Background: Vehicle-induced air pollution may increase the prevalence and severity of asthma. Pollens are important sources of outdoor allergens associated with asthma. Outdoor pollution may influence the structure of pollen… Click to show full abstract
Background: Vehicle-induced air pollution may increase the prevalence and severity of asthma. Pollens are important sources of outdoor allergens associated with asthma. Outdoor pollution may influence the structure of pollen grains, resulting in enhanced immune reactions. Objective: This study aims to investigate the impact that artemisia pollen extracts exposed to diesel emissions (APEDE) may induce – allergic airway inflammation, pulmonary pathology and immune imbalance – in mice. Methods: Sixty male Balb/c mice were equally randomized into 5 groups, sensitized with 30 μL artemisia pollen extracts (APE) or APEDE adsorbed on 2 mg aluminum hydroxide gel by intraperitoneal injection on day 0, 7, 14, and 22, and challenged intranasally once per day with 30 μL APE or APEDE from day 29 to 36. The controlling group used phosphate-buffered saline as control. Results: In mice immunized and challenged by APEDE, the clinical phenotype of eosinophils, neutrophils in bronchoalveolar lavage fluid (BALF), tracheal wall thickness, airway smooth muscle thickness and airway resistance increased significantly. Pathophysiological parameters such as interleukin (IL)-17A and tumour necrosis factor-α production in BALF and serum, and the ratio of Th17/Treg cells in CD4+ cells increased significantly, while IL-10 in BALF and serum and the ratio of Treg cells decreased significantly. It was further found that the expression of oxidative stress marker 3-nitrotyrosine (3-NT) and the activation of nuclear factor kappa B (NF-κB) were significantly increased. The correlation analysis showed that the expression of 3-NT was positively correlated with the activation of NF-κB. Conclusion: Our findings suggested that pollens exposed to diesel exhaust enhance allergic responses, which may contribute to an increased prevalence of allergic diseases in urban environments with serious exhaust emissions.
               
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