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Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental

Malte A Kluger1, Gunther Zahner, Hans-Joachim Paust

  • 1III.Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.

Kidney International
|January 25, 2013
PubMed

Insights

Matrix metalloproteinase 9 (MMP9) drives kidney inflammation in glomerulonephritis by recruiting macrophages. MMP9 deficiency in leukocytes reduces kidney injury and macrophage infiltration during experimental nephritis.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Matrix metalloproteinase 9 (MMP9) is upregulated in glomerulonephritis, but its specific role is unclear.
  • Glomerulonephritis involves leukocyte infiltration and renal failure.

Purpose of the Study:

  • To elucidate the function of MMP9 in experimental crescentic glomerulonephritis.
  • To determine if leukocyte-derived MMP9 mediates macrophage recruitment in kidney disease.

Main Methods:

  • Induction of nephrotoxic serum nephritis (NTN) in wild-type and MMP9-deficient mice.
  • Assessment of histological injury, albuminuria, and leukocyte infiltration.
  • In vitro chemotaxis assays of macrophages.
  • Bone marrow transplantation experiments.

Main Results:

  • MMP9 upregulation correlated with leukocyte infiltration, albuminuria, and renal failure in NTN.
  • MMP9 deficiency ameliorated NTN, reducing histological damage and proinflammatory macrophage infiltration.
  • MMP9-deficient macrophages showed impaired chemotaxis in vitro.
  • Bone marrow transplantation from wild-type to MMP9-deficient mice restored renal injury and macrophage recruitment.

Conclusions:

  • Leukocyte-derived MMP9 is crucial for recruiting proinflammatory macrophages to the kidneys during experimental crescentic glomerulonephritis.
  • Targeting MMP9 may offer a therapeutic strategy for glomerulonephritis.

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