Journal
JOURNAL OF DERMATOLOGICAL SCIENCE
Volume 49, Issue 1, Pages 21-31Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jdermsci.2007.05.007
Keywords
impetigo; staphylococcal scalded-skin syndrome; exfoliative toxin; desmoglein; exudative epidermitis
Categories
Ask authors/readers for more resources
Bullous impetigo and its generalized form, staphylococcal scalded-skin syndrome (SSSS), are highly contagious, blistering skin diseases caused by Staphylococcus aureus infection. Virulent strains of the bacteria produce exfoliative toxins (ETs) that cause the loss of keratinocyte cell-cell adhesion in the superficial epidermis. Recent studies have indicated that the three isoforms of ETs, i.e., ETA, ETB, and ETD, are glutamate-specific serine proteases that specifically and efficiently cleave a single peptide bond in the extracellular region of human and mouse desmoglein 1 (Dsg1), a desmosomal intercellular adhesion molecule. In addition, four isoforms of S. hyicus exfoliative toxin, ExhA, ExhB, ExhC, and ExhD, cleave swine Dsg1, resulting in skin exfoliation similar to that observed in pigs with exudative epidermitis. In this review, we describe recent advances in our knowledge of the mechanisms of action of staphylococcal exfoliative toxins, which act as molecular scissors to facilitate percutaneous bacterial. invasion of mammalian skin by cleavage of keratinocyte cell-cell adhesion molecules. The species-specificity of staphylococcal exfoliative toxins to cleave Dsg1 in certain mammalian species is discussed. (C) 2007 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available