OBJECTIVETo study the role of dendritic cells (DCs) in initiating delayed-type hypersensitivity (DTH) to fluorescein isothiocyanate (FITC) after trauma-hemorrhage in mice.

METHODSInbred BALB/c mice (6-8 weeks old, male) were epicutaneously sensitized with FITC 12 hours, 1 day, 2 days, 4 days and 7 days after closed bilateral femur fractures combined with hemorrhage. And 5 days after sensitization, DTH was evaluated by ear swelling after a challenge of FITC. Draining lymph node cells were examined for the percentages of FITC-positive cells, cluster of differentiation (CD)11c-positive cells and major histocompatibility complex II (MHC II)-positive cells by means of flow cytometry. In vitro proliferative responses of syngeneic lymphocytes and in vivo passive transfer of DTH to naive recipients induced by isolated DCs from the draining lymph nodes were determined.

RESULTSThe time of DTH to FITC decreased more significantly in the mice with trauma-hemorrhage (12 hours to 4 days) than in the mice with sham injury. After sensitization, the relative percentages of FITC+ cells, FITC+/CD11c+ cells and FITC+/CD11c+/MHC II+ cells from the draining lymph nodes were all significantly reduced following injury. And the capacity of DCs from the draining lymph nodes in stimulating proliferative responses of lymphocytes and transferring DTH to naive recipients were also inhibited after injury.

CONCLUSIONSTrauma-hemorrhage induces repressive DTH in mice, which may be attributed, at least partially, to the reduced trafficking of DCs into the draining lymph nodes and insufficient maturation during DC migration.