TY - JOUR
T1 - Staphylococcal exfoliative toxins
T2 - "Molecular scissors" of bacteria that attack the cutaneous defense barrier in mammals
AU - Nishifuji, Koji
AU - Sugai, Motoyuki
AU - Amagai, Masayuki
N1 - Funding Information:
The authors thank Dr. Takayuki Yamaguchi for his invaluable contribution to this work and for his unpublished data, introduced in this article. Our work was supported by Grants-In-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (to KN, MS and MA) and a Research Fellowship of the Japan Society for the Promotion of Science for Young Scientists (to KN).
PY - 2008/1
Y1 - 2008/1
N2 - 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.
AB - 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.
KW - Desmoglein
KW - Exfoliative toxin
KW - Exudative epidermitis
KW - Impetigo
KW - Staphylococcal scalded-skin syndrome
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UR - http://www.scopus.com/inward/citedby.url?scp=36849014403&partnerID=8YFLogxK
U2 - 10.1016/j.jdermsci.2007.05.007
DO - 10.1016/j.jdermsci.2007.05.007
M3 - Review article
C2 - 17582744
AN - SCOPUS:36849014403
VL - 49
SP - 21
EP - 31
JO - Journal of Dermatological Science
JF - Journal of Dermatological Science
SN - 0923-1811
IS - 1
ER -