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Published in: Journal of Inflammation 1/2015

Open Access 01-12-2015 | Short Report

Chronic Kidney Disease is associated with an increase of Intimal Dendritic cells in a comparative autopsy study

Authors: Miguel Hueso, Joan Torras, Marta Carrera, August Vidal, Estanis Navarro, Josep Grinyó

Published in: Journal of Inflammation | Issue 1/2015

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Abstract

Background

Chronic Kidney Disease (CKD) and inflammation are risk factors for atherosclerotic vascular disease (ASVD). In inflammatory conditions, Nuclear Factor-κB (NF-κB) is frequently activated and it has been detected in human ASVD. In this work, we investigated if the degree of inflammation and of NF-κB activation were increased in the aorta of patients with CKD.

Methods

This is a case–control pilot study performed on 30 abdominal aorta samples from 10 human autopsies. Cases were patients with CKD and controls patients with normal glomerular filtration rate (eGFR). Infiltrating mononuclear cells (S100+, CD3+, CD40+, CD40L+) and activation of NF-κB were identified by immunohistochemistry.

Findings

The number of cells in the intima which showed activated nuclear NF-κB correlated with severity of ASVD lesions (r = 0.56, p = 0.003), with numbers of CD3+ lymphocytes in adventitia (r = 0.50, p = 0.008), with numbers of CD40+ cells in the intima (r = 0.59, p = 0.002) or in the adventitia (r = 0.45, p = 0.02), and with numbers of CD40L+ cells in the intima (r = 0.51, p = 0.011). Increased numbers of S100+ Intimal Dendritic cells (IDCs) were associated with ASVD (p = 0.03) and CKD (p = 0.01).

Conclusions

Number of CD3+ cells, of CD40+ cells, of CD40L+ cells and the degree of NF-κB activation were increased in ASVD lesions suggesting a role for the adaptive T cell in the development of ASVD lesions. IDCs were associated both with ASVD and CKD suggesting a role of these cells in the pathogenesis of ASVD in CKD.
Literature
1.
go back to reference London GM, Guerin AP, Marchais SJ, Métivier F, Pannier B, Adda H. Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality. Nephrol Dial Transplant. 2003;18:1731–40.CrossRefPubMed London GM, Guerin AP, Marchais SJ, Métivier F, Pannier B, Adda H. Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality. Nephrol Dial Transplant. 2003;18:1731–40.CrossRefPubMed
3.
go back to reference Hernandez-Presa M, Bustos C, Ortego M, Tuñon J, Renedo G, Ruiz-Ortega M. Angiotensin-converting enzyme inhibition prevents arterial nuclear factor-kappa B activation, monocyte chemoattractant protein-1 expression, and macrophage infiltration in a rabbit model of early accelerated atherosclerosis. Circulation. 1997;95:1532–41.CrossRefPubMed Hernandez-Presa M, Bustos C, Ortego M, Tuñon J, Renedo G, Ruiz-Ortega M. Angiotensin-converting enzyme inhibition prevents arterial nuclear factor-kappa B activation, monocyte chemoattractant protein-1 expression, and macrophage infiltration in a rabbit model of early accelerated atherosclerosis. Circulation. 1997;95:1532–41.CrossRefPubMed
4.
go back to reference Zhang W, Xing SS, Sun XL, Xing QC. Overexpression of activated nuclear factor-kappa B in aorta of patients with coronary atherosclerosis. Clin Cardiol. 2009;32:E42–7.CrossRefPubMed Zhang W, Xing SS, Sun XL, Xing QC. Overexpression of activated nuclear factor-kappa B in aorta of patients with coronary atherosclerosis. Clin Cardiol. 2009;32:E42–7.CrossRefPubMed
5.
go back to reference Zheng L, Sinniah R, Hsu SI. Pathogenic role of NF-kappaB activation in tubulointerstitial inflammatory lesions in human lupus nephritis. J Histochem Cytochem. 2008;56:517–29.CrossRefPubMedCentralPubMed Zheng L, Sinniah R, Hsu SI. Pathogenic role of NF-kappaB activation in tubulointerstitial inflammatory lesions in human lupus nephritis. J Histochem Cytochem. 2008;56:517–29.CrossRefPubMedCentralPubMed
6.
go back to reference Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20:1262–75.CrossRefPubMed Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20:1262–75.CrossRefPubMed
7.
go back to reference Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. 2004;351:1296–305.CrossRefPubMed Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. 2004;351:1296–305.CrossRefPubMed
8.
go back to reference Massy ZA, Ivanovski O, Nguyen-Khoa T, Angulo J, Szumilak D, Mothu N. Uremia accelerates both atherosclerosis and arterial calcification in apolipoprotein E knockout mice. J Am Soc Nephrol. 2005;16:109–16.CrossRefPubMed Massy ZA, Ivanovski O, Nguyen-Khoa T, Angulo J, Szumilak D, Mothu N. Uremia accelerates both atherosclerosis and arterial calcification in apolipoprotein E knockout mice. J Am Soc Nephrol. 2005;16:109–16.CrossRefPubMed
9.
10.
go back to reference Alberts-Grill N, Denning TL, Rezvan A, Jo H. The role of the vascular dendritic cell network in atherosclerosis. Am J Physiol Cell Physiol. 2013;305:C1–C21.CrossRefPubMedCentralPubMed Alberts-Grill N, Denning TL, Rezvan A, Jo H. The role of the vascular dendritic cell network in atherosclerosis. Am J Physiol Cell Physiol. 2013;305:C1–C21.CrossRefPubMedCentralPubMed
11.
12.
go back to reference Bobryshev YV, Lord RS. S-100 positive cells in human arterial intima and in atherosclerotic lesions. Cardiovasc Res. 1995;29:689–96.CrossRefPubMed Bobryshev YV, Lord RS. S-100 positive cells in human arterial intima and in atherosclerotic lesions. Cardiovasc Res. 1995;29:689–96.CrossRefPubMed
13.
go back to reference Cybulsky MI, Jongstra-Bilen J. Resident intimal dendritic cells and the initiation of atherosclerosis. Curr Opin Lipidol. 2010;21:397–403.CrossRefPubMed Cybulsky MI, Jongstra-Bilen J. Resident intimal dendritic cells and the initiation of atherosclerosis. Curr Opin Lipidol. 2010;21:397–403.CrossRefPubMed
14.
go back to reference Jung S, Unutmaz D, Wong P, Sano G, De los Santos K, Sparwasser T. In vivo depletion of CD11c + dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens. Immunity. 2002;17:211–20.CrossRefPubMedCentralPubMed Jung S, Unutmaz D, Wong P, Sano G, De los Santos K, Sparwasser T. In vivo depletion of CD11c + dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens. Immunity. 2002;17:211–20.CrossRefPubMedCentralPubMed
15.
go back to reference Packard RR, Libby P. Inflammation in atherosclerosis: from vascular biology to biomarker discovery and risk prediction. Clin Chem. 2008;54:24–38.CrossRefPubMed Packard RR, Libby P. Inflammation in atherosclerosis: from vascular biology to biomarker discovery and risk prediction. Clin Chem. 2008;54:24–38.CrossRefPubMed
Metadata
Title
Chronic Kidney Disease is associated with an increase of Intimal Dendritic cells in a comparative autopsy study
Authors
Miguel Hueso
Joan Torras
Marta Carrera
August Vidal
Estanis Navarro
Josep Grinyó
Publication date
01-12-2015
Publisher
BioMed Central
Published in
Journal of Inflammation / Issue 1/2015
Electronic ISSN: 1476-9255
DOI
https://doi.org/10.1186/s12950-015-0073-4

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