|CD14CD16 monocyte subset levels in heart failure patients.|
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|PMID: 20364047 Owner: NLM Status: MEDLINE|
|Our aim was to define the distribution of monocyte subsets in a cohort of congestive heart failure (CHF) patients, to verify whether increased severity of CHF is linked to the expansion of specific monocyte subsets, and finally to investigate the relationship between monocyte subset relative frequencies, laboratory parameters of inflammation, and monocyte ACE expression. Thirty consecutive CHF patients and 26 healthy control subjects were evaluated for peripheral blood monocyte expression of CD14, CD16 and CD143 (ACE) by flow-cytometry, and for endothelial-derived soluble CD146 levels by ELISA. CD14++ CD16+ frequency was significantly higher in CHF patients than in Controls (%, median value and IQ) (12.3, 8.7-14.8 vs 5.9, 4.7-6.9, p< 0.05, CHF vs Controls), and it increased depending on how high NYHA class was, on worsening LV ejection fraction and on circulating pro-BNP values. Furthermore, it was associated with increasing creatinine and with decreasing GFR and albumin levels. Monocyte CD143 expression was significantly elevated in CHF patients as compared to Controls, and positively associated with CD14++ CD16+ levels. Frequencies of CD14+ CD16+ monocytes were significantly lower in CHF patients as compared to Controls, and negatively correlated with levels of soluble CD146 (r=-0.529; p 0.048). In conclusion, monocytic CD14++ CD16+ frequency and CD143 levels are increased and reflect disease status and progressive cardiac deterioration in CHF patients. The CD14+ CD16+ subset is depleted in CHF and is linked to endothelial damage in this group of patients. Although the question of whether differences in monocyte CD14CD16 expansion are causal or whether they represent a marker of HF progression which is potentially relevant for risk prediction remains unanswered, we believe that our data represent an important tool for exploring the role of selective inflammatory pathways in CHF progression.|
|Chiara Barisione; Silvano Garibaldi; Giorgio Ghigliotti; Patrizia Fabbi; Paola Altieri; Maria Carla Casale; Paolo Spallarossa; Giovanni Bertero; Manrico Balbi; Luca Corsiglia; Claudio Brunelli|
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|Type: Journal Article|
|Title: Disease markers Volume: 28 ISSN: 1875-8630 ISO Abbreviation: Dis. Markers Publication Date: 2010|
|Created Date: 2010-04-05 Completed Date: 2010-06-29 Revised Date: 2013-12-17|
Medline Journal Info:
|Nlm Unique ID: 8604127 Medline TA: Dis Markers Country: Netherlands|
|Languages: eng Pagination: 115-24 Citation Subset: IM|
|APA/MLA Format Download EndNote Download BibTex|
Antigens, CD14 / blood*
Biological Markers / blood
C-Reactive Protein / metabolism
Heart Failure / blood*, physiopathology
Inflammation Mediators / blood
Kidney / physiopathology
Monocytes / classification*, enzymology, immunology*
Peptidyl-Dipeptidase A / blood
Receptors, IgG / blood*
|0/Antigens, CD14; 0/Biological Markers; 0/FCGR3B protein, human; 0/GPI-Linked Proteins; 0/Inflammation Mediators; 0/Receptors, IgG; 9007-41-4/C-Reactive Protein; EC 22.214.171.124/Peptidyl-Dipeptidase A|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Journal ID (nlm-ta): Dis Markers
Journal ID (iso-abbrev): Dis. Markers
Journal ID (publisher-id): DM
Publisher: IOS Press
Copyright © 2010 Hindawi Publishing Corporation.
Received Day: 25 Month: 3 Year: 2010
Accepted Day: 25 Month: 3 Year: 2010
Print publication date: Year: 2010
Electronic publication date: Day: 2 Month: 4 Year: 2010
Volume: 28 Issue: 2
First Page: 115 Last Page: 124
PubMed Id: 20364047
Article Id: 236405
|CD14CD16 Monocyte Subset Levels in Heart Failure Patients|
|Maria Carla Casale1|
1Division of CardiologyDepartment of Internal MedicineResearch Center of Cardiovascular BiologyUniversity of GenovaV.le Benedetto XV6 16132 GenovaItaly
2Casa Di Cura Istituto Cardiovascolare Camogli (ISC)CamogliItaly
|Correspondence: *Giorgio Ghigliotti: firstname.lastname@example.org
Keywords: Angiotensin, congestive heart failure, monocytes, peptidyl-dipeptidase A, antigens, CD14, receptors, IgG, kidney failure, chronic.
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