Reduced occludin and claudin-7 expression is associated with urban locations and exposure to second-hand smoke in allergic rhinitis patients

Abstract

The breakdown of nasal epithelial barrier occurs in allergic rhinitis (AR) patients. Impairment of cell junction molecules including tight junctions (TJs) and desmosomes plays causative roles in the pathogenesis of AR. In this study, we investigated the transcript expression levels of TJs including occludin (OCLN), claudin-3 and -7 (CLDN3 and CLDN7), desmoglein 3 (DSG3) and thymic stromal lymphopoietin (TSLP) in AR patients (n = 30) and non-allergic controls (n = 30). Nasal epithelial cells of non-allergic controls and AR patients were collected to examine their mRNA expression levels, and to correlate with clinico-demographical and environmental parameters. We demonstrated that the expression of OCLN (p = 0.009), CLDN3 (p = 0.032) or CLDN7 (p = 0.004) transcript was significantly lower in AR patients compared with non-allergic controls. No significant difference was observed in the expression of DSG3 (p = 0.750) or TSLP (p = 0.991) transcript in AR patients compared with non-allergic controls. A significant association between urban locations and lower OCLN expression (p = 0.010), or exposure to second-hand smoke with lower CLDN7 expression (p = 0.042) was found in AR patients. Interestingly, none of the TJs expression was significantly associated with having pets, frequency of changing bedsheet and housekeeping. These results suggest that defective nasal epithelial barrier in AR patients is attributable to reduced expression of OCLN and CLDN7 associated with urban locations and exposure to second-hand smoke, supporting recent findings that air pollution represents one of the causes of AR.

Higher Wheal Sizes of Dermatophagoides farinae Sensitization Exhibit Worse Nasal Symptoms in Allergic Rhinitis Patients

“…We acknowledge the limitations of the study as follows: (1) Small sample size; (2) Sample size calculation had been conducted previously according to past gene expression studies, but not studies pertaining to SPT wheal sizes in AR patients, as this study was part of our previously published cross-sectional gene expression study (23); (3) Lack of correlation studies with other symptom questionnaires such as the total nasal symptom score (TNSS) (44)(45)(46), or with the levels of total and specific IgE. Future investigations addressing these limitations are thus recommended.…”

Nasal Epithelial Barrier Integrity and Tight Junctions Disruption in Allergic Rhinitis: Overview and Pathogenic Insights

“…Previous studies have shown the defect in epithelial barrier due to decreased expression of CLDNs that contribute to AR in both patients and animal models. Recently, we demonstrated a decreased expression of CLDN3 and CLDN7 in nasal epithelial cells (NECs) of HDM-induced AR patients compared to nonallergic controls (34). CLDN1, CLDN3, CLDN7 and CLDN12 mRNA and protein expressions were significantly decreased in nasal epithelium of AR patients compared to controls subject (32).…”

“…Nasal epithelial barrier function has been known to be impaired in HDM-induced AR patients (33). Lower OCLN mRNA expression also occurred in HDM-induced AR patients compared to non-allergic controls (33,34). Moreover, reduced ordered arrangement of OCLN was found in AR patients and the defect might expedite the passage of allergens and environmental pro-inflammatory agents through nasal epithelial barrier (33).…”

“…Environmental factors such as urban locations, air pollutants and presence of airborne allergens play contributive roles to the disruption of TJs in AR. We recently demonstrated that OCLN and CLDN7 mRNA expressions were significantly reduced in AR patients sensitized to HDMs compared with non-allergic controls, and lower OCLN or CLDN7 expression was associated with urban locations or exposure to second-hand smoke, respectively (34). This is comparable with recent findings that air pollution represents a risk factor for AR onset whereby epithelial barrier can be negatively affected by air pollutant such as diesel exhaust particles (DEPs) and fine particulate matter ≤2.5 mm (PM2.5) causing sinonasal diseases (38)(39)(40)(41).…”

Priorities in Management of Children with Bronchial Obstruction Associated with Acute Respiratory Viral Infection: What’s New?

“…Оказалось, что некоторые респираторные вирусы способны сдвигать баланс иммунной системы человека в сторону Th2-ответа, что может стать одним из факторов риска развития и/или обострения бронхиальной астмы. Чаще всего этот феномен наблюдается у детей с частыми (более 6 раз в год) респираторными инфекциями, при инфицировании риновирусами и респираторно-синтициальными вирусами [11,12].…”