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International Journal of Endocrinology
Volume 2017, Article ID 2912763, 9 pages
https://doi.org/10.1155/2017/2912763
Research Article

Circulatory Immune Cells in Cushing Syndrome: Bystanders or Active Contributors to Atherometabolic Injury? A Study of Adhesion and Activation of Cell Surface Markers

1Group of Endocrine Disorders, IDIBAPS, Barcelona, Spain
2Department of Endocrinology and Nutrition, Hospital Clinic Universitari, Barcelona, Spain
3Cytometry Department, IDIBAPS, Barcelona, Spain
4Centro de Investigación en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain
5University of Barcelona, Barcelona, Spain
6Biochemistry and Molecular Genetics Service, Hospital Clinic Universitari and IDIBAPS and CIBERehd, Barcelona, Spain
7Department of Neurosurgery, Hospital Clinic Universitari, Barcelona, Spain

Correspondence should be addressed to Felicia A. Hanzu; tac.cinilc@uznahf

Received 22 February 2017; Revised 18 June 2017; Accepted 16 July 2017; Published 20 September 2017

Academic Editor: Sabrina Corbetta

Copyright © 2017 Gloria Aranda et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Glucocorticoids (GC) induce cardiometabolic risk while atherosclerosis is a chronic inflammation involving immunity. GC are immune suppressors, and the adrenocorticotrophic hormone (ACTH) has immune modulator activities. Both may act in atherothrombotic inflammation involving immune cells (IMNC). Aim. To investigate adhesion and activation surface cell markers (CDs) of peripheral IMNC in endogenous Cushing syndrome (CS) and the immune modulator role of ACTH. Material and Methods. 16 ACTH-dependent CS (ACTH-D), 10 ACTH-independent (ACTH-ID) CS, and 16 healthy controls (C) were included. Leukocytes (Leuc), monocytes (MN), lymphocytes (Lym), and neutrophils (N) were analyzed by flow cytometry for atherosclerosis previously associated with CDs. Results. Leuc, N, and MN correlated with CS (), WC (), WHR (), BMI (), and hs-CRP (). CD14++CD16+ (); CD14+CD16++ () MN; CD15+ (); CD15+CD16+ () N; and NK-Lym () were higher in CS. CD14+CD16++ MN were higher in ACTH-ID (8.9 ± 3.5%) versus ACTH-D CS (4.2 ± 1.9%) versus C (4.9 ± 2.3%). NK-Lym correlated with c-LDL (r = 0.433, ) and CD15+ N with hs-CRP (r = 0.446, ). In multivariate analysis, Leuc, N, and MN depended on BMI (), WC (), and WHR (), while CD15+ and CD15+CD16+ N on hypercortisolism and CS (). Conclusion. In CS, IMNC present changes in activation and adhesion CDs implicated in atherothrombotic inflammation. ACTH-IDCS presents a particular IMNC phenotype, possibly due to the absence of the immune modulator effect of ACTH.