barrier and immune systems.10-12,18 Primary (eg, genetic) barrier defects are coupled with secondary defects due to inflammation affecting expression and activity of proteases, lipids, and structural proteins.5,10-12,18 When comparing healthy skin to ADaffected skin, features such as hyperkeratosis, edema, and an increased number in and activity of immune cells are observed.12 The immune response could be a primary feature of AD itself or a response to allergens penetrating the leaky skin barrier.5,6,12,14,18 Also, skin pH values are higher in patients with active AD lesions than in asymptomatic individuals18,19; the elevated level of skin pH can be expected to delay barrier recovery and facilitate barrier breakdown.18
Antimicrobial Defense
S. aureus microbial colonization and invasion are thought to play a critical role in the development of AD.20-23 In a defective skin barrier, the reduced levels of NMF lead to a decreased ability of the corneocytes to hold water with a concomitantly elevated surface skin pH.6 The elevated pH favors serine protease activity and inhibits enzymes involved in the synthesis of lipid lamellae, weakening the skin’s defense mechanism against pathogens.6,20-23 Many microorganisms such as S. aureus and Streptococcus pyogenes (S. pyogenes) are inhibited by the skin’s acid pH, which also regulates the activity of antimicrobial peptides.20-23 The elevated level of skin pH can be expected to delay barrier recovery, further facilitating skin barrier breakdown.18 Additionally, the skin cannot retain sufficient water, which leads to dry skin and the “itch, scratch, damaged skin, and inflammation cycle” (Figure 3).4 Moreover, mechanical damage to the skin due to scratching enables pathogens to penetrate and to enhance inflammation. 4,22,23
Statement 7: Many available soaps and cleansers have a high pH, which potentially disrupt the skin barrier.
A defective skin barrier can be triggered by genetic and environmental factors such as a ‘western’ lifestyle, frequent bathing,
Antimicrobial Defense
S. aureus microbial colonization and invasion are thought to play a critical role in the development of AD.20-23 In a defective skin barrier, the reduced levels of NMF lead to a decreased ability of the corneocytes to hold water with a concomitantly elevated surface skin pH.6 The elevated pH favors serine protease activity and inhibits enzymes involved in the synthesis of lipid lamellae, weakening the skin’s defense mechanism against pathogens.6,20-23 Many microorganisms such as S. aureus and Streptococcus pyogenes (S. pyogenes) are inhibited by the skin’s acid pH, which also regulates the activity of antimicrobial peptides.20-23 The elevated level of skin pH can be expected to delay barrier recovery, further facilitating skin barrier breakdown.18 Additionally, the skin cannot retain sufficient water, which leads to dry skin and the “itch, scratch, damaged skin, and inflammation cycle” (Figure 3).4 Moreover, mechanical damage to the skin due to scratching enables pathogens to penetrate and to enhance inflammation. 4,22,23
Statement 7: Many available soaps and cleansers have a high pH, which potentially disrupt the skin barrier.
A defective skin barrier can be triggered by genetic and environmental factors such as a ‘western’ lifestyle, frequent bathing,
