)在重大野火之前(2019年10月至2020年3月;空气质量指数=37)和期间(2020年8月;空气质量指数=80)提供了血液样本。11天收集暴露样本(范围,10-12天)连续暴露于野火烟雾后。我们确定了506种蛋白质的改变,包括zonulin家族肽(ZFP);通过飞行时间(CyTOF)进行细胞计数的免疫细胞表型;以及使用相关矩阵的相互关系。
■靶向蛋白质组分析(n=15)显示spondin-2减少,粒酶A增加,B,H,杀伤细胞免疫球蛋白样受体3DL1,IL-16,nibrin,聚(ADP-核糖)聚合酶1,C1qTNF相关蛋白,成纤维细胞生长因子19和vonWillebrand因子平均连续暴露于大型野火烟雾后11天(P<0.05)。我们还观察到免疫调节途径(IL-16,颗粒酶A,B,H,和杀伤细胞免疫球蛋白样受体3DL1),DNA修复[聚(ADP-核糖)1,nibrin],和自然杀伤细胞。我们没有观察到ZFP水平的变化,表明上皮屏障的变化。然而,ZFP与免疫细胞表型(幼稚CD4+,TH2细胞)。
■我们观察到野火烟雾暴露过程中关键免疫细胞及其蛋白质的功能变化。未来在更大的队列或暴露于野火烟雾的消防员中的研究应进一步评估免疫变化和干预目标。
UNASSIGNED: Given the increasing prevalence of wildfires worldwide, understanding the effects of wildfire air pollutants on human health-particularly in specific immunologic pathways-is crucial. Exposure to air pollutants is associated with cardiorespiratory disease; however, immune and epithelial barrier alterations require further investigation.
UNASSIGNED: We sought to determine the impact of wildfire smoke exposure on the immune system and epithelial barriers by using proteomics and immune cell phenotyping.
UNASSIGNED: A San Francisco Bay area cohort (n = 15; age 30 ± 10 years) provided blood samples before (October 2019 to March 2020; air quality index = 37) and during (August 2020; air quality index = 80) a major wildfire. Exposure samples were collected 11 days (range, 10-12 days) after continuous exposure to wildfire smoke. We determined alterations in 506 proteins, including zonulin family peptide (ZFP); immune cell phenotypes by cytometry by time of flight (CyTOF); and their interrelationship using a correlation matrix.
UNASSIGNED: Targeted proteomic analyses (n = 15) revealed a decrease of spondin-2 and an increase of granzymes A, B, and H, killer cell immunoglobulin-like receptor 3DL1, IL-16, nibrin, poly(ADP-ribose) polymerase 1, C1q TNF-related protein, fibroblast growth factor 19, and von Willebrand factor after 11 days\' average continuous exposure to smoke from a large wildfire (P < .05). We also observed a large correlation cluster between immune regulation pathways (IL-16, granzymes A, B, and H, and killer cell immunoglobulin-like receptor 3DL1), DNA repair [poly(ADP-ribose) 1, nibrin], and natural killer cells. We did not observe changes in ZFP levels suggesting a change in epithelial barriers. However, ZFP was associated with immune cell phenotypes (naive CD4+, TH2 cells).
UNASSIGNED: We observed functional changes in critical immune cells and their proteins during wildfire smoke exposure. Future studies in larger cohorts or in firefighters exposed to wildfire smoke should further assess immune changes and intervention targets.