• S Drechsler, P Rademann, J Zipperle, T Klotz, S Bahrami, and M Osuchowski.
• Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, AUVA Research Center, Vienna, Austria.
• Shock. 2015 Oct 1;44 Suppl 2:23-4.

IntroductionIn preclinical and clinical setting, severe polytrauma affects the immune system frequently triggering strong immunological deregulation, which predisposes patients for secondary complications. Yet not all body compartments are equally responsive to development of immunosuppression.MethodsFocusing on blood/bone marrow compartment, we investigated early immune responses developing in a severe murine polytrauma model. 3-month old, female, Balb/c mice (n=35) underwent unilateral femur fracture, splenectomy and hemorrhagic shock with 30% blood loss (TSH). Whole blood (WB) and bone marrow (BM) were collected at baseline and 24 or 48 h post-TSH. In WB and BM, leukocyte populations and mean fluorescence intensity (MFI) of total MHC-2 expression were compared to baseline. Specifically, T-helper, cytotoxic and regulatory T-cells in WB and phagocytic capacity of leukocytes were evaluated by flow cytometry.ResultsAt 48hrs, TSH induced neutrophilia and lymphocytosis (p<0.05). In BM, at 48 h a 20% decrease in granulocytes (CD11b+/Ly6G+) MFI occurred (p < 0.05). MHC-2 on pertinent BM cells decreased by 3-fold, while a contrasting trend occurred in circulation. Within 48 h of TSH, there was a relative reduction of CD4+ and CD8+ T-lymphocytes (by 25% and 30%; p < 0.05), while regulatory T-cells (CD4+CD24+CD127-) increased by 1.5-fold (p < 0.05). Plasma level of C5a increased by 2-fold at 48hrs (p < 0.05). Phagocytic capacity of WB cells did not decline; it gradually increased until 48 h post-TSH.ConclusionThe above results of the blood-bone marrow compartment show a simultaneous activation and impairment of the murine innate and adaptive immune response post-TSH. Assessment of any single compartment is insufficient to characterize the magnitude of the developing immunosuppression.

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