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Updated: Mar 26, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
[Ability of human monocytes to activate in atherosclerosis]
Insights
Individual immune response characteristics, not cholesterol, dictate monocyte activation. This study reveals significant patient variations in macrophage activation, impacting immune responses in atherosclerosis.
Area of Science:
- Immunology
- Cardiovascular Science
- Cell Biology
Background:
- Monocytes play a key role in immune responses and are implicated in atherosclerosis.
- Intima-media thickness (IMT) and atherosclerotic plaques indicate cardiovascular risk.
- Macrophage activation markers include TNF-α and CCL18.
Purpose of the Study:
- To investigate individual differences in monocyte activation capacity.
- To explore the relationship between intracellular cholesterol and monocyte activation.
- To determine if atherogenic lipoproteins influence monocyte activation.
Main Methods:
- Isolation of monocytes from patients with varying carotid IMT and atherosclerotic plaque status.
- Measurement of TNF-α and CCL18 cytokine/chemokine concentrations in culture medium.
- In vitro culture of monocytes with modified low-density lipoprotein to induce cholesterol accumulation.
Main Results:
- Significant individual variations in TNF-α and CCL18 levels were observed across all patient groups.
- An inverse correlation was found between intracellular cholesterol levels and monocyte activation.
- Induced intracellular cholesterol accumulation did not affect cytokine secretion or gene expression.
Conclusions:
- Individual differences in monocyte activation capacity are not solely determined by intracellular cholesterol accumulation from atherogenic lipoproteins.
- The findings suggest that inherent individual characteristics of the immune response are crucial in modulating monocyte activation.
- Understanding these individual variations may offer new insights into personalized approaches for managing atherosclerosis.
Abstract:
Monocytes were isolated from blood of patients belonging to three groups: those with normal intima-media thickness (IMT) of carotid arteries, patients with increased IMT and patients with atherosclerotic plaques. The degree of activation of the macrophages was determined by the concentration of the cytokine TNF-α and chemokine CCL18 in the culture medium. When comparing the average values of the concentrations of TNF-α and CCL18 for patients in all groups dramatic individual differences were revealed. These individual differences were found within each group and in the pool. An inverse relationship between intracellular cholesterol levels and the ability of monocytes to activate was found. To clarify the cause of this relationship, monocytes were cultured with atherogenic modified low-density lipoprotein, causing accumulation of cholesterol in cultured cells. The accumulation of intracellular cholesterol had no effect neither on the secretion of cytokines nor on the expression of their genes. Therefore, individual differences in the activation capacity of monocytes is not determined by the accumulation of intracellular cholesterol caused by atherogenic lipoproteins. The data obtained can be explained by the individual characteristics of the immune response in different patients.
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