THE ROLE OF FILAGGRIN IN THE FORMATION OF SKIN BARRIER DYSFUNCTION

Abstract

Dysfunction of the epidermal barrier plays an important role in the development of skin inflammatory processes. Pathological changes in the intracellular composition of keratinocytes are an integral part of the modern understanding of the pathogenesis of atopic dermatitis (AD). One of the significant proteins involved in the formation of the skin barrier is filaggrin (FLG). The purpose of our review is to summarize the available data on the role of FLG in the formation of skin barrier dysfunction in AD. Material and methods. An analysis of domestic sources was carried out using the scientific electronic libraries Cyberleninka and Elibrary, and foreign sources using the PubMed/Medline databases. Results. Excessive accumulation of FLG monomers in keratinocytes during skin barrier dysfunction induces premature cell death. Intracellular vesicles/exosomes remove FLG from keratinocytes for further transport through the bloodstream. Staphylococcus aureus is able to influence intracellular vesicles, enhancing FLG transport. More than 140 variants of FLG gene mutations are known, leading to a deficiency of the protective skin protein. In AD there is an increased level of FLG in the blood serum. The level of FLG increases with the severity of the skin inflammatory process. Pregnant women with AD have higher serum FLG levels compared to nonpregnant women with AD, healthy pregnant women, and nonpregnant women. Conclusion. FLG plays a significant role in maintaining the skin barrier function. Pronounced changes in the level of FLG in the blood serum in AD allow us to consider FLG as a biomarker of exacerbation of this disease. Given the transport of FLG into the blood, further in-depth study of the role of FLG in localizations distant from the skin is necessary.