Dissecting the role of infections in atopic dermatitis.
In patients with atopic dermatitis the skin is highly susceptible to infection by bacteria, fungi and viruses. Increasing knowledge about the complex immune network that regulates anti-microbial responses has helped to dissect further the role of infections in atopic dermatitis. Conserved patterns of microbes are recognized by the innate immune system, which mediates microbicidal activity, either directly or through inflammatory responses. New evidence suggests that components of the innate immune system, such as anti-microbial peptides, humoural lectins, nucleotide-binding oligomerization domain-containing (NOD) proteins, and Toll-like receptors not only protect from microbial invasion, but contribute to skin inflammation in atopic dermatitis. In addition, atopic patients tend to develop Th2-dominated immune responses that weaken anti-microbial immunity. This impairment of an appropriate anti-microbial defence compounded by amplified microbe-driven innate and adaptive immune responses leads to the vicious circle of skin inflammation. New microbial management in atopic dermatitis will foster a well-balanced microbial flora, which establishes natural defence mechanisms to maintain immuno-surveillance of the skin. In addition to anti-microbial therapies, other innate immune stimuli may suppress pro-inflammatory signals and help to break the vicious circle of cutaneous inflammation. To elucidate further these different interactions of the skin immune system and microbes in atopic dermatitis, clinical studies and further efforts in basic research are needed.
Biedermann
Tilo
T
Department of Dermatology, Eberhard Karls University Tuebingen, Germany. tilo.biedermann@med.uni-tuebingen.de
D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D023181:Antimicrobial Cationic Peptides / Q000276:immunology; D001424:Bacterial Infections / Q000188:drug therapy / Q000276:immunology*; D003876:Dermatitis, Atopic / Q000188:drug therapy / Q000276:immunology*; D004198:Disease Susceptibility; D006801:Humans; D007113:Immunity, Innate; D018418:Th2 Cells / Q000276:immunology; D051193:Toll-Like Receptors / Q000276:immunology
D000900:Anti-Bacterial Agents; D023181:Antimicrobial Cationic Peptides; D051193:Toll-Like Receptors