The Effect Of Trauma On Cell Immunity Function And Antigen Presenting Ability Of Dendritic Cells

Objective:Study DC's changes after trauma and the relations between these changes and the disorderly cell immunity under trauma, and explore the mechanism of these changes following trauma. Learning the mechanism of DC's involvement in trauma will undoubtedly spur new therapeutic strategy and drug development to protect human from severe trauma.Methods: With the model of trauma (hemorrhagic injury combined with closed fracture), DTH responses were induced by DNFB and FITC to evaluation of cell immunity function after trauma. In addition, the FITC+, CD11c+ and MHC II+ cells in pooled inguinal lymph nodes were analysed by FACScan after FITC skin painting.In both early and later stage of DTH response, Cell transfer sensitization for DTH induced by DNFB after trauma in mice. DCs from spleens were separated by the method of Nycodenz density gradient enrichment. The low-density cells (3 %-5 % of the total) as DC were collected at the interface. Then their ability to stimulate nonadherent splenocytes proliferation in the presence of conalbumin in vitro was detected. Determination of IL-12 and IL-10 levels in splenic DCs culture supernatants. At last A FACSCalibur was used for analysis of surface molecules CD11c, MHC II, CD40, CD80 and CD86 of cells from spleen, thymus gland, pooled inguinal lymph nodes and mesenteric lymph nodes.Results: The degree of ear edema of 24 h post-injury decreased significantly compared with that of control group. However, after 24 h post-injury, the DTH response increased, and there was almost no difference between 7 day post-injury and control group. FACS can analyses show FITC+ cells, FITC+/CD11c+ cells and FITC+/CD11c+/MHC II+ cells are all significantly reduced following trauma. Inguinal lymph nodes cells from mice of 24 h post-injury induced significantly weaker sensitization compared with that from normal mice. The proliferation index (PI) of nonadherent splenocytes from normal mice is obviously higher than that from injured mice. In addition, the antigen presenting ability of splenic DCs is affected by 1-MT (inhibitor of IDO). IL-12 from DCs of injured mice is obviously reduced than that from normal mice, while IL-10 is not affected by trauma. When splenic DCs are cultured with LPS, IL-12 from DCs of injured mice rises, but IL-10 is obviously reduced. For spleen, the number of mature DCs has decreased, while the number of immature DCs has increased. For inguinal lymph nodes and mesenteric lymph nodes, the number of costimulator molecules is not changed, but the number of total DC, immature DCs and mature DCs is declined following trauma.Conclusion: With in vitro and in vivo experiments, we found that severe trauma causes the cell immunity function weakened, which has significant relations to the changes of number, surface molecules, phenotypes, and antigen presenting ability of DC following trauma. In addition, in order to correct the imbalanced immune system after severe injury, a preliminary study has been made, and we found that supply of lymph node cells can promote the recovery of severe trauma.