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Alterations in intestinal permeability and immune function were investigated in a murine femur fracture (FFx) model. We postulated that soft tissue injury associated with closed FFx (crush injury) would result in greater immunosuppression that open FFx (surgical division). AKR mice were randomized to four groups (Normal, Sham, Open FFx, Closed FFx) and studied at 24 and 96 h post-injury. Immune function was assessed by splenocyte blastogenic response and class-specific immunoglobulin production. Intestinal permeability was assessed by measurement of whole blood fluorometry after gavage administration of fluorescein-dextran (FITC-dextran). Closed FFx is associated with increased splenocyte blastogenesis and increased immunoglobulin production at 24 h post-injury. This immunostimulatory response was associated with altered intestinal permeability early after injury (FITC-dextran: .185 ± .070 Closed FFx vs. .069 ± .011 Normal, p = .06). Immunosuppression was evident at 96 h post-injury in the closed FFx group, documented by significant reductions in splenocyte blastogenesis to all mitogens studied. The Open FFx group did not demonstrate any reduction in splenocyte blastogenesis at 96 h post-injury. These data suggest that the soft tissue injury associated with Closed FFx is associated with significant immunosuppression and altered gastrointestinal permeability, which may adversely affect the host by increasing the relative risk of post-trauma infection.