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Contrib Nephrol. 2011;171:57-61. doi: 10.1159/000327134. Epub 2011 May 23.

CD14+CD16+ monocytes from chronic kidney disease patients exhibit increased adhesion ability to endothelial cells.

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1
Nephrology Unit, Hospital Universitario Reina Sofía, Córdoba, Spain.

Abstract

Chronic kidney disease (CKD) patients present an inflammatory process that induces endothelial damage and therefore plays a role in the high rates of cardiovascular morbidity and mortality reported in these patients. Although new therapies have reduced the elevated serum levels of inflammatory mediators such as cytokines and CRP in CKD patients, the rise in the level of activated immunocompetent cells is maintained in peripheral blood, which appears to play a prominent role in the endothelial damage suffered by these patients. CD14+CD16+ monocytes are a subset of activated monocytes that are found in greater numbers in the peripheral blood of CKD patients. The increased presence of these cells is related to the endothelial damage suffered by these patients. However, the mechanism through which these cells damage the vascular endothelium is still unclear. One of the characteristics that differentiate CD14+CD16+ monocytes is their powerful ability to produce inflammatory cytokines, which may be responsible for causing damage to endothelial cells. However, it is difficult to imagine that the cytokines produced by a relatively small proportion of these cells are capable of damaging the endothelium. For this reason, we have suggested that these cells do not release their cytokines into the bloodstream, but that they possess cellular mechanisms that lead them to produce and release cytokines after adhering to the layer of endothelial cells. This hypothesis is based on the fact that unlike the CD14++CD16- monocytes found in healthy subjects, CD14+CD16+ monocytes in CKD patients show a high level of expression of chemokines that favors their migration to the vascular wall, and a low level of chemokines such as CCR2 that would prevent such migration. Furthermore, these CD14+CD16+ monocytes express a large number of adhesion molecules, which helps them attach to endothelial cells. In view of this scenario, it is easy to suggest that a moderate number of CD14+CD16+ monocytes might well be capable of producing endothelial damage; therefore, the rise in the number of these cells in CKD patients may play an important role in the development of vascular disease.

PMID:
21625090
DOI:
10.1159/000327134
[Indexed for MEDLINE]
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