Increased Accumulation of CD16+ Monocytes at Local Sites of Inflammation in Patients with Chronic Kidney Disease

Authors

  • C. Wallquist,

    1. Department of Nephrology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden
    2. Division of Nephrology, Department of Medicine, Västmanlands Hospital, Västerås, Sweden
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  • J. M. Paulson,

    1. Department of Clinical Immunology and Allergy, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden
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  • B. Hylander,

    1. Department of Nephrology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden
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  • J. Lundahl,

    1. Department of Clinical Immunology and Allergy, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden
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  • S. H. Jacobson

    Corresponding author
    1. Department of Nephrology, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden
    • Correspondence to: S. Jacobson, Department of Nephrology, Karolinska Institutet, Danderyd University Hospital, Danderyd Hospital AB, 182 88 Stockholm Sweden. E-mail: Stefan.Jacobson@ds.se

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Abstract

Patients with chronic kidney disease (CKD) display a high prevalence of cardiovascular events and acute infections. Potential effector cells are the CD16+ monocytes, known to be increased in the peripheral circulation in CKD. The aim of this study was to assess the expression of CD16 and CX3CR1 on peripheral and in vivo extravasated monocytes in patients with CKD (GFR < 20 ml/min × 1.73 m²) using flow cytometry. In vivo extravasated monocytes were collected from a local inflammatory site, induced by a skin blistering technique. Soluble markers were assessed by Luminex. The number of CD16+ monocytes was significantly higher in patients with CKD compared with healthy subjects, both in the peripheral circulation (P < 0.05) and at the site of induced inflammation (P < 0.001). Patients with CKD displayed significantly higher concentration of soluble CX3CL1 both in the peripheral circulation (P < 0.01) and in the interstitial fluid (P < 0.001). In addition, patients with CKD had a significantly higher concentration of TNF-α in the peripheral circulation (P < 0.001). On the contrary, at the inflammatory site, concentrations of both TNF-α and IL-10 were significantly lower in patients with CKD compared with healthy controls (P < 0.05 for both). In conclusion, patients with CKD have an increased percentage of CD16+ monocytes in both circulation and at the inflammatory site, and this finding is in concurrence with simultaneous changes in CX3CR1. Together with distorted TNF-α and IL-10 levels, this may have potential impact on the altered inflammatory response in CKD.

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