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Endogenous and exogenous pentraxin-3 limits postischemic acute and chronic kidney injury

Maciej Lech1, Christoph Römmele, Regina Gröbmayr

  • 1Division of Nephrology, Medizinische Klinik und Poliklinik IV, Campus Innenstadt, University of Munich-LMU, Munich, Germany.

Kidney International
|January 18, 2013
PubMed

Insights

Pentraxin 3 (PTX3) deficiency worsens kidney injury after ischemia-reperfusion, increasing inflammation and long-term damage. PTX3 treatment protects against this injury, highlighting its therapeutic potential for acute kidney injury.

Area of Science:

  • Immunology
  • Nephrology
  • Inflammation Research

Background:

  • Ischemia-reperfusion injury (IRI) triggers innate immunity and sterile inflammation, leading to acute kidney injury (AKI).
  • Pentraxin 3 (PTX3) is a key regulator of innate immunity and tissue inflammation.

Purpose of the Study:

  • To investigate the role of PTX3 in renal IRI.
  • To determine if PTX3 deficiency exacerbates AKI and if PTX3 administration offers protection.

Main Methods:

  • Induction of renal ischemia-reperfusion in wild-type and Ptx3-deficient mice.
  • Measurement of PTX3 serum levels and kidney expression.
  • Assessment of kidney injury markers, inflammatory cytokine release (TNF, IL-6), and immune cell infiltration.
  • In vivo microscopy to observe leukocyte dynamics.
  • Administration of recombinant PTX3 post-reperfusion.

Main Results:

  • Renal IRI increased PTX3 levels, primarily in intrarenal mononuclear phagocytes.
  • Ptx3-deficient mice exhibited aggravated AKI, including tubular necrosis, increased TNF/IL-6, and greater neutrophil/macrophage infiltration.
  • Long-term Ptx3 deficiency led to tubular atrophy, fibrosis, and kidney shrinking.
  • Recombinant PTX3 administration up to 6 hours post-reperfusion prevented leukocyte recruitment and kidney injury.

Conclusions:

  • Local PTX3 release from mononuclear phagocytes limits post-ischemic renal inflammation.
  • PTX3 deficiency predisposes to AKI and subsequent chronic kidney disease.
  • Delayed PTX3 treatment is a potential therapeutic strategy for post-ischemic AKI.

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