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Staphylococcal scalded skin syndrome: exfoliative toxin A (ETA) induces serine protease activity when combined with A431 cells
Author(s) -
Ladhani S,
Poston SM,
Joannou CL,
Evans RW
Publication year - 1999
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1999.tb00042.x
Subject(s) - proteases , staphylococcal scalded skin syndrome , serine protease , protease , staphylococcus aureus , serine , microbiology and biotechnology , medicine , biology , biochemistry , enzyme , bacteria , genetics
Staphylococcal scalded skin syndrome is the term used for a spectrum of primarily neonatal blistering skin diseases caused by the exfoliative toxins, ETA and ETB, of Staphylococcus aureus. Despite 25 y of research, the toxins' mechanism of action is still poorly understood, although evidence suggests that they may act as serine proteases. In this study, 0.1 mg purified ETA isolated from a baby with pemphigus neonatorum was incubated with A431 cells (a human squamous cell line) at 37 ˚ C for 8, 24 and 48 h and the supernatant tested for protease activity using azocasein as a non‐specific substrate. Phosphate‐buffered saline was also incubated as negative control. Incubation of ETA with A431 cells for 48 h resulted in a four‐fold increase in supernatant azocaseinolytic activity compared with buffer and cells, ETA alone and buffer alone ( p < 0.001). Furthermore, this proteolytic activity was inhibited by PMSF ( p