IL-10 deficiency increases renal ischemia-reperfusion injury

Nephron Exp Nephrol. 2014;128(1-2):37-45. doi: 10.1159/000366130. Epub 2014 Oct 31.

Abstract

Background: Renal ischemia-reperfusion (IR) injury is a frequent cause of acute kidney injury, which results in high morbidity and mortality. Inflammation is an important factor that is involved in kidney repair after renal IR injury. IL-10 is a potent anti-inflammatory cytokine that inhibits inflammatory pathways, but the role of IL-10 in repairing renal IR injury is not known. Here, we investigated the role of IL-10 in kidney repair after renal IR injury.

Methods: We used an IL-10(-/-) mouse model and examined the serologic and histomorphology of kidney after IR injury. We also measured ki67, TNF-α, IL-6, and macrophages with immunohistochemistry or Western blotting.

Results: There was a greater increase in serum creatinine in IL-10(-/-) mice than in wild-type (WT) mice. And compared with WT mice, IL-10(-/-) mice had increased histologic renal injury and decreased proliferation. Moreover, the expression of TNF-α, IL-6 and macrophages was clearly increased in IL-10(-/-) mice compared with the WT mice.

Conclusion: These data reveal an important role for IL-10 in the improvement of renal IR injury, acting through suppression of inflammatory mediators, and that IL-10 would be a crucial target for the treatment of IR injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Proliferation
  • Disease Models, Animal
  • Disease Progression*
  • Interleukin-10 / deficiency*
  • Interleukin-10 / genetics
  • Interleukin-10 / physiology
  • Interleukin-6 / metabolism
  • Ki-67 Antigen / metabolism
  • Kidney / blood supply*
  • Kidney / metabolism
  • Kidney / pathology
  • Macrophages / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology*
  • Reperfusion Injury / physiopathology*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-6
  • Ki-67 Antigen
  • Tumor Necrosis Factor-alpha
  • Interleukin-10