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J Card Fail. 2016 May;22(5):358-65. doi: 10.1016/j.cardfail.2015.12.014. Epub 2015 Dec 17.

Monocyte Subsets and Inflammatory Cytokines in Acute Decompensated Heart Failure.

Author information

1
University of Michigan, Ann Arbor, Michigan; Ann Arbor Veterans Affairs Health System, Ann Arbor, Michigan. Electronic address: sngoonew@med.umich.edu.
2
University of Michigan, Ann Arbor, Michigan.
3
University of Michigan, Ann Arbor, Michigan; Ann Arbor Veterans Affairs Health System, Ann Arbor, Michigan. Electronic address: scothumm@med.umich.edu.

Abstract

BACKGROUND:

Distinct monocyte subsets predict cardiovascular risk and contribute to heart failure progression in murine models, but they have not been examined in clinical acute decompensated heart failure (ADHF).

METHODS AND RESULTS:

Blood samples were obtained from 11 healthy control subjects (HCs) and at admission and discharge from 19 ADHF patients. Serologic markers of inflammation were assessed at admission and discharge. Monocyte populations were defined with the use of flow cytometry for cell-surface expression of CD14 and CD16: CD14++CD16- (classic), CD14++CD16+ (intermediate), and CD14+CD16++ (nonclassic). In ADHF patients, C-reactive protein (CRP) and interleukin-6 (IL-6) were higher compared with HCs (both P < .001) and decreased from admission to discharge (CRP: 12.1 ± 10.1 to 8.6 ± 8.4 mg/L [P = .005]; IL-6: 19.8 ± 34.5 to 7.1 ± 4.7 pg/mL [P = .08]). In ADHF patients, the admission proportion of CD14++CD16- monocytes was lower (68% vs 85%; P < .001) and that of CD14++CD16+ (15% vs 8%; P = .002) and CD14+CD16++ (17% vs 7%, P = .07) monocytes higher compared with HCs. Additionally, the proportion of CD14++CD16- monocytes increased (68% to 79%, P = .04) and the CD14+CD16++ monocytes decreased (17% to 7%, P = .049) between admission and discharge.

CONCLUSIONS:

Following standard treatment of ADHF, the monocyte profile and circulating inflammatory markers shifts to more closely resemble those of HC, suggesting a resolution of the acute inflammatory state. Functional studies are warranted to understand how specific monocyte subsets and systemic inflammation may contribute to ADHF pathophysiology.

KEYWORDS:

Heart failure; inflammation; innate immunity; monocytes

Comment in

PMID:
26705751
PMCID:
PMC4861694
DOI:
10.1016/j.cardfail.2015.12.014
[Indexed for MEDLINE]
Free PMC Article

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