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Updated: May 16, 2026

Characterization of Human Monocyte Subsets by Whole Blood Flow Cytometry Analysis
Published on: October 17, 2018
Changes in the monocytic subsets CD14(dim)CD16(+) and CD14(++)CD16(-) in chronic systolic heart failure patients
Offer Amir1, Ilia Spivak, Idit Lavi
1Heart Failure Center, Division of Cardiology, Lady Davis Carmel Medical Center and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, 34362 Haifa, Israel.
Insights
In heart failure (HF) patients, classical monocytes decrease while nonclassical monocytes increase, potentially counteracting adverse heart remodeling. These nonclassical monocytes also produce IL-13, a cytokine linked to HF severity.
Area of Science:
- Immunology
- Cardiology
- Biomedical Science
Background:
- Monocytic subsets play roles in inflammation and tissue remodeling.
- Heart failure (HF) involves inflammation, but monocytic subset roles in HF remain unclear.
Purpose of the Study:
- To investigate the distribution and function of monocytic subsets in chronic systolic heart failure patients.
- To explore the relationship between monocytic subsets, inflammation, and cardiac remodeling in HF.
Main Methods:
- Flow cytometry was used to analyze monocytic subsets (CD14++CD16-, CD14+CD16+, CD14dimCD16+) in 59 HF patients and 29 controls.
- Serum cytokine levels (TNFα, IL-1β, IL-10, IL-13) were measured.
- Intracellular cytokine staining was performed to identify cytokine-producing monocytes.
Main Results:
- HF patients showed decreased classical (CD14++CD16-) and expanded nonclassical (CD14dimCD16+) monocyte subsets compared to controls.
- The expansion of nonclassical monocytes was inversely associated with HF severity (increased end-diastolic dimension).
- Serum IL-13 levels were elevated in HF patients and positively correlated with the nonclassical monocyte subset, which was found to produce IL-13.
Conclusions:
- The altered distribution of monocytic subsets in HF may reflect an attempt to counterbalance adverse cardiac remodeling.
- Nonclassical monocytes producing IL-13 might play a protective role in mitigating HF-associated tissue remodeling.
Abstract:
Different monocytic subsets are important in inflammation and tissue remodelling, but although heart failure (HF) is associated with local and systemic inflammation, their roles in HF are yet unknown. We recruited 59 chronic systolic HF patients (aged 58 ± 13 years, 45 males and 14 females) and 29 age-matched controls with no pervious heart disease. Compared to the controls, we found no change in the distribution of the CD14(+)CD16(+) monocytic subset, whereas the classical CD14(++)CD16(-) subset was decreased by 11% (P < 0.001), and the nonclassical CD14(dim)CD16(+) subset was expanded by 4% (P < 0.001) in HF patients and was inversely associated with severe HF (P = 0.015), as assessed by increased end-diastolic dimension (EDD). Compared to the control group, serum TNFα, IL-1β, IL-10, and IL-13 levels were significantly elevated in the HF patients. Specifically, IL-13 levels were positively correlated to the CD1CD14(dim)CD16(+) monocytic subset (r = 0.277, P = 0.017), and intracellular staining of IL-13 demonstrated that some of these monocytes produce the cytokine in HF patients, but not in the controls. We suggest that the inverse association between EDD values and the expansion of CD14(dim)CD16(+) monocytes that can produce IL-13 could be explained as a measure to counterbalance adverse remodelling, which is a central process in HF.
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