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揭示了巨驱动的炎症失调:NF-κB介导的高炎症将6PPD-Q暴露与病毒免疫病理学联系在一起

Xia-Wen Qiu¹, Jiajun Chen², Jiayan Wang³

¹Jinhua Academy of Zhejiang Chinese Medical University, Jinhua, Zhejiang 321015, China; Zhejiang Key Laboratory of Ecological Environmental Damage Control and Value Transformation, College of Environment and Resources, College of Carbon Neutral, Zhejiang A & F University, Hangzhou, Zhejiang 311300, China.

Journal of hazardous materials

|March 5, 2026

概括

环境污染物6PPD-Q (N-(1,3-二甲基) -N'--p-phenylenediamine quinone) 的暴露增加了对呼吸道病毒感染的易感性. 这种污染物通过调节免疫反应并增加死亡率来加剧病毒性肺炎.

科学领域:

环境科学环境科学
免疫学免疫学免疫学
毒理学毒理学毒理学

背景情况:

呼吸道病毒感染对全球健康构成重大威胁.
N-(1,3-二甲基) -N'--p-phenylenediamine (6PPD-Q) 是一种已知的生态毒性环境污染物.
6PPD-Q对宿主免疫防御对呼吸道病毒的影响尚不清楚.

研究的目的:

调查6PPD-Q暴露对宿主免疫反应和对呼吸道病毒感染的易感性的影响.
阐明病毒性肺炎期间6PPD-Q诱导的免疫调节背后的机制.

主要方法:

通过内注射6PPD-Q,随后感染甲型流感病毒 (IAV) 或膀性口腔炎病毒 (VSV),建立了一种小鼠模型.
评估了死亡率,病毒传播,肺病理和炎症性细胞因子水平 (IL-6,TNF-α,IL-1β,IL-10).
进行了免疫细胞分析和巨细胞枯竭实验,以确定关键细胞参与者和信号通路 (NF-κB).

主要成果:

6PPD-Q预暴露导致感染小鼠的死亡率增加,病毒传播和严重的肺病理.
暴露于6PPD-Q失调的炎症,有过度的细胞因子生产和中性粒细胞,单细胞和单细胞衍生的巨细胞 (MDMs) 在肺部的积累.
巨细胞枯竭取消了6PPD-Q的有害影响,并且发现6PPD-Q可以激活肺部MDM中的NF-κB信号.

结论:

6PPD-Q显著增加了宿主对病毒性肺炎的敏感性,加剧了疾病的严重程度和死亡率.
这些发现强调了6PPD-Q诱导的肺MDM激活和NF-κB信号传递在驱动过度炎症中的作用.
环境卫生管理对于减轻6PPD-Q等污染物对呼吸道传染病结果的影响至关重要.

关键词:

6PPD - 氨酸 - 氨酸的使用情况免疫系统的调节失调.巨细胞是一个巨细胞.呼吸道暴露呼吸道暴露病毒感染病毒感染.

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