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Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
12:27

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration

Published on: June 7, 2014

Influence of TH1/TH2 switched immune response on renal ischemia-reperfusion injury

Vilmar Paiva Marques1, Giselle Martins Gonçalves, Carla Quarin Feitoza

  • 1Laboratório de Imunologia Clínica e Experimental, Division of Nephrology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil.

Nephron. Experimental Nephrology
|June 3, 2006
PubMed

Insights

Interleukin-4 knockout mice showed worsened kidney injury and impaired regeneration after ischemia-reperfusion injury. This suggests Th1 cell responses exacerbate renal injury by increasing chemokine production.

Area of Science:

  • Immunology
  • Renal Physiology
  • Inflammation Biology

Background:

  • CD4+ T cells, specifically the Th1/Th2 paradigm, play a role in ischemia-reperfusion injury (IRI).
  • A polarized Th1 response may negatively impact renal IRI.
  • This impact could be mediated by chemokine production (MCP-1) and tissue response (HO-1).

Purpose of the Study:

  • To investigate the role of Interleukin-4 (IL-4) and Interleukin-12 (IL-12) in renal ischemia-reperfusion injury.
  • To determine if a Th1-polarized response exacerbates renal IRI.
  • To examine the relationship between Th1 response, chemokine production (MCP-1), and heme oxygenase-1 (HO-1) expression in renal IRI.

Main Methods:

  • C57BL/6 mice with IL-4 and IL-12 knockout were subjected to renal ischemia.
  • Serum urea levels and histomorphometric analysis for tubular necrosis/regeneration were performed.
  • mRNA expression of HO-1, t-bet, Gata-3, and MCP-1 was evaluated using real-time PCR.

Main Results:

  • IL-4 knockout mice exhibited significantly higher serum urea levels post-IRI compared to controls.
  • IL-4 deficient mice showed increased tubular injury and impaired cell regeneration.
  • IRI in IL-4 deficient mice was associated with elevated HO-1, t-bet, and later MCP-1 upregulation.

Conclusions:

  • IL-4 deficiency exacerbates renal IRI, indicating a protective role for IL-4.
  • IL-12 deficiency did not significantly affect renal IRI outcomes.
  • Deleterious effects of Th1 cells in renal IRI appear linked to increased MCP-1 production.
Abstract

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