| Abstrakt: |
The article is devoted to atopic dermatitis, which is a chronic skin disease that significantly affects the quality of life of children and their relatives. The incidence of atopic dermatitis is constantly increasing. The development of the disease is accompanied by significant changes in the composition of skin microbiome. The adequate commensal colonization prevents invasion of pathogens. Furthermore, epithelial cells produce antimicrobial proteins (human ß-defensin-1, -2 and -3, cathelicidin LL-37, ribonuclease 7) that directly kill or inhibit the growth of the pathogens. Patients with atopic dermatitis have impaired skin immunity. It manifests in a decrease of T-cells cytokines (IL-4 and IL-13), high sensitivity to alpha-toxin-induced cell death, decreased level of lamellar bodies and acid sphingomyelinase, suppressed filaggrin expression, contributing to a high level of Staphylococcus aur eus skin colonization. S. aureus secretes a variety of pathogenicity factors that facilitate its persistence on the infected skin. Staphylococcal enterotoxins A, B, C and toxic shock syndrome toxin also play the role of superantigens, which increase inflammation by a massive release of proinflammatory cytokines, including TNF-a and IL-1ß. Affected by S. aureus superantigens regulatory T-cells lose their immunosuppressive activity. Moreover, enterotoxins act like a new group of allergens provoking IgE inflammation. S.aureus pathogenicity is enhanced by the ability to form biofilms. Thus, impaired skin immunity function, decrease of commensals and increase growth of S. aureus play an essential role in the development of skin inflammation in atopic dermatitis and should be considered as the main reference points in the study of the disease in the futur e. [ABSTRACT FROM AUTHOR] |
