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Updated: Feb 18, 2026
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory
Thomas A Angelovich1, Anna C Hearps2, Anna Maisa3
1Centre for Biomedical Research, Burnet Institute; School of Health and Biomedical Sciences, RMIT University.
Insights
A new human in vitro model assesses monocyte activation and foam cell formation, crucial early steps in atherosclerosis development. This model aids in understanding coronary artery disease risk in various patient groups.
Area of Science:
- Cardiovascular Research
- Immunology
- Atherosclerosis Pathogenesis
Background:
- Coronary artery disease (CAD) is a major global health burden, primarily driven by atherosclerosis.
- Atherosclerosis begins with monocyte transmigration and lipid accumulation, leading to foam cell formation.
- Chronic inflammatory conditions and aging increase atherosclerosis risk, linked to monocyte activation.
Purpose of the Study:
- To develop a novel human in vitro model for evaluating monocyte atherogenic potential.
- To overcome limitations of existing models that assess monocyte transmigration and foam cell formation separately.
- To enable the study of atherogenesis in the context of human comorbid diseases.
Main Methods:
- Isolated human monocytes transmigrate across endothelial cells into a collagen matrix.
- Monocyte maturation into foam cells is measured with or without exogenous lipids.
- The protocol is validated using monocytes from HIV-infected and elderly HIV-uninfected individuals.
Main Results:
- The model successfully measures monocyte transmigration and foam cell formation.
- It allows for the assessment of atherogenic factors in patient serum or plasma.
- Validated for use with diverse human patient populations, including those with HIV.
Conclusions:
- This versatile human in vitro model accurately reflects early atherogenesis stages.
- It provides a platform for studying monocyte-driven atherosclerosis in various disease states.
- The model facilitates research into CAD risk factors and potential therapeutic targets.
Abstract:
Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Atherosclerosis, a leading cause of CAD, is initiated by the transmigration of innate immune monocytes to inflammatory sites of deposited lipid called fatty streaks, which are present in arterial walls of medium to large arteries. The key pathogenic feature of lesions at this early stage of atherosclerosis is the maturation of monocytes which migrate into arteries to form foam cells or lipid-laden macrophages. Considerable evidence supports the hypothesis that risk of atherosclerosis is increased by chronic inflammatory conditions accompanying diseases such as rheumatoid arthritis and HIV, as well as general ageing, and that this risk is predicted by monocyte activation. While mouse models provide a good platform to investigate the role of monocytes in atherogenesis in vivo, they require genetic alteration of natural cholesterol metabolism and drastic alteration of normal mouse diets, and have limited suitability for the study of atherogenic influences of human comorbid diseases. This motivated us to develop a human in vitro model to measure the atherogenic potential of monocytes isolated from individuals with defined disease states. Currently, human in vitro models are limiting in that they evaluate monocyte transmigration and foam cell formation in isolation. Here we describe a protocol in which monocytes isolated from patient blood transmigrate across human endothelial cells into a type 1 collagen matrix, and their propensity to mature into foam cells in the presence or absence of exogenous lipid is measured. The protocol has been validated for the use of human monocytes purified from individuals with HIV infection and elderly HIV uninfected individuals. This model is versatile and allows monocyte transmigration and foam cell formation to be evaluated using either microscopy or flow cytometry as well as allowing the assessment of atherogenic factors present in serum or plasma.
