ECE2016 Eposter Presentations Neuroendocrinology (43 abstracts)
Impaired innate immunity in Cushing’s syndrome: increase CD14+CD16++ monocytes
Gloria Aranda Velazquez 1, , Cristina Lopez 2 , Yaiza Esteban 3 , Mireia Mora 1, , Irene Halperin 1, , Gregori Casals 4 , Joaquim Enseñat 5 & Felicia Alexandra Hanzu 1,
1Endocrinology Department, HCB, Barcelona, Spain; 2Citometry Plataform. IDIBAPS, Barcelona, Spain; 3IDIBAPS-CIBERDEM, Barcelona, Spain; 4Hormonal Laboratory, HCB, Barcelona, Spain; 5Neurosurgery, HCB, Barcelona, Spain.
Introduction: Chronic hypercortisolism is marked by an increased cardiovascular risk pattern. Atherosclerosis is a chronic inflammation that involves both innate and adaptive immunity. Glucocorticoids (GC) are immune-suppressors and adrenocorticotrophic hormone (ACTH) possesses immune-modulatory activities. GC and ACTH may act in atherothrombotic inflammatory pathways.
Aim: To analyze the immune cells pattern in endogenous Cushing syndrome (CS) in order to investigate their atherovascular risk phenotype and to evaluate the immune modulator role of ACTH on this pattern.
Material and Methods: 26 CS: 16 ACTH dependent (D), 10 ACTH independent (ID) and 12 healthy controls (C) were included and peripheral immune cells, respectively monocytes (MN), lymphocytes (L) and neutrophils (N) analyzed by flow cytometry for the presence of cell surface activation markers previously associated with atherosclerosis.
Results: Leukocytes, N, M, NKL were increased in CS (P*<0.05). Atypical CD14+CD16++M were higher in ACTH-ID CS (8.9±3.5%) vs ACTH-D CS (4.2±1.9%). Other tendencies: CD11b+ cells increased in ACTH-ID CS; CD15+, CD15+CD16+ and CD15+CD16+11b+N were higher in CS.
Conclusion: High chronic exposure to GC in CS increase in the absence of the protective immune-modulator presence of ACTH the non-classical atherovascular risk CD14+CD16++ monocytes.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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