Figure 2.

The cycle of S. aureus biofilm formation and its impact on skin barrier function in AD. The increased expression of adhesion molecules, epidermal lipid aberrations, and paucity of AMPs predispose AD patients to S. aureus colonization. Initially, planktonic S. aureus cells adhere to the skin surface via microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) and start producing extracellular polymeric substances (EPS), which results in the establishment of a bacterial community associated in the biofilm. The growing biofilm causes hypoxia and the apoptosis of keratinocytes. Once the bacterial quorum is achieved, the Agr system activates the upregulation of virulence factors including proteases and toxins, and the downregulation of colonization and adhesion molecules with the dispersal of biofilm to new locations. Collectively, S. aureus biofilm contributes to the destruction of the epidermal barrier by downregulating EDC proteins and TJ components, and by stimulating Th2-skewing as a result of aberrant innate immune response. FLG—filaggrin; LOR—loricrin.