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Updated: Jan 17, 2026
Use of Animal Model of Sepsis to Evaluate Novel Herbal Therapies
Published on: April 11, 2012
Spices to Combat Sepsis: Curcumin and Piperine Combination Increases Survival and Modulates Immune Response in a
Christina Schwenk1, Nadja Muehlhaupt1, Laura Heimann2
1Department of Experimental Trauma Surgery, Department of Trauma Surgery, TUM Klinikum Rechts der Isar, School of Medicine and Health, Technical University of Munich, Munich, Germany.
Background:
Following trauma, SIRS and CARS interact in a sensitive balance with CD4 + Tregs considered as protective. Previously we showed a reciprocal activation of CD4 + Tregs and platelets early after trauma. Here, we investigated the immunomodulatory potential and survival advantage due to treatment with curcumin + piperine (C + P) or ancrod in a long-term two-hit trauma model.
Methods:
C57BL/6N mice were subjected to SIRS by burn injury, followed by sepsis induction via CLP 7 days later. At a maximum follow-up period of 23 days pathohistology, immunohistochemistry, (phospho-)flow cytometry and multiplex Enzyme-linked Immunosorbent Assay were performed.
Results:
C + P-treated mice showed a clear survival advantage ( P = 0.0097) with alterations in cytokine levels. Organ damage was similar to Sham group. CD8 + T cells exhibited lower major histocompatibility complex II and CD69 expression in C + P group compared with Burn/CLP group ( P = 0.0215; P = 0.0347). In CD4 + T cells, the enhancement of extracellular markers CD38 ( P = 0.0130) and major histocompatibility complex II ( P = 0.0330) proved an increased activity, underlined by elevated intracellular signal molecules ZAP-70 ( P = 0.0002) and PKC-θ ( P = 0.0001) and their phosphorylated forms, with distinct differences between CD4 + Tregs and non-Tregs (ZAP-70: P = 0.0153; PKC-θ: P = 0.0085). Platelets expressed lower levels of the activation marker CD62 ( P = 0.0229).
Conclusion:
C + P improves the long-term outcome in a murine two-hit trauma model by balancing the posttraumatic immune response. CD4 + Tregs seem to be primed for further activation, whereas downregulation of CD8 + T cells and platelets may reduce proinflammatory signals.
