The staphylococcal alpha-toxin and leukotoxins

Author(s):  
Gilles Prévost ◽  
Mira Y. Tawk ◽  
Gaëlle Zimmermann-Meisse ◽  
Emmanuel Jover
Keyword(s):  
2016 ◽  
Vol 1 (3) ◽  
pp. 0-0
Author(s):  
Amin Rostami ◽  
Fatemeh Goshadrou ◽  
Gholamreza Ahmadian

1992 ◽  
Vol 24 ◽  
pp. 36
Author(s):  
Cornelis van Breemen ◽  
Junji Nishimura ◽  
Suzanne Moreland ◽  
Robert S. Moreland

1993 ◽  
Vol 10 (3) ◽  
pp. 627-634 ◽  
Author(s):  
J. Ballard ◽  
Y. Sokolov ◽  
W.-L. Yuan ◽  
B. L. Kagan ◽  
R. K. Tweten

2002 ◽  
Vol 184 (7) ◽  
pp. 2034-2038 ◽  
Author(s):  
Milena M. Awad ◽  
Julian I. Rood

ABSTRACT The pathogenesis of Clostridium perfringens-mediated gas gangrene or clostridial myonecrosis involves the extracellular toxins alpha-toxin and perfringolysin O. Previous studies (T. Shimizu, A. Okabe, J. Minami, and H. Hayashi, Infect. Immun. 59:137-142, 1991) carried out with Escherichia coli suggested that the perfringolysin O structural gene, pfoA, was positively regulated by the product of the upstream pfoR gene. In an attempt to confirm this hypothesis in C. perfringens, a pfoR-pfoA deletion mutant was complemented with isogenic pfoA+ shuttle plasmids that varied only in their ability to encode an intact pfoR gene. No difference in the ability to produce perfringolysin O was observed for C. perfringens strains carrying these plasmids. In addition, chromosomal pfoR mutants were constructed by homologous recombination in C. perfringens. Again no difference in perfringolysin O activity was observed. Since it was not possible to alter perfringolysin O expression by mutation of pfoR, it was concluded that the pfoR gene product is unlikely to have a role in the regulation of pfoA expression in C. perfringens.


2001 ◽  
Vol 45 (3) ◽  
pp. 724 ◽  
Author(s):  
B. T. Heier ◽  
A. Lovland ◽  
K. B. Soleim ◽  
M. Kaldhusal ◽  
J. Jarp

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