| Autor: |
Walz, C. R., Zedler, S., Schneider, C. P., Mayr, S., Loehe, F., Bruns, C. J., Faist, E., Jauch, K. W., Angele, M. K. |
| Předmět: |
|
| Zdroj: |
Langenbeck's Archives of Surgery; Jul2007, Vol. 392 Issue 3, p339-343, 5p, 1 Diagram, 2 Graphs |
| Abstrakt: |
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. 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-γ and IL-12 for APC responses were measured in the supernatants by the multiplex assay. The release of IFN-γ 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-γ 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. 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Full text from SpringerLink