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IL-10 increases tissue injury after selective intestinal ischemia/reperfusion
Natascha C Nüssler1, Andrea R Müller, Hans Weidenbach
1Department of Surgery, Charité, Campus Virchow-Klinikum, Humboldt University of Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. natascha.nuessler@charite.de
Annals of Surgery
|July 2, 2003
Summary
Interleukin-10 (IL-10) worsened intestinal ischemia/reperfusion injury, while Interleukin-2 (IL-2) showed protective effects. These cytokine impacts on tissue damage are linked to nitric oxide synthase-2 (NOS-2) and heme oxygenase-1 (HO-1) expression.
Area of Science:
- Immunology
- Gastroenterology
- Molecular Biology
Background:
- Ischemia/reperfusion injury (IRI) involves oxidative stress and inflammation.
- Stress proteins like inducible nitric oxide synthase (NOS-2) and heme oxygenase-1 (HO-1) may offer protection against IRI.
Purpose of the Study:
- To investigate the impact of immunoregulatory cytokines (IL-2, IL-10) on intestinal IRI.
- To evaluate the roles of nitric oxide, HO-1, and NF-kappaB/Rel in IRI pathogenesis.
Main Methods:
- Lewis rats underwent intestinal ischemia/reperfusion (IR).
- Interleukin-2 (IL-2) or Interleukin-10 (IL-10) was administered intravenously before reperfusion.
- Tissue damage, oxidative stress markers (glutathione), NF-kappaB/Rel activation, and NOS-2/HO-1 expression were analyzed post-IR.
Main Results:
- IR induced tissue destruction and reduced glutathione levels.
- NF-kappaB/Rel activation and increased NOS-2/HO-1 mRNA were observed post-IR.
- IL-2 improved outcomes, increasing NF-kappaB/Rel, NOS-2, and HO-1; IL-10 worsened injury and reduced these markers.
Conclusions:
- IL-10 exacerbated intestinal IR, potentially due to decreased NOS-2 and HO-1 expression.
- IL-2 demonstrated beneficial effects, possibly mediated by enhanced HO-1 expression and NOS-2 activity.
- Cytokine-mediated regulation of NOS-2 and HO-1 gene expression influences intestinal IR outcomes.