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在产前暴露于[a]pyrene会在后代小鼠中加剧OVA诱导的喘

Wenge Li¹, Lihong Wu², Xue Lu³

¹Department of Maternal, Child and Adolescent Health, School of Public Health, Anhui Medical University, No 81 Meishan Road, Hefei, Anhui 230032, China; Key Laboratory of Population Health Across Life Cycle (Anhui Medical University), Ministry of Education of the People's Republic of China, No 81 Meishan Road, Hefei, Anhui 230032, China; Anhui Provincial Key Laboratory of Environment and Population Health across the Life Course, Anhui Medical University, No 81 Meishan Road, Hefei, Anhui 230032, China.

Ecotoxicology and environmental safety

|November 14, 2025

概括

产前暴露于甲 (B[a]P) 会通过增加呼吸道炎症和粘液,使后代的喘恶化. 这项研究强调了早期的肠道微生物群变化是B[a]P诱导喘恶化的关键因素.

科学领域:

环境健康环境健康
免疫学免疫学免疫学
微生物学微生物学

背景情况:

产前暴露于[a]pyrene (B[a]P) 等环境毒素与喘风险增加有关.
妊娠期间B[a]P暴露影响后代喘表型和肠道微生物群的作用的具体机制尚未完全理解.

研究的目的:

用小鼠模型研究产前B[a]P暴露对后代喘发展的影响.
阐明潜在的机制,包括免疫反应和肠道微生物群的改变.

主要方法:

怀孕的小鼠在怀孕期间暴露在B[a]P或载体中.
后代接受了卵蛋白 (OVA) 诱导的喘模型.
评估了呼吸道的高反应性,肺部病理,免疫标记物和肠道微生物群组成 (16S rRNA测序).

主要成果:

产前B[a]P暴露加剧了OVA诱导的喘,增加了气道炎症,粘液产生和气道壁厚度.
观察到IFN-γ和TGF-β的水平升高,支气管洗液 (BALF) 中的中性粒细胞和单细胞数量增加,以及Muc5ac表达的增加.
确定了肠道微生物群组成的显著变化,包括增加的α多样性和Clostridia_UCG-014丰度的显著增加.

结论:

产前B[a]P暴露会通过促进呼吸道炎症,粘液过分分泌和肠道失调症来加剧后代的喘.
早期的肠道微生物群变化代表了预测和干预B[a]P诱导喘的潜在治疗目标.

关键词:

气道的过度反应性呼吸道的炎症呼吸道的炎症喘喘是一种子[a]二烯是一种二烯.我们的肠道微生物群.

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