Premium
Increased Accumulation of CD 16 + Monocytes at Local Sites of Inflammation in Patients with Chronic Kidney Disease
Author(s) -
Wallquist C.,
Paulson J. M.,
Hylander B.,
Lundahl J.,
Jacobson S. H.
Publication year - 2013
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12115
Subject(s) - kidney disease , peripheral , inflammation , medicine , in vivo , flow cytometry , monocyte , kidney , gastroenterology , endocrinology , immunology , biology , microbiology and biotechnology
Patients with chronic kidney disease ( CKD ) display a high prevalence of cardiovascular events and acute infections. Potential effector cells are the CD 16 + monocytes, known to be increased in the peripheral circulation in CKD . The aim of this study was to assess the expression of CD 16 and CX 3 CR 1 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 L uminex. The number of CD 16 + 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 CX 3 CL 1 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 CD 16 + monocytes in both circulation and at the inflammatory site, and this finding is in concurrence with simultaneous changes in CX 3 CR 1 . Together with distorted TNF ‐α and IL ‐10 levels, this may have potential impact on the altered inflammatory response in CKD .