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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Monocytes from people with Familial Hypercholesterolaemia are inflammatory, despite statin-treatment
Helen Williams1,2, Habib Francis1,2, Jasmin Huang1,2
1Vascular Biology Research Centre, Department of Surgery, WSLHD Research and Education Network Building, Westmead Hospital, Hawkesbury Road, Westmead, NSW, Australia.
Insights
Monocytes in individuals with Familial Hypercholesterolaemia (FH) are inflammatory and form inflammatory macrophages, even with statin treatment. This inflammation may drive cardiovascular disease risk in FH patients.
Area of Science:
- Cardiovascular Science
- Immunology
- Metabolic Disorders
Background:
- Familial Hypercholesterolaemia (FH) is linked to premature cardiovascular disease, with inflammation being a key factor in atherosclerotic plaque development.
- Inflammation in FH, particularly involving monocytes and macrophages, remains understudied despite their role in plaque destabilization.
Purpose of the Study:
- To investigate if monocytes from FH individuals exhibit an inflammatory profile.
- To determine if these monocytes readily differentiate into inflammatory macrophages.
- To assess if this inflammatory tendency persists in statin-treated FH patients.
Main Methods:
- Whole blood flow cytometry was used to analyze monocyte inflammatory marker expression in FH patients (statin-treated and untreated) and healthy controls.
- Monocytes were cultured with autologous serum to assess their differentiation into macrophages.
- Lipid profiles were obtained for all participants.
Main Results:
- Both treated and untreated FH groups showed elevated inflammatory monocytes (high CD86).
- The inflammatory monocyte marker ratio (CD86/CD163) correlated with LDL-C and ApoB/ApoA1 ratio, suggesting high cholesterol promotes monocyte inflammation.
- Monocyte-derived macrophages from FH individuals also displayed a more inflammatory phenotype.
Conclusions:
- Monocytes in FH individuals are inherently inflammatory, even with cholesterol-lowering treatment.
- These inflammatory monocytes readily form pro-inflammatory macrophages, potentially contributing to plaque instability and cardiovascular events.
- Targeting inflammatory monocytes presents a potential strategy to mitigate residual cardiovascular risk in FH.
Background And Aims:
Familial Hypercholesterolaemia (FH) is characterised by high cholesterol and premature cardiovascular disease. While hypercholesterolaemia and inflammation are both key drivers in the formation of atherosclerotic plaques, inflammation remains understudied in FH. Inflammatory (M1) macrophages contribute to plaque destabilisation and macrophage precursors, monocytes, can be skewed towards an inflammatory state. Aims: Determine; whether monocytes of FH individuals are inflammatory, if they readily form inflammatory macrophages, and whether this remains so in statin-treated individuals.
Methods:
Blood samples were collected from people with FH (statin-treated and untreated) and healthy controls. Lipid profile was obtained and monocyte inflammatory marker expression was determined by whole blood flow cytometry. Monocytes were cultured with autologous serum and resultant macrophage profile determined by flow cytometry.
Results:
Total cholesterol and low-density lipoprotein cholesterol (LDL-C) were higher in the Untreated-FH group compared to the Treated-FH group and controls. In both Treated-FH and Untreated-FH groups, monocytes were inflammatory with high CD86 (M1). The ratio of inflammatory/anti-inflammatory markers (CD86/CD163) significantly correlated with LDL-C and ApoB/ApoA1 ratio across the cohort, indicating the high LDL-C of FH may promote an inflammatory monocyte profile. Monocyte-derived-macrophages from (Treated) FH individuals also had a more inflammatory profile (CD86 and CD86/CD163).
Conclusions:
Overall, monocytes show inflammatory skewing in FH individuals, even those with moderately-reduced cholesterol levels. These monocytes readily become inflammatory macrophages. This, along with subsequent inflammatory macrophage formation, could contribute to plaque destabilisation and downstream clinical events. This supports inflammatory monocyte targeting as a potential approach to reduce residual risk in FH individuals.
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