Barrier dysfunction in the nasal allergy
Epithelial cells form the first physiological barrier against invasion by pathogens and the infiltration of allergens. Tight junctions (TJ), a cell–cell junctional complex located on the apical side of epithelial cells, have a critical role in the maintenance of epithelial barrier function. Impaired...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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Elsevier
2018-01-01
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| Series: | Allergology International |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1323893017301594 |
| _version_ | 1828328779096784896 |
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| author | Ayumi Fukuoka Tomohiro Yoshimoto |
| author_facet | Ayumi Fukuoka Tomohiro Yoshimoto |
| author_sort | Ayumi Fukuoka |
| collection | DOAJ |
| description | Epithelial cells form the first physiological barrier against invasion by pathogens and the infiltration of allergens. Tight junctions (TJ), a cell–cell junctional complex located on the apical side of epithelial cells, have a critical role in the maintenance of epithelial barrier function. Impaired TJ structures are observed in patients with asthma, atopic dermatitis and nasal allergy; therefore, the dysfunction of epithelial barriers might be involved in the initiation or progression of allergic diseases. Protease-containing allergens and environmental pollutants enhance paracellular transport in epithelial cells through disruption of epithelial barrier function. This suggests that the disruption of TJ leads to the promotion of allergen delivery into the subepithelia, resulting in the progression of allergic diseases. Thus, protection of the epithelial barrier function might prevent or inhibit the development or exacerbation of allergic diseases. Recently, we reported that diesel exhaust particles (DEP), the main component of particulate patter 2.5, exacerbated allergic rhinitis (AR) in a mouse model through TJ disruption. In addition, we revealed that the oxidative stress-mediated pathway is involved in the effects caused by DEP and that nasal treatment with a reactive oxygen species (ROS) scavenger suppressed DEP-induced TJ disruption and exacerbation of AR. In this review, we focus on the relationship between TJ disruption and allergic disease. Furthermore, we discuss our recent findings regarding TJ disruption and the exacerbation of AR. |
| first_indexed | 2024-04-13T20:14:48Z |
| format | Article |
| id | doaj.art-b64a871e9f724e1b85f33aa4fcfba754 |
| institution | Directory Open Access Journal |
| issn | 1323-8930 |
| language | English |
| last_indexed | 2024-04-13T20:14:48Z |
| publishDate | 2018-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Allergology International |
| spelling | doaj.art-b64a871e9f724e1b85f33aa4fcfba7542022-12-22T02:31:44ZengElsevierAllergology International1323-89302018-01-01671182310.1016/j.alit.2017.10.006Barrier dysfunction in the nasal allergyAyumi Fukuoka0Tomohiro Yoshimoto1Department of Immunology, Hyogo College of Medicine, Hyogo, JapanDepartment of Immunology, Hyogo College of Medicine, Hyogo, JapanEpithelial cells form the first physiological barrier against invasion by pathogens and the infiltration of allergens. Tight junctions (TJ), a cell–cell junctional complex located on the apical side of epithelial cells, have a critical role in the maintenance of epithelial barrier function. Impaired TJ structures are observed in patients with asthma, atopic dermatitis and nasal allergy; therefore, the dysfunction of epithelial barriers might be involved in the initiation or progression of allergic diseases. Protease-containing allergens and environmental pollutants enhance paracellular transport in epithelial cells through disruption of epithelial barrier function. This suggests that the disruption of TJ leads to the promotion of allergen delivery into the subepithelia, resulting in the progression of allergic diseases. Thus, protection of the epithelial barrier function might prevent or inhibit the development or exacerbation of allergic diseases. Recently, we reported that diesel exhaust particles (DEP), the main component of particulate patter 2.5, exacerbated allergic rhinitis (AR) in a mouse model through TJ disruption. In addition, we revealed that the oxidative stress-mediated pathway is involved in the effects caused by DEP and that nasal treatment with a reactive oxygen species (ROS) scavenger suppressed DEP-induced TJ disruption and exacerbation of AR. In this review, we focus on the relationship between TJ disruption and allergic disease. Furthermore, we discuss our recent findings regarding TJ disruption and the exacerbation of AR.http://www.sciencedirect.com/science/article/pii/S1323893017301594Allergic rhinitisDiesel exhaust particlesNasal epithelial cellsProteaseTight junctions |
| spellingShingle | Ayumi Fukuoka Tomohiro Yoshimoto Barrier dysfunction in the nasal allergy Allergology International Allergic rhinitis Diesel exhaust particles Nasal epithelial cells Protease Tight junctions |
| title | Barrier dysfunction in the nasal allergy |
| title_full | Barrier dysfunction in the nasal allergy |
| title_fullStr | Barrier dysfunction in the nasal allergy |
| title_full_unstemmed | Barrier dysfunction in the nasal allergy |
| title_short | Barrier dysfunction in the nasal allergy |
| title_sort | barrier dysfunction in the nasal allergy |
| topic | Allergic rhinitis Diesel exhaust particles Nasal epithelial cells Protease Tight junctions |
| url | http://www.sciencedirect.com/science/article/pii/S1323893017301594 |
| work_keys_str_mv | AT ayumifukuoka barrierdysfunctioninthenasalallergy AT tomohiroyoshimoto barrierdysfunctioninthenasalallergy |