CX3CR1 Reduces Kidney Fibrosis by Inhibiting Local Proliferation of Profibrotic Macrophages

DOI PDF 被引用文献4件
  • Daniel R Engel
    Institute of Experimental Immunology, Rheinische Friedrich-Wilhelms University , 53105 Bonn ,
  • Torsten A Krause
    Institute of Experimental Immunology, Rheinische Friedrich-Wilhelms University , 53105 Bonn ,
  • Sarah L Snelgrove
    Centre for Inflammatory Diseases, Department of Medicine, Monash University , Clayton, Victoria 3168 ,
  • Stephanie Thiebes
    Institute of Experimental Immunology, Rheinische Friedrich-Wilhelms University , 53105 Bonn ,
  • Michael J Hickey
    Centre for Inflammatory Diseases, Department of Medicine, Monash University , Clayton, Victoria 3168 ,
  • Peter Boor
    Institute of Pathology, Rheinisch-Westfälische Technische Hochschule , 52074 Aachen ,
  • A Richard Kitching
    Centre for Inflammatory Diseases, Department of Medicine, Monash University , Clayton, Victoria 3168 ,
  • Christian Kurts
    Institute of Experimental Immunology, Rheinische Friedrich-Wilhelms University , 53105 Bonn ,

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公開日
2015-02
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.1402149
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>A dense network of macrophages and dendritic cells (DC) expressing the chemokine receptor CX3CR1 populates most tissues. We recently reported that CX3CR1 regulates the abundance of CD11c+ DC in the kidney and thereby promotes renal inflammation in glomerulonephritis. Given that chronic inflammation usually causes fibrosis, we hypothesized that CX3CR1 deficiency should attenuate renal fibrosis. However, when we tested this hypothesis using the DC-independent murine fibrosis model of unilateral ureteral obstruction, kidney fibrosis was unexpectedly more severe, despite less intrarenal inflammation. Two-photon imaging and flow cytometry revealed in kidneys of CX3CR1-deficient mice more motile Ly6C/Gr-1+ macrophages. Flow cytometry verified that renal macrophages were more abundant in the absence of CX3CR1 and produced more of the key profibrotic mediator, TGF-β. Macrophages accumulated because of higher intrarenal proliferation, despite reduced monocyte recruitment and higher signs of apoptosis within the kidney. These findings support the theory that tissue macrophage numbers are regulated through local proliferation and identify CX3CR1 as a regulator of such proliferation. Thus, CX3CR1 inhibition should be avoided in DC-independent inflammatory diseases because it may promote fibrosis.</jats:p>

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