Prognostic usefulness of lymphocyte V β receptor determination in toxic shock syndrome

Ohashi, Reiko; Takaya, Junji; Tsuji, Shoji; Yamato, Fumiko; Hasui, Masafumi; Kinoshita, Yoh; Kobayashi, Yohnosuke

doi:10.1007/s00431-005-1711-2

Cited by 4 publications

(4 citation statements)

References 5 publications

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“…However, TSS is rare in France, with only one case per 10 6 inhabitants per year. Also, markers of T‐cell activation, e.g., CD45RO, used in neonatal TSS‐like exanthematous disease or in some TSS cases associated with TSST‐1 production [14,34], were not employed. Activation of an expanded Vβ subset may provide indications of superantigen production, and may be useful for distinguishing expansion caused by superantigen toxins from relative expansion caused by age‐related changes in the T‐cell repertoire or proliferative disorders, e.g., myeloma, myelodysplasic syndromes and T‐cell lymphoproliferation [41,42].…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown previously that the in‐vivo Vβ signature of superantigenic toxins can be used to confirm a diagnosis of TSS [13,14]; indeed, expansion of Vβ 2 T‐cells, which corresponds to TSST‐1 superantigenic activity, has been detected in patients with TSS [13–15]. Selective expansion of Vβ T‐cells has not yet been investigated in patients with enterotoxin‐associated non‐menstrual TSS or in patients with S. aureus septic shock.…”

Section: Introductionmentioning

confidence: 99%

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Analysis of superantigenic toxin Vβ T-cell signatures produced during cases of staphylococcal toxic shock syndrome and septic shock

Ferry

Thomas

Perpoint

et al. 2008

Clinical Microbiology and Infection

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Most clinical isolates of Staphylococcus aureus harbour genes encoding superantigenic toxins that bind the Vbeta domain of T-cells, but little information is available concerning superantigenic toxin production during staphylococcal toxic shock syndrome (TSS) and septic shock. This prospective study investigated 14 patients with staphylococcal TSS or septic shock; the toxin gene profile of each isolate was determined and flow-cytometry was used to identify the discriminant Vbeta signature (DVbetaS) of each superantigenic toxin in vitro. Attempts were also made to identify in-vivo production of superantigenic toxin DVbetaS in patients' blood. The DVbetaS identified in vitro were: toxic shock syndrome toxin (TSST)-1, Vbeta 2; staphylococcal enterotoxin (SE), Vbeta 9, Vbeta 22; SEB, Vbeta 3, Vbeta 14, Vbeta 17; SED, Vbeta 1, Vbeta 8; egc, Vbeta 5.3, Vbeta 7.1, Vbeta 9, Vbeta 23; and SElK, Vbeta 5.1. The DVbetaS of TSST-1 and SEB were detected in patients with menstrual and non-menstrual TSS, respectively, whereas no Vbeta signature was detected during septic shock. All patients with septic shock (but only one patient with TSS) had lymphopenia and/or impaired cellular immunity. Detection of a superantigenic toxin DVbetaS may help to show which toxin is produced during staphylococcal TSS, thus confirming the diagnosis and hastening the administration of anti-toxin therapy. In contrast, this approach failed to demonstrate superantigenic toxin involvement in cases of septic shock. In this latter condition, a superantigenic toxin may not be produced by S. aureus, or its production may occur without expansion of targeted T-cells because of T-cell apoptosis and/or anergy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Analysis of superantigenic toxin Vβ T-cell signatures produced during cases of staphylococcal toxic shock syndrome and septic shock

Ferry

Thomas

Perpoint

et al. 2008

Clinical Microbiology and Infection

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“…macrophages plus monocytes) and T cells [96,97]. These toxins each bind a distinct repertoire of V -bearing T-cells, thus revealing a unique biological "fingerprint" useful for confirming a diagnosis of TSS [98,99]. One very unusual exception has been noted, as SEH evidently stimulates T cells in a V -specific mode [100].…”

Section: Binding Of Ses and Tsst-1 To Target Cellsmentioning

confidence: 99%

Staphylococcus aureus: The Toxic Presence of a Pathogen Extraordinaire

Larkin¹,

Carman²,

Krakauer³

et al. 2009

CMC

123

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Staphylococcus aureus is a facultative, Gram-positive coccus well known for its disease-causing capabilities. In particular, methicillin and vancomycin resistant strains of S. aureus (MRSA and VRSA, respectively) isolated globally represent daunting medical challenges for the 21(st) Century. This bacterium causes numerous illnesses in humans such as food poisoning, skin infections, osteomyelitis, endocarditis, pneumonia, enterocolitis, toxic shock, and autoimmune disorders. A few of the many virulence factors attributed to S. aureus include antibiotic resistance, capsule, coagulase, lipase, hyaluronidase, protein A, fibronectin-binding protein, and multiple toxins with diverse activities. One family of protein toxins is the staphylococcal enterotoxins (SEs) and related toxic shock syndrome toxin-1 (TSST-1) that act as superantigens. There are more than twenty different SEs described to date with varying amino acid sequences, common conformations, and similar biological effects. By definition, very low (picomolar) concentrations of these superantigenic toxins activate specific T-cell subsets after binding to major histocompatibility complex class II. Activated T-cells vigorously proliferate and release proinflammatory cytokines plus chemokines that can elicit fever, hypotension, and other ailments which include a potentially lethal shock. In vitro and in vivo models are available for studying the SEs and TSST-1, thus providing important tools for understanding modes of action and subsequently countering these toxins via experimental vaccines or therapeutics. This review succinctly presents the pathogenic ways of S. aureus, with a toxic twist. There will be a particular focus upon the biological and biochemical properties of, plus current neutralization strategies targeting, staphylcoccocal superantigens like the SEs and TSST-1.

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“…As SAgs are active at very low concentrations (less than 1 pg/ml) (44), which are barely detectable in vivo, SAg-related diseases might theoretically be identified by determining TCR V␤ specificities in vitro. For example, an expansion of V␤2 T cells on the one hand and of V␤3, -14, and -17 T cells on the other hand, which correspond to TSST-1 and SEB superantigenic activities, respectively, has been detected in patients with TSS (6,10,25,29). Such an approach would be particularly useful for investigating suspected SAg-related diseases, including some inflammatory disorders, Kawasaki disease, and atopy (11).…”

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confidence: 99%

Staphylococcus aureusSuperantigens Elicit Redundant and Extensive Human Vβ Patterns

et al. 2009

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Staphylococcus aureus can produce a wide variety of exotoxins, including toxic shock syndrome toxin 1 (TSST-1), staphylococcal enterotoxins, and staphylococcal enterotoxin-like toxins. These toxins share superantigenic activity. To investigate the ␤ chain (V␤) specificities of each of these toxins, TSST-1 and all known S. aureus enterotoxins and enterotoxin-like toxins were produced as recombinant proteins and tested for their ability to induce the selective in vitro expansion of human T cells bearing particular V␤ T-cell receptors (TCR). Although redundancies were observed between the toxins and the V␤ populations, each toxin induced the expansion of distinct V␤ subsets, including enterotoxin H and enterotoxin-like toxin J. Surprisingly, the V␤ signatures were not associated with a specific phylogenic group of toxins. Interestingly, each human V␤ analyzed in this study was stimulated by at least one staphylococcal superantigen, suggesting that the bacterium derives a selective advantage from targeting the entire human TCR V␤ panel.Staphylococcus aureus produces a broad range of exoproteins, including staphylococcal enterotoxins (SEs) and toxic shock syndrome toxin 1 (TSST-1) (9). These toxins were initially implicated in staphylococcal food poisoning (SEs) and TSS (TSST-1) (39). Since the first characterization of SEA and SEB in 1959 to 1960 by Casman and Bergdoll, 18 different SEs have been described; they are designated SEA to SEV, in the chronological order of their discovery (2,5,41). Some were renamed SE-like toxins (SEl), because either no emetic properties were detected or because they were not tested in primate models (21, 41).SEs, SEls, and TSST-1 share certain structural and biological properties. They have similar sizes (23 to 29 kDa), and their crystal structures, established for SEA, SEB, SEC, SED, SEH, SElI, SElK, and TSST-1, reveal significant homology in their secondary and tertiary conformations (26).

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Prognostic usefulness of lymphocyte V β receptor determination in toxic shock syndrome

Cited by 4 publications

References 5 publications

Analysis of superantigenic toxin Vβ T-cell signatures produced during cases of staphylococcal toxic shock syndrome and septic shock

Analysis of superantigenic toxin Vβ T-cell signatures produced during cases of staphylococcal toxic shock syndrome and septic shock

Staphylococcus aureus: The Toxic Presence of a Pathogen Extraordinaire

Staphylococcus aureusSuperantigens Elicit Redundant and Extensive Human Vβ Patterns

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