کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3398631 1222306 2008 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Analysis of superantigenic toxin Vβ T-cell signatures produced during cases of staphylococcal toxic shock syndrome and septic shock
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی میکروب شناسی
پیش نمایش صفحه اول مقاله
Analysis of superantigenic toxin Vβ T-cell signatures produced during cases of staphylococcal toxic shock syndrome and septic shock
چکیده انگلیسی

ABSTRACTMost clinical isolates of Staphylococcus aureus harbour genes encoding superantigenic toxins that bind the Vβ 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 Vβ signature (DVβS) of each superantigenic toxin in vitro. Attempts were also made to identify in-vivo production of superantigenic toxin DVβS in patients’ blood. The DVβS identified in vitro were: toxic shock syndrome toxin (TSST)-1, Vβ 2; staphylococcal enterotoxin (SE), Vβ 9, Vβ 22; SEB, Vβ 3, Vβ 14, Vβ 17; SED, Vβ 1, Vβ 8; egc, Vβ 5.3, Vβ 7.1, Vβ 9, Vβ 23; and SE/K, Vβ 5.1. The DVβS of TSST-1 and SEB were detected in patients with menstrual and non-menstrual TSS, respectively, whereas no Vβ 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 DVβS 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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Clinical Microbiology and Infection - Volume 14, Issue 6, June 2008, Pages 546–554
نویسندگان
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