Abstract |
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. 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 Vbeta subpopulations. Contrary to SEG, however, SEA induced a strong proinflammatory/Th1 response, including TNF-alpha and MIP-1alpha 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.
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Authors | Olivier Dauwalder, Damien Thomas, Tristan Ferry, Anne-Lise Debard, Cédric Badiou, François Vandenesch, Jerome Etienne, Gerard Lina, Guillaume Monneret |
Journal | Journal of leukocyte biology
(J Leukoc Biol)
Vol. 80
Issue 4
Pg. 753-8
(Oct 2006)
ISSN: 0741-5400 [Print] United States |
PMID | 16885504
(Publication Type: Comparative Study, Journal Article)
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Chemical References |
- Antigens, CD
- Antigens, Differentiation, T-Lymphocyte
- CD69 antigen
- Chemokine CCL3
- Chemokine CCL4
- Enterotoxins
- Lectins, C-Type
- Macrophage Inflammatory Proteins
- Superantigens
- Tumor Necrosis Factor-alpha
- enterotoxin G, staphylococcal
- enterotoxin A, Staphylococcal
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Topics |
- Antigens, CD
(biosynthesis, drug effects)
- Antigens, Differentiation, T-Lymphocyte
(biosynthesis, drug effects)
- Chemokine CCL3
- Chemokine CCL4
- Dose-Response Relationship, Drug
- Enterotoxins
(immunology, pharmacology)
- Humans
- Inflammation
(immunology)
- Lectins, C-Type
- Leukocytes, Mononuclear
(drug effects, immunology)
- Macrophage Inflammatory Proteins
(biosynthesis)
- Shock, Septic
(immunology)
- Structure-Activity Relationship
- Superantigens
(immunology, pharmacology)
- T-Lymphocytes
(drug effects, immunology)
- Th1 Cells
(drug effects, immunology)
- Tumor Necrosis Factor-alpha
(biosynthesis, drug effects)
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