Protective effect ofAquaphilus dolomiaeextract-G1, ADE-G1, on tight junction barrier function in aStaphylococcus aureus-infected atopic dermatitis model

Background Atopic dermatitis (AD) is a common skin disease characterized by recurrent pruritic inflammatory skin lesions and defects of the skin barrier. Bacterial infection withStaphylococcus aureuscontributes to increased severity of AD by compromising the barrier further. A microorganism component of Avene Thermal Spring Water,Aquaphilus dolomiae, is thought to contribute to some of its beneficial effects to skin, eg AD alleviation. Aims Here, we have investigated the effects of an extract ofA. dolomiae,A. dolomiaeextract-G1 (ADE-G1), on the structural barrier function of keratinocytes, tight junction (TJ) protein expression and the expression of several genes altered in AD patients. Methods An epidermal cell culture model mimicking the AD environment and phenotype was used, in whichS. aureus-infected cell cultures of normal human epidermal keratinocytes were exposed to a proinflammatory environment. Endpoints measured included the transepithelial electrical resistance (TER) and immunohistological staining of the epidermal TJ proteins, claudin and occludin. Additional analysis was made of several genes known to be differentially regulated in skin from AD patients (C-C motif chemokine ligand 20 (CCL20), interleukin-8 (IL-8), S100 calcium binding protein A7 (S100A7), defensin beta 4 (DEFB4) and filaggrin). Results Aquaphilus dolomiaeextract-G1 strongly increased TER in non-infected cells and provided protection against infection by overcoming the decrease in TER induced by the infection withS. aureus. In infected cells exposed to a pro-inflammatory environment - depicting AD-like conditions - TER protection by ADE-G1 was still observed. Gene expression analysis of infected and pro-inflammatory stimulated cells indicated that ADE-G1 modulated the inflammatory response (induced IL-8 and attenuated CCL20 expression), increased antimicrobial activities (induced DEFB4 and A100A7) and strengthened barrier function (restored filaggrin expression). Conclusions ADE-G1 reinforces barrier function and strongly protects TJ barrier disruption induced by bacterial infection and inflammation.