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Nasal epithelial barrier dysfunction increases sensitization and mast cell degranulation in the absence of allergic inflammation

机译：在没有过敏性炎症的情况下，鼻上皮屏障功能障碍增加了敏化和肥大细胞脱粒

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Abstract Background Increased epithelial permeability has been reported in allergic rhinitis, with histamine and type‐2 inflammation being responsible for tight junction dysfunction. The impact of an epithelial barrier defect on allergic sensitization and mast cell (MC) degranulation remains speculative. Methods Transepithelial passage of allergens was evaluated on primary human nasal epithelial cell cultures. Active sensitization was attempted by repeated intranasal ovalbumin (OVA) applications in Na?ve mice. In a passive sensitization model, mice were injected with IgE to Dermatophagoides pteronyssinus (r Der p )2 and then exposed intranasally to the allergen. Chitosan was used to disrupt nasal epithelial integrity in vitro and in vivo . Results Chitosan strongly reduced transepithelial electrical resistance and facilitated transepithelial allergen passage in cultured primary nasal epithelial cells. In vivo , intranasal chitosan affected occludin expression and facilitated allergen passage. After epithelial barrier disruption, intranasal OVA application induced higher OVA‐specific IgG1 and total IgE in serum, and increased eosinophilia and interleukin‐5 in bronchoalveolar lavage (BAL) compared to sham‐OVA mice. Chitosan exposure, prior to r Der p 2 allergen challenge in passively sensitized mice, resulted in increased β‐hexosaminidase levels in serum and BAL compared to sham‐r Der p 2 mice. Intranasal treatment with the synthetic glucocorticoid fluticasone propionate prevented chitosan‐induced barrier dysfunction, allergic sensitization, and MC degranulation. Conclusion Epithelial barrier dysfunction facilitates transepithelial allergen passage, allergic sensitization, and allergen‐induced MC degranulation even in the absence of inflammatory environment. These results emphasize the crucial role of an intact epithelial barrier in prevention of allergy.
机译：抽象背景增加上皮通透性有报道在过敏性鼻炎，组胺和2型炎症负责紧密连接功能障碍。关于变应性致敏和肥大细胞（MC）的脱颗粒上皮屏障缺陷的影响仍然推测性的。变应原的方法跨上皮通道上的原代人鼻粘膜上皮细胞培养物进行了评价。主动致敏通过反复娜鼻内卵清蛋白（OVA）应用程序试图？实验的小鼠。在一个被动致敏模型中，小鼠与IgE注入屋尘螨（R的Der p）2，然后经鼻内暴露于变应原。脱乙酰壳多糖用于破坏在体外和体内鼻上皮的完整性。结果壳聚糖强烈降低的经上皮电阻和促进跨上皮过敏原通道在培养的原代鼻上皮细胞。在体内，鼻内壳聚糖影响闭合蛋白表达和促进过敏原的通道。上皮屏障破坏后，鼻内OVA诱导应用OVA特异性更高IgG1和总IgE血清，并与假-OVA小鼠支气管肺泡灌洗（BAL）增加嗜酸性粒细胞和白细胞介素-5。脱乙酰壳多糖接触，前至r的Der p过敏原2在被动致敏小鼠的挑战，导致血清和BAL增加β氨基己糖苷酶水平相比于假-R的Der p 2小鼠。与合成的糖皮质激素丙酸氟替卡松防止脱乙酰壳多糖诱导屏障功能障碍治疗鼻内，变应性致敏和MC脱粒。结论上皮屏障功能障碍功能有助于跨上皮过敏原通道，变应性致敏，和过敏原诱导的MC的脱颗粒甚至在没有炎症的环境。这些结果强调在预防过敏的完整上皮屏障的重要作用。

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