Diesel exhaust particles exacerbate allergic rhinitis in mice by disrupting the nasal epithelial barrier

Summary Background Diesel exhaust particles (DEP), traffic‐related air pollutants, are considered environmental factors that affect allergic diseases adversely. However, the exact effect of DEP on allergic rhinitis (AR) is unclear. Objective We thought to investigate the effect of DEP on seasonal AR...

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Bibliographic Details
Published in:Clinical and experimental allergy 2016-01, Vol.46 (1), p.142-152
Main Authors: Fukuoka, A., Matsushita, K., Morikawa, T., Takano, H., Yoshimoto, T.
Format: Article
Language:English
Subjects:
Air Pollutants - adverse effects
Allergens - immunology
allergic rhinitis
Ambrosia - adverse effects
Animals
antioxidant
Antioxidants - metabolism
diesel exhaust particles
Disease Models, Animal
Disease Progression
Epithelial Cells - metabolism
Female
Immunization
Mice
nasal epithelial cells
Nasal Mucosa - immunology
Nasal Mucosa - pathology
Particulate Matter - adverse effects
Permeability
Pollen - immunology
reactive oxygen species
Rhinitis, Allergic - diagnosis
Rhinitis, Allergic - etiology
Tight Junctions
Vehicle Emissions - toxicity
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Summary:Summary Background Diesel exhaust particles (DEP), traffic‐related air pollutants, are considered environmental factors that affect allergic diseases adversely. However, the exact effect of DEP on allergic rhinitis (AR) is unclear. Objective We thought to investigate the effect of DEP on seasonal AR using a mouse model. Methods Ragweed‐pollen‐sensitized mice were nasally challenged with ragweed pollen in the presence or absence of DEP. The frequency of sneezing was evaluated immediately after each nasal challenge. The expression of a tight junction (TJ) protein, zonula occludens‐1 (ZO‐1), was examined by immunohistochemistry in AR mice. RPMI 2650 cells were used for in vitro examination of paracellular permeability. Results Mice challenged with ragweed pollen plus DEP showed increased frequency of sneezing compared with mice challenged with pollen alone. Interestingly, intranasal DEP pretreatment before ragweed pollen challenge increased ragweed‐pollen‐induced sneezing to levels comparable with the co‐administration group. In vitro examination revealed that DEP reduced ZO‐1 expression in RPMI 2650 cells. In addition, intranasal administration of DEP, but not ragweed pollen, disrupted nasal mucosal TJs in vivo. The effect of a single DEP treatment on ragweed‐induced sneezing and ZO‐1 expression persisted for at least 4 days and was inversely correlated. Finally, an antioxidant substance, N‐acetyl‐L‐cysteine, inhibited DEP‐mediated TJ disruption and exacerbation of sneezing in AR. Conclusions and Clinical Relevance DEP disrupts TJs by a reactive oxygen species‐mediated pathway, leading to the increased permeability of nasal epithelial cells. This may result in the promotion of allergen delivery into subepithelial tissues contributing to the exacerbation of immediate allergic responses.
ISSN:0954-7894
1365-2222
DOI:10.1111/cea.12597