DOI 10.1016/j.cyto.2016.09.010
Coexistence of Th1/Th2 and Th17/Treg imbalances in patients with post traumatic sepsis.
Аннотация
INTRODUCTION
Multiple organ dysfunction syndrome (MODS) developed due to the insult of trauma is a leading cause of death. The high mortality rate in these patients with and without sepsis has been reported up to 50%, throughout the world and thus required an urgent insight to overcome this problem.
OBJECTIVE
The aim of this study is to examine the differential changes in subsets of T cells, imbalance in cytokine profile, immune-paralysis (T cell anergy) in Trauma hemorrhagic shock (THS) and post traumatic sepsis patients.
METHODOLOGY: 114, THS patients and 50 healthy controls were recruited in the present study. We have measured the T cell proliferation assay using dominant antigens of both gram positive (LTA, 100ng/ml) and gram negative (LPS-100ng/ml) bacteria and PHA (4μg/ml) using radioactive thymidine (1H3) assay. Simultaneously, we have measured the culture supernatant level of cytokines using Cytokine bead assay (CBA). The other parts of this study include the analysis of different subsets of T cells.
RESULTS AND
CONCLUSION
We observed significantly (P<0.05) reduced T cell proliferation in THS patients as compared to control. Our study also showed patients died due to sepsis/septic shock, had significantly (p<0.05) lower T cell response and had significantly elevated levels of IL-4, IL-10andTGF-β, but low level of IL-2andIFN-γ in culture supernatant. THS patients who developed sepsis complication had significantly higher T regulatory cells and lower Th17 cells in comparison to non-sepsis. In conclusion, our study showed an imbalance in cell mediated immune response and disturbance in Th1/Th2/Th17 and T reg population of T helper cells and also the shifts towards Th2 and T17 in THS patients who had developed sepsis and showed poor outcomes.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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