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Published online before print August 2, 2006
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Article |
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@
*Université Claude Bernard, INSERM E230, IFR-62, Faculté de Médecine Laennec, Lyon, France; and
Hospices Civils de Lyon, CH Lyon-Sud, and
Hôpital Neurologique, Laboratoire d’Immunologie, Lyon, France
@ To whom correspondence should be addressed. E-mail: guillaume.monneret{at}chu-lyon.fr.
| Abstract |
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The severity of Staphylococcus aureus sepsis is positively associated with staphylococcal enterotoxin A (SEA) and negatively associated with the enterotoxin gene cluster (egc), which encodes five staphylococcal enterotoxins [1]. We postulated that the variable, clinical severity of S. aureus sepsis might be a result of differences in the inflammatory properties of staphylococcal superantigens. We therefore compared the inflammatory properties of SEA with those of staphylococcal entérotoxin G (SEG), a member of the five egc superantigens. We found that SEA and SEG had similar superantigenic properties, as they induced CD69 expression on T lymphocytes and selective expansion of V
subpopulations. Contrary to SEG, however, SEA induced a strong proinflammatory/Th1 response, including TNF-
and MIP-1
production. These results suggest that the association of SEA with the severity of S. aureus septic shock, characterized by a deleterious, inflammatory cascade, may be explained partly by the specific proinflammatory properties of this superantigen.
Key Words: superantigens bacterial cytokines chemokines Staphylococcus aureus
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