Staphylococcal enterotoxin B‐ and lipopolysaccharide‐induced toxic shock syndrome in a burn patient

Author(s):  
Osamu Yamasaki ◽  
Satoru Sugihara ◽  
Ai Kajita ◽  
Emi Yokoyama ◽  
Tomoko Miyake ◽  
...  
2012 ◽  
Vol 287 (30) ◽  
pp. 25203-25215 ◽  
Author(s):  
Hatice Karauzum ◽  
Gang Chen ◽  
Laura Abaandou ◽  
Mahta Mahmoudieh ◽  
Atefeh R. Boroun ◽  
...  

2003 ◽  
Vol 31 (4) ◽  
pp. 373-378 ◽  
Author(s):  
Vladimir Savransky ◽  
Victor Rostapshov ◽  
Dmitriy Pinelis ◽  
Yury Polotsky ◽  
Sergey Korolev ◽  
...  

2010 ◽  
Vol 175 (11) ◽  
pp. 917-922 ◽  
Author(s):  
Teresa Krakauer ◽  
Marilyn Buckley ◽  
Diana Fisher

2005 ◽  
Vol 73 (6) ◽  
pp. 3375-3384 ◽  
Author(s):  
Timur O. Yarovinsky ◽  
Michael P. Mohning ◽  
Mary A. Bradford ◽  
Martha M. Monick ◽  
Gary W. Hunninghake

ABSTRACT Staphylococcal enterotoxin B induces toxic shock and is a major virulence factor of staphylococcal diseases. We examined the effects of systemic adenoviral infection on responses to staphylococcal enterotoxin B in a murine model. We found that adenoviral infection markedly increases the severity of liver injury following exposure to staphylococcal enterotoxin B without d-galactosamine sensitization. In adenovirus-infected mice, staphylococcal enterotoxin B triggered a more profound hypothermia and increased apoptosis in the liver. Consistent with these observations, we also found that adenoviral infection primed for an increased production of gamma interferon in vivo and in vitro following stimulation with staphylococcal enterotoxin B. Gamma-interferon-knockout mice did not show increased sensitivity to staphylococcal enterotoxin B following adenoviral infection. These data suggest that a preexisting viral infection primes mice for subsequent staphylococcal enterotoxin B exposure, possibly via a gamma-interferon-mediated mechanism.


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