Barrier dysfunction in the nasal allergy

Abstract

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.

Blocking histone deacetylase activity as a novel target for epithelial barrier defects in patients with allergic rhinitis

“…Endogenous HDAC activity was significantly greater in ALI cultures of patients compared with control subjects (Fig 1, A). In line with previous publications, 7,32 we observed that TER of ALI cultures of patients was significantly decreased compared with that in healthy control subjects (Fig 1, B). Individual patient data demonstrated that endogenous HDAC activity negatively correlated with TER of both patients and healthy control subjects (Fig 1, C).…”

Associations of greenness, greyness and air pollution exposure with children’s health: a cross-sectional study in Southern Italy

“…Differently from other studies, we found that very low (1st quartile) exposure to greenness measured by NDVI, an objective measure capturing even small-scale green spaces, was associated with a higher risk of self-reported nasal symptoms. We hypothesized that this finding might be ascribed to the lack of mitigation effect of greenness on pollutants from vehicular sources, such as diesel exhaust particles (DEP) recently shown to be involved in the oxidative stress-mediated pathway leading to the dysfunction of epithelial barriers of nasal mucosa [ 41 ]. However, we do underline that these results have to be considered with caution and cannot be generalized since NDVI is not able to identify which, if any, particular vegetation types, pathways of exposure or duration of exposures are present [ 9 ].…”

Aeroallergens, air pollutants, and chronic rhinitis and rhinosinusitis

“… 58 Interestingly, these negative effects of DEP were suppressed by treatment with a reactive oxygen species scavenger. 58 , 59 A second possible mechanism of sinonasal inflammatory disease aggravation is through DEP-mediated induction of pro-inflammatory cytokines. Kim et al 60 stimulated nasal fibroblasts with DEP and performed a cytokine and chemokine array where they found increased levels of interleukin-6 (IL-6) and interleukin-8 (IL-8).…”