PM<sub>2.5</sub> Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model
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 intr...
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MDPI AG
2021-07-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/22/15/8173 |
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| author | Chun Hua Piao Yanjing Fan Thi Van Nguyen Hee Soon Shin Hyoung Tae Kim Chang Ho Song Ok Hee Chai |
| author_facet | Chun Hua Piao Yanjing Fan Thi Van Nguyen Hee Soon Shin Hyoung Tae Kim Chang Ho Song Ok Hee Chai |
| author_sort | Chun Hua Piao |
| collection | DOAJ |
| description | 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 (PM<sub>2.5</sub>) solution, and then by intraperitoneal injection of ovalbumin (OVA) with alum and intranasal challenging with 10 mg/mL OVA. The effects of PM<sub>2.5</sub> 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. PM<sub>2.5</sub> 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 PM<sub>2.5</sub> 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 PM<sub>2.5</sub> exposure reinforced this impairment in OVA-induced AR mice. Long-term PM<sub>2.5</sub> 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 PM<sub>2.5</sub> exposed AR mice. Furthermore, PM<sub>2.5</sub> exposure increased the histopathological changes of nasal and lung tissues and related the inflammatory cytokine, and clearly enhanced PM<sub>2.5</sub> 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 PM<sub>2.5</sub> exposure. |
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| language | English |
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| spelling | doaj.art-5302a5199e71472984ffe5e1af1e5e9e2023-11-22T05:44:22ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-07-012215817310.3390/ijms22158173PM<sub>2.5</sub> Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse ModelChun Hua Piao0Yanjing Fan1Thi Van Nguyen2Hee Soon Shin3Hyoung Tae Kim4Chang Ho Song5Ok Hee Chai6Department of Pulmonary and Critical Care Medicine, Yantai Yuhuangding Hospital, Yantai 264000, ChinaDepartment of Anatomy, Jeonbuk National University Medical School, Jeonju 54896, Jeonbuk, KoreaDepartment of Anatomy, Jeonbuk National University Medical School, Jeonju 54896, Jeonbuk, KoreaDivision of Food Functionality Research, Korea Food Research Institute, 245 Nongsaengmyeong-ro, Iseo-myeon, Wanju-gun 55365, Jeonbuk, KoreaDepartment of Anatomy, Jeonbuk National University Medical School, Jeonju 54896, Jeonbuk, KoreaDepartment of Anatomy, Jeonbuk National University Medical School, Jeonju 54896, Jeonbuk, KoreaDepartment of Anatomy, Jeonbuk National University Medical School, Jeonju 54896, Jeonbuk, KoreaAir 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 (PM<sub>2.5</sub>) solution, and then by intraperitoneal injection of ovalbumin (OVA) with alum and intranasal challenging with 10 mg/mL OVA. The effects of PM<sub>2.5</sub> 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. PM<sub>2.5</sub> 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 PM<sub>2.5</sub> 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 PM<sub>2.5</sub> exposure reinforced this impairment in OVA-induced AR mice. Long-term PM<sub>2.5</sub> 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 PM<sub>2.5</sub> exposed AR mice. Furthermore, PM<sub>2.5</sub> exposure increased the histopathological changes of nasal and lung tissues and related the inflammatory cytokine, and clearly enhanced PM<sub>2.5</sub> 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 PM<sub>2.5</sub> exposure.https://www.mdpi.com/1422-0067/22/15/8173particulate matter (PM<sub>2.5</sub>)allergic rhinitis (AR)Nrf2NF-κBoxidative stressinflammation |
| spellingShingle | Chun Hua Piao Yanjing Fan Thi Van Nguyen Hee Soon Shin Hyoung Tae Kim Chang Ho Song Ok Hee Chai PM<sub>2.5</sub> Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model International Journal of Molecular Sciences particulate matter (PM<sub>2.5</sub>) allergic rhinitis (AR) Nrf2 NF-κB oxidative stress inflammation |
| title | PM<sub>2.5</sub> Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model |
| title_full | PM<sub>2.5</sub> Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model |
| title_fullStr | PM<sub>2.5</sub> Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model |
| title_full_unstemmed | PM<sub>2.5</sub> Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model |
| title_short | PM<sub>2.5</sub> Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model |
| title_sort | pm sub 2 5 sub exacerbates oxidative stress and inflammatory response through the nrf2 nf κb signaling pathway in ova induced allergic rhinitis mouse model |
| topic | particulate matter (PM<sub>2.5</sub>) allergic rhinitis (AR) Nrf2 NF-κB oxidative stress inflammation |
| url | https://www.mdpi.com/1422-0067/22/15/8173 |
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