PM(2.5) Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model.
PM(2.5) Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model.
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PM（2.5）通过Nrf 2/NF-κB信号通路加重OVA诱导的变应性鼻炎小鼠模型中的氧化应激和炎症反应
DOI：
10.3390/ijms22158173
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发表时间：
2021-07-29
影响因子：
5.6
通讯作者：
Chai OH
中科院分区：
文献类型：
--
作者：
Piao CH;Fan Y;Nguyen TV;Shin HS;Kim HT;Song CH;Chai OH
据报道，与空气污染相关的颗粒物（PM）暴露会加剧过敏性气道炎症。一些研究表明PM暴露与过敏性鼻炎（AR）风险之间存在关联。然而，PM对AR的影响尚未完全了解。通过鼻内给予100 μg/小鼠的空气动力学直径（PM 2.5）小于或等于2.5 μm的PM溶液，然后通过腹腔内注射含有明矾的卵清蛋白（OVA）和鼻内给予10 mg/mL的OVA来建立AR小鼠模型。通过组织学、血清和蛋白质分析检测PM2. 5对有或无AR小鼠中通过Nrf 2/NF-κB信号通路的氧化应激和炎症反应的影响。在OVA诱导的AR小鼠中，PM2.5给药通过增加炎性细胞因子的表达和减少Treg细胞因子的释放来增强鼻粘膜中的变应性炎性细胞表达，尽管PM2.5暴露本身既不诱导变应性反应也不损伤鼻和肺组织。值得注意的是，反复的OVA免疫明显损害了鼻中隔区域的鼻粘膜。此外，AR与PM2.5暴露强化了OVA诱导的AR小鼠的这种损害。长期PM2.5暴露通过诱导丙二醛产生而增强过敏反应。本研究还首次提供了证据，表明Nrf 2信号通路的活性在PM2.5暴露的AR小鼠中受到抑制。此外，PM2. 5暴露可引起鼻和肺组织病理学改变，并与炎性细胞因子的产生有关，还可通过激活NF-κB信号通路增强肺泡巨噬细胞对PM2. 5的吞噬作用。这些获得的结果表明，AR患者可能会在长期暴露于PM2.5的区域发生过敏反应加重。
Air pollution-related particulate matter (PM) exposure reportedly enhances allergic airway inflammation. Some studies have shown an association between PM exposure and a risk for allergic rhinitis (AR). However, the effect of PM for AR is not fully understood. An AR mouse model was developed by intranasal administration of 100 μg/mouse PM with a less than or equal to 2.5 μm in aerodynamic diameter (PM2.5) solution, and then by intraperitoneal injection of ovalbumin (OVA) with alum and intranasal challenging with 10 mg/mL OVA. The effects of PM2.5 on oxidative stress and inflammatory response via the Nrf2/NF-κB signaling pathway in mice with or without AR indicating by histological, serum, and protein analyses were examined. PM2.5 administration enhanced allergic inflammatory cell expression in the nasal mucosa through increasing the expression of inflammatory cytokine and reducing the release of Treg cytokine in OVA-induced AR mice, although PM2.5 exposure itself induced neither allergic responses nor damage to nasal and lung tissues. Notably, repeated OVA-immunization markedly impaired the nasal mucosa in the septum region. Moreover, AR with PM2.5 exposure reinforced this impairment in OVA-induced AR mice. Long-term PM2.5 exposure strengthened allergic reactions by inducing the oxidative through malondialdehyde production. The present study also provided evidence, for the first time, that activity of the Nrf2 signaling pathway is inhibited in PM2.5 exposed AR mice. Furthermore, PM2.5 exposure increased the histopathological changes of nasal and lung tissues and related the inflammatory cytokine, and clearly enhanced PM2.5 phagocytosis by alveolar macrophages via activating the NF-κB signaling pathway. These obtained results suggest that AR patients may experience exacerbation of allergic responses in areas with prolonged PM2.5 exposure.
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影响因子：
2.1
作者：
Riva, D. R.;Magalhaes, C. B.;Zin, W. A.
通讯作者：
Zin, W. A.
影响因子：
9.8
作者：
Alghamdi, Mansour A.;Shamy, Magdy;Elserougy, Safaa
通讯作者：
Elserougy, Safaa
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影响因子：
2.6
作者：
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通讯作者：
Zhang, Ru-Xin
影响因子：
2.8
作者：
Kzhyshkowska, Julia;Neyen, Claudine;Gordon, Siamon
通讯作者：
Gordon, Siamon
DOI：
10.1016/j.mrgentox.2008.08.015
发表时间：
2008-12-08
影响因子：
1.9
作者：
Mehta, Manju;Chen, Lung-Chi;Gordon, Terry;Rom, William;Tang, Moon-shong
通讯作者：
Tang, Moon-shong