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  • Title: Depressed T cell-derived IFN-gamma following trauma-hemorrhage: a potential mechanism for diminished APC responses.
    Author: Walz CR, Zedler S, Schneider CP, Mayr S, Loehe F, Bruns CJ, Faist E, Jauch KW, Angele MK.
    Journal: Langenbecks Arch Surg; 2007 May; 392(3):339-43. PubMed ID: 17377804.
    Abstract:
    INTRODUCTION: Prolonged immunosuppression has been demonstrated after trauma-hemorrhage resulting in an increased susceptibility to sepsis. The contribution of antigen-presenting cells (APC) vs T cells to this diminished immune response, however, remains unknown. MATERIALS AND METHODS: To study this, male mice were trauma-hemorrhaged (35 +/- 5 mmHg for 90 min and resuscitation) or sham operated. At 24 h thereafter, spleens were harvested and T cells (via Microbeads) and APC (via adherence) were isolated. Cocultures of combined T cells and APC were established for 48 h, stimulated with ConA and LPS. The T cell-derived cytokine IFN-gamma and IL-12 for APC responses were measured in the supernatants by the multiplex assay. RESULTS: The release of IFN-gamma was suppressed by T cells after trauma-hemorrhage irrespective of whether sham or trauma-hemorrhage APC were added. Trauma-hemorrhaged APC did not affect T cells-derived IFN-gamma release by sham T cells. In contrast, trauma-hemorrhaged T cells depressed the release of IL-12 by APC. The release of IL-12 by trauma-hemorrhaged APC was not altered when sham T cells were cocultured. CONCLUSION: Prolonged immunosuppression after trauma-hemorrhage appears to be predominantly due to diminished T cell function. Thus, attempts to prevent immunodysfunction should be directed towards T cells.
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