Lau Carmen H, Pendleton Drew, Drury Nicholas L, Zhao Jiayun, Li Yixin, Zhang Renyi, Wright Gus A, Hoffmann Aline Rodrigues, Johnson Natalie M
Department of Veterinary Pathobiology, Texas A&M University, College Station, TX 77843, USA.
Department of Environmental and Occupational Health, Texas A&M University, College Station, TX 77843, USA.
Antioxidants (Basel). 2022 Jan 21;11(2):202. doi: 10.3390/antiox11020202.
Early life exposure to particulate matter (PM) air pollution negatively impacts neonatal health. The underlying mechanisms following prenatal exposure, particularly to ultrafine particles (UFP, diameter ≤ 0.1 μm), are not fully understood; To evaluate the role of in response to in utero UFP exposure, we exposed time-mated -deficient () or wildtype (WT) mice to filtered air (FA) or 100 μg/m ultrafine PM daily throughout pregnancy. Offspring were evaluated for pulmonary immunophenotypes and pulmonary/systemic oxidative stress on postnatal day 5, a timepoint at which we previously demonstrated viral respiratory infection susceptibility; offspring exposed to FA had significantly lower average body weights compared to FA-exposed WT pups. Moreover, PM-exposed offspring weighed significantly less than PM-exposed WT pups. Notably, PM-exposed offspring showed a decreased pulmonary Th1/Th2 ratio, indicating a Th2 bias. Th17 cells were increased in FA-exposed neonates yet decreased in PM-exposed neonates. Analysis of oxidative stress-related genes in lung and oxidative stress biomarkers in liver tissues did not vary significantly across exposure groups or genotypes. Collectively, these findings indicate that the lack of causes growth inhibitory effects in general and in response to gestational UFP exposure. Prenatal UFP exposure skews CD4+ T lymphocyte differentiation toward Th2 in neonates lacking , signifying its importance in maternal exposure and infant immune responses.
生命早期暴露于颗粒物（PM）空气污染会对新生儿健康产生负面影响。产前暴露，尤其是暴露于超细颗粒物（UFP，直径≤0.1μm）后的潜在机制尚未完全了解；为了评估[具体物质名称缺失]在子宫内暴露于UFP后的反应中的作用，我们在整个孕期将经时间匹配的[基因名称缺失]缺陷（[基因名称缺失]）或野生型（WT）小鼠每天暴露于过滤空气（FA）或100μg/m³超细颗粒物中。在出生后第5天对后代进行肺部免疫表型和肺部/全身氧化应激评估，这是我们之前证明存在病毒性呼吸道感染易感性的时间点；与暴露于FA的WT幼崽相比，暴露于FA的[基因名称缺失]后代平均体重显著更低。此外，暴露于PM的[基因名称缺失]后代体重显著低于暴露于PM的WT幼崽。值得注意的是，暴露于PM的[基因名称缺失]后代肺部Th1/Th2比值降低，表明存在Th2偏向。在暴露于FA的[基因名称缺失]新生儿中Th17细胞增加，而在暴露于PM的[基因名称缺失]新生儿中Th17细胞减少。肺组织中氧化应激相关基因和肝组织中氧化应激生物标志物的分析在不同暴露组或基因型之间没有显著差异。总体而言，这些发现表明，[基因名称缺失]的缺乏一般会导致生长抑制作用，并且在孕期暴露于UFP时也会如此。产前UFP暴露会使缺乏[基因名称缺失]的新生儿的CD4 + T淋巴细胞分化偏向Th2，这表明其在母体暴露和婴儿免疫反应中的重要性。
