Abstract
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.
Highlights
Atmospheric particulate matter (PM) is a complex mixture of inorganic substances, dust, smoke, metal elements, various liquid and solid substances, as well as biological components including bacteria, fungi, and viruses [1]
The results showed that inflammatory cells increased in OVA-induced allergic rhinitis (AR) mice compared with those in the Naive group, especially eosinophils, and these reactions were exacerbated by AR with exposure to PM2.5 (Figure 2A,B)
The results revealed that the level of MDA significantly increased by AR with PM2.5 exposed group, followed by down-regulation of Superoxide dismutase (SOD) activity and production of HO-1 in Nasal Lavage Fluid (NALF), which subsequently induced the oxidative stress in AR (Figure 5A)
Summary
Atmospheric particulate matter (PM) is a complex mixture of inorganic substances (such as oxides of transition metals), dust, smoke, metal elements, various liquid and solid substances, as well as biological components including bacteria, fungi, and viruses [1]. Acute and chronic exposure to PM, especially the fine particles (aerodynamic diameters less than or equal to 2.5 μm, PM2.5), are harmful to human health because they can penetrate into the bronchi and alveoli of the respiratory tract and cause lung and cardiovascular diseases [2,3,4]. Increasing epidemiologic studies have demonstrated that PM exposure is closely associated with morbidity and mortality due to chronic respiratory diseases [5]. Practical evidence gathered through environmental and epidemiological studies shows a strong association between fine particulate air pollution and health problems such as respiratory illnesses including respiratory tract inflammation, asthma, acute bronchitis, and lung cancer [6,7]. There is increasing evidence from epidemiological and laboratory-based studies that exposure to air pollutants can play an important role in the nasal symptoms of allergic and non-allergic airway diseases
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