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IL-15 Prevents Renal Fibrosis by Inhibiting Collagen Synthesis: A New Pathway in Chronic Kidney Disease?

Aurore Devocelle1,2, Lola Lecru1,2, Sophie Ferlicot3

  • 1INSERM UMR-S-MD 1197/Ministry of the Armed Forces, Biomedical Research Institute of the Armed Forces (IRBA), Paul-Brousse Hospital Villejuif and CTSA Clamart, 94807 Villejuif, France.

International Journal of Molecular Sciences
|November 13, 2021
PubMed

Insights

Interleukin-15 (IL-15) reduces kidney fibrosis by inhibiting extracellular matrix production in myofibroblasts and decreasing macrophage infiltration. This suggests IL-15 as a potential therapy for chronic kidney disease (CKD).

Area of Science:

  • Nephrology
  • Immunology
  • Fibrosis Research

Background:

  • Chronic kidney disease (CKD) is a significant public health issue driven by renal fibrogenesis.
  • Interstitial myofibroblast activation and excessive extracellular matrix (ECM) deposition are key pathological features of CKD.
  • Interleukin-15 (IL-15) shows potential in protecting organs from fibrosis, but its role in kidney fibrosis is largely unexplored.

Purpose of the Study:

  • To investigate the renoprotective role of Interleukin-15 (IL-15) in the context of renal fibrogenesis.
  • To explore the therapeutic potential of IL-15, alone or with its soluble receptor (IL-15Rα), in preventing kidney fibrosis.

Main Methods:

  • Utilized the unilateral ureteral obstruction (UUO) model in rodents to induce kidney fibrosis.
  • Administered IL-15, with or without IL-15Rα, to assess its effects on fibrotic markers.
  • Examined the impact of IL-15 on primary myofibroblast cultures stimulated with transforming growth factor-β (TGF-β).
  • Assessed the expression of monocyte chemoattractant protein 1 (MCP-1) and macrophage infiltration.

Main Results:

  • IL-15 treatment, with or without IL-15Rα, significantly prevented tubulointerstitial fibrosis (TIF) in the UUO model.
  • Reduced collagen and fibronectin deposition was observed following IL-15 administration.
  • IL-15 directly inhibited collagen and fibronectin secretion by TGF-β-treated myofibroblasts.
  • IL-15 treatment decreased MCP-1 expression and subsequent macrophage infiltration in the UUO model.

Conclusions:

  • IL-15 demonstrates a significant renoprotective effect against kidney fibrosis in the UUO model.
  • The antifibrotic action of IL-15 involves direct inhibition of ECM synthesis by myofibroblasts and modulation of macrophage infiltration.
  • IL-15 represents a promising therapeutic candidate for managing renal fibrosis and potentially treating chronic kidney disease.
Keywords:
chronic kidney diseaseextracellular matrixfibrosisinterleukin-15myofibroblastsunilateral ureteral obstruction

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