Femur fracture induces site-specific changes in T-cell immunity

Trauma is associated with altered host defense and susceptibility to infection, in part due to cytokine dysregulation and altered T-cell immunity. The gut-associated lymphoid tissue (GALT) provides a defense against infection and contributes to the process of mucosal healing by T-cell activation and cytokine production.

To determine whether femur fracture induces alterations in Peyer's patch and splenic T-cell phenotype, proliferative response, and cytokine expression following traumatic injury.

Mice underwent femur fracture or sham procedure and, 48 h later, lymphocytes were isolated from spleen and Peyer's patches. Lymphocytes were cultured, and lipopolysaccharide (10 microg/ml) was added in some cultures. Cells and supernatant were harvested at 48 h. Proliferation was analyzed by [3H]thymidine, and interleukin-10 (IL-10) protein was measured by ELISA in the culture supernatant. T-cell phenotype was determined by flow cytometry.

Femur fracture induced a significant increase in proliferative response in Peyer's patch immunocytes. In contrast, no significant differences were identified in splenocyte proliferative response 48 h after femur fracture injury. Femur fracture induced a significant decrease in IL-10 protein expression of both splenocytes and Peyer's patches. Femur fracture also induced a significant increase in the fraction of CD3(+), CD4(+), and T-cell receptor-alpha beta Peyer's patch immunocytes, whereas splenocytes demonstrated no significant phenotypic change.

Femur fracture is associated with significant alterations in Peyer's patch but not splenic T-cell phenotype and proliferative response early (48 h) after injury. Changes in the GALT immune response may contribute to intestinal mucosal dysfunction and increased susceptibility to gut-derived sepsis after traumatic injury.