Atopic dermatitis: pathogenetic mechanisms, skin barrier function, commensal bacteria and Staphylococcus aureus
Th2/Th1-lymphocytes and Th17/Th22-lymphocytes in acute and chronic illness. The detected skin barrier anomaly, its defense failure, lesser production of commensal bacteria promote skin lesion colonization by opportunistic flora. As of today, there have been published enough papers proving the negative role of the strains of staphylococcus aureus in intensifying local inflammatory responses in AD. A better understanding of the possible pathogenetic mechanisms of the disease will contribute to working out more effective AD treatment techniques.
Key words: atopic dermatitis, staphylococcus aureus, immunity, microbiome, skin.
For citation: Kudryavtseva A.V., Gelezhe K.A., Farber I.M. Atopic dermatitis: pathogenetic mechanisms, skin barrier function, commensal bacteria and Staphylococcus aureus. Vopr. prakt. pediatr. (Clinical Practice in Pediatrics). 2019; 14(4): 51–57. (In Russian).