Keratinocytes as sensors and central players in the immune defense against Staphylococcus aureus in the skin. Issue 3 (September 2017)

• Record Type: Journal Article
• Authors: Bitschar, Katharina; Wolz, Christiane; Krismer, Bernhard; Peschel, Andreas; Schittek, Birgit
• Is Part Of: Journal of dermatological science. Volume 87:Issue 3(2017:Sep.)
• Page Start: 215
• Page End: 220
• Publication Date: 2017-09
• Subjects: AMP antimicrobial peptides -- AD atopic dermatitis -- ECM extracellular matrix -- FPR2 formyl-peptide receptor 2 -- HMGB1 High-Mobility-Group-Box 1 -- LPP lipopeptides -- MAMP microbe-associated molecular pattern -- MyD88 myeloid differentiation factor 88 -- NRF2 nuclear factor erythroid 2–related factor 2 -- ROS reactive oxygen species -- RTK receptor-tyrosine kinase -- TLR toll-like receptors -- PSM phenol-soluble modulins; Keratinocytes -- Skin -- Staphylococcus aureus -- Atopic dermatitis -- Immune response; Dermatology -- Periodicals; Skin Diseases -- Periodicals; Dermatologie -- Périodiques; 616.5005
• DOI: 10.1016/j.jdermsci.2017.06.003
• Languages: English
• ISSNs: 0923-1811

Abstract

Abstract: Healthy human skin provides an effective mechanical as well as immunologic barrier against pathogenic microorganisms with keratinocytes as the main cell type in the epidermis actively participating and orchestrating the innate immune response of the skin. As constituent of the outermost layer encountering potential pathogens they have to sense signals from the environment and must be able to initiate a differential immune response to harmless commensals and harmful pathogens. Staphylococci are among the most abundant colonizers of the skin: Whereas Staphylococcus epidermidis is part of the skin microbiota and ubiquitously colonizes human skin, Staphylococcus aureus is only rarely found on healthy human skin, but frequently colonizes the skin of atopic dermatitis (AD) patients. This review highlights recent advances in understanding how keratinocytes as sessile innate immune cells orchestrate an effective defense against S. aureus in healthy skin and the mechanisms leading to an impaired keratinocyte function in AD patients.