title: Comparative inflammatory properties of staphylococcal superantigenic enterotoxins SEA and SEG: implications for septic shock.
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.
authors.affiliation: Université Claude Bernard, INSERM E230, IFR-62, Lyon, France.
authors.forename: Olivier
authors.initials: O
authors.lastname: Dauwalder
authors.forename: Damien
authors.initials: D
authors.lastname: Thomas
authors.forename: Tristan
authors.initials: T
authors.lastname: Ferry
authors.forename: Anne-Lise
authors.initials: AL
authors.lastname: Debard
authors.forename: Cédric
authors.initials: C
authors.lastname: Badiou
authors.forename: François
authors.initials: F
authors.lastname: Vandenesch
authors.forename: Jerome
authors.initials: J
authors.lastname: Etienne
authors.forename: Gerard
authors.initials: G
authors.lastname: Lina
authors.forename: Guillaume
authors.initials: G
authors.lastname: Monneret
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis / Q000187:drug effects; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis / Q000187:drug effects; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D004305:Dose-Response Relationship, Drug; D004768:Enterotoxins / Q000276:immunology* / Q000494:pharmacology; D006801:Humans; D007249:Inflammation / Q000276:immunology; D037181:Lectins, C-Type; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis; D012772:Shock, Septic / Q000276:immunology*; D013329:Structure-Activity Relationship; D018089:Superantigens / Q000276:immunology* / Q000494:pharmacology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000187:drug effects; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D004768:Enterotoxins; D037181:Lectins, C-Type; D019402:Macrophage Inflammatory Proteins; D018089:Superantigens; D014409:Tumor Necrosis Factor-alpha; D000099192:CD69 Antigens; C419397:enterotoxin G, staphylococcal; C026066:enterotoxin A, Staphylococcal