Cytokine profiles in patients with Staphylococcus aureus skin infections (P3136)
العنوان: | Cytokine profiles in patients with Staphylococcus aureus skin infections (P3136) |
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المؤلفون: | Luqiu Chen, Caroline Bartman, Anita Chong, Robert Daum, Maria-Luisa Alegre |
المصدر: | The Journal of Immunology. 190:186.15-186.15 |
بيانات النشر: | The American Association of Immunologists, 2013. |
سنة النشر: | 2013 |
مصطلحات موضوعية: | Immunology, Immunology and Allergy |
الوصف: | Methicillin-resistant Staphylococcus aureus (MRSA) causes skin infections in epidemic proportions among otherwise healthy individuals. Previous evidence shows that Th17 cells may be crucial to prevent localized S. aureus infections, as they occur in patients deficient in STAT3 or mice lacking IL-17A and F. In this study, we hypothesized that patients presenting to the emergency room (ER) with skin infections but no known genetic deficiency may have a reduction in Th17 differentiation, either globally or specifically to S. aureus antigens because of inhibitory factors produced by MRSA strains. Sera from 72 patients and 143 controls were collected and cytokines were measured by MultiPlex beads assay. It showed elevated cytokines in patients with skin abscesses on day 0. PBMCs from the same groups were stimulated with MRSA lysates, or anti-CD3, and supernatants were collected at 24h for detection of cytokines by ELISA. The production of IFNγ and IL-17 in response to anti-CD3 was similar in patients and controls, but MRSA stimulation triggered greater secretion of IL-6 and IFNγ in select groups of patients than in controls. These data suggest that our skin infected patients do not have a global defect in Th17 differentiation but may have a specific increase in IFNγ production in response to S. aureus antigens. Future experiments in mice will investigate whether this response may be detrimental to prevent S. aureus infections. |
تدمد: | 1550-6606 0022-1767 |
DOI: | 10.4049/jimmunol.190.supp.186.15 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_________::ceb3e22b992c197fd1d7bb406a84a132 https://doi.org/10.4049/jimmunol.190.supp.186.15 |
رقم الانضمام: | edsair.doi...........ceb3e22b992c197fd1d7bb406a84a132 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15506606 00221767 |
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DOI: | 10.4049/jimmunol.190.supp.186.15 |