IL-10 administration attenuates pulmonary neutrophil infiltration and alters pulmonary iNOS activation following hemorrhagic shock
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- Kobbe, P., Schmidt, J., Stoffels, B. et al. Inflamm. Res. (2009) 58: 170. doi:10.1007/s00011-009-8116-z
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Objective and design:
Several studies report immuno-modulatory effects of endogenous IL-10 after trauma. This study investigates the effect of IL-10 administration on systemic and pulmonary inflammation in hemorrhagic shock.
Material and Methods:
Male C57/BL6 mice (4–6 animals per group) were subjected to volume controlled hemorrhagic shock for 3 hrs followed by resuscitation. Animals were either subcutaneously injected with 0.9 % saline (Shock group) or with recombinant mouse IL-10 (Shock+IL-10 group) 1 h before and 1 h after the induction of hemorrhagic shock. Serum TNF-α, IL-6, and keratinocyte (KC) concentrations were measured with the LuminexTM multiplexing platform. Acute pulmonary inflammation was assessed by pulmonary myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) activity.
IL-10 administration significantly decreased serum TNF-α (10.30 ± 1.68 vs 37.42 ± 10.64; p < 0.05), IL-6 (44.22 ± 6.65 vs 85.24 ± 7.94; p < 0.05), and KC (276.74 ± 52.67 vs 465.61 ± 58.98; p < 0.05) levels following hemorrhagic shock. Further, pulmonary MPO activity was significantly lower (2698.85 ± 431.10 vs 4580.67 ± 294.38; p < 0.05) and pulmonary iNOS activity upregulated.
These findings suggest that administration of IL-10 modulates the degree of hemorrhage-induced systemic and pulmonary inflammation and support the notion of a central role for iNOS in acute lung injury.