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Filaggrin Mutations, Skin Barrier Dysfunction, and Sensitization in Allergic Rhinitis

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Filaggrin

Abstract

Allergic rhinitis (AR) is a common disorder with an estimated prevalence of 20,000 per 100,000 Europeans. Classical clinical signs include sneezing, coughing, and itchy and runny nose and eyes, which may be accompanied by more severe symptoms such as headaches, fatigue, and cognitive impairment.

AR occurs in the context of the atopic syndrome, and it is assumed that it is a part of the atopic march, in which asthma and AR follow atopic dermatitis (AD). Until now, little is known about the genetics of AR. However, from the literature, it is obvious that individuals with AD and filaggrin gene (FLG) mutations are at higher risk of developing AR.

Filaggrin is an important protein of the epidermal barrier, and impairment of this protein causes increased risk of irritation, inflammation, and sensitization. Therefore, it is considered that the association between FLG mutations and AR in the context of AD is caused by cutaneous sensitization to pollen, house dust mite, and cat dander followed by secondary systemic allergies. The concept of cutaneous sensitization to aeroallergens is demonstrated by the mechanism of atopy patch tests in which aeroallergens are patch tested on the skin and can cause eczematous reactions.

Cutaneous sensitization and consequential systemic allergies in the context of allergic rhinitis could be inhibited by creating oral tolerance through the administration of small amounts of allergens to an unsensitized individual at a young age. Besides, the epithelial barrier has to be restored with topical emollients to prevent irritation and inflammation.

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Correspondence to Marie-Louise A. Schuttelaar MD, PhD .

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Vogel, T.A., Schuttelaar, ML.A. (2014). Filaggrin Mutations, Skin Barrier Dysfunction, and Sensitization in Allergic Rhinitis. In: Thyssen, J., Maibach, H. (eds) Filaggrin. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-54379-1_18

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