IL-10 administration attenuates pulmonary neutrophil infiltration and alters pulmonary iNOS activation following hemorrhagic shock

Inflamm Res. 2009 Mar;58(3):170-4. doi: 10.1007/s00011-009-8116-z.

Abstract

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-alpha, IL-6, and keratinocyte (KC) concentrations were measured with the Luminex multiplexing platform. Acute pulmonary inflammation was assessed by pulmonary myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) activity.

Results: IL-10 administration significantly decreased serum TNF-alpha (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.

Conclusion: 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.

MeSH terms

  • Acute Lung Injury* / enzymology
  • Acute Lung Injury* / immunology
  • Acute Lung Injury* / pathology
  • Animals
  • Cytokines / blood
  • Enzyme Activation
  • Interleukin-10* / administration & dosage
  • Interleukin-10* / immunology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neutrophil Infiltration / drug effects*
  • Nitric Oxide Synthase Type II / metabolism*
  • Peroxidase / metabolism
  • Shock, Hemorrhagic / blood
  • Shock, Hemorrhagic / immunology*

Substances

  • Cytokines
  • Interleukin-10
  • Peroxidase
  • Nitric Oxide Synthase Type II