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Published on: May 6, 2014
IMMUNE RESPONSE OF CULTURED MONOCYTES OF ATHEROSCLEROTIC PATIENTS RECEIVING STATIN THERAPY
T Kirichenko1, I Yudina2, M Lukina2
11Petrovsky National Research Centre of Surgery, Moscow; 2Petrovsky Medical University, Moscow, Russia.
Insights
Statin therapy, including rosuvastatin and atorvastatin, significantly reduces inflammatory cytokine secretion from monocytes in patients with coronary atherosclerosis. This reduction correlates with lower cholesterol and LDL levels, highlighting statins
Area of Science:
- Immunology
- Cardiovascular Medicine
- Pharmacology
Background:
- Atherosclerosis is a chronic inflammatory disease characterized by lipid deposition and immune cell infiltration in arterial walls.
- Monocytes/macrophages play a crucial role in the inflammatory processes underlying atherosclerosis.
- Statins are widely used for lipid-lowering but also possess pleiotropic anti-inflammatory effects.
Purpose of the Study:
- To evaluate the impact of hydrophilic (rosuvastatin) and lipophilic (atorvastatin) statins on the inflammatory response of monocytes/macrophages from atherosclerotic patients.
- To assess the effect of statin therapy on the secretion of key inflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), by circulating monocytes.
- To investigate the relationship between serum lipid levels and monocyte inflammatory cytokine production in patients with coronary atherosclerosis.
Main Methods:
- Inclusion of three groups: 20 patients receiving atorvastatin, 20 receiving rosuvastatin, and 20 without statin therapy, all with coronary atherosclerosis.
- Isolation of CD14+ monocytes from whole blood via immunomagnetic separation.
- Culture of isolated monocytes for 7 days with or without lipopolysaccharide (LPS) stimulation, followed by ELISA measurement of TNF-α and IL-1β secretion.
Main Results:
- Both atorvastatin and rosuvastatin significantly reduced basal TNF-α secretion compared to the statin-free group.
- Rosuvastatin, but not atorvastatin, significantly reduced basal IL-1β secretion.
- Both statins significantly reduced LPS-stimulated IL-1β secretion, while TNF-α secretion differences were not significant. Rosuvastatin also reduced re-stimulated TNF-α secretion.
Conclusions:
- Statin therapy demonstrably decreases inflammatory cytokine secretion from monocytes in patients with coronary atherosclerosis.
- Rosuvastatin exhibited a more pronounced effect on reducing inflammatory cytokine secretion compared to atorvastatin.
- The observed reduction in TNF-α and IL-1β secretion correlated with lower total cholesterol and LDL serum levels.
Aim:
The current study was aimed to evaluate the immune response of monocytes/macrophages derived from atherosclerotic patients receiving hydrophilic and lipophilic statins and without lipid-lowering therapy, in order to evaluate the effect of statins on the inflammatory status of circulating monocytes.
Materials And Methods:
Three groups of 20 patients with atherosclerosis of the coronary arteries were included in the study: patients receiving atorvastatin or rosuvastatin therapy for at least 12 months before inclusion in the study and participants without statin therapy within a year before the inclusion in the study. CD14+ monocytes were derived from the whole blood of study participants by immunomagnetic separation. The isolated cells were cultured for 7 days under inflammatory stimulation with LPS and without stimulation. The level of basal, LPS-stimulated and re-stimulated secretion of inflammatory cytokines TNF-α and IL-1β was determined by ELISA.
Results:
The significantly lower basal secretion of TNF-α was revealed in atorvastatin and rosuvastatin groups in comparison with statin-free group (p=0.003; p<0.001); the basal secretion of IL-1β was lower only in rosuvastatin recipients (p=0.020). LPS-stimulated secretion of TNF-α wasn't significantly different in all groups while secretion of IL-1β was significantly reduced in both atorvastatin and rosuvastatin groups (p=0.002; p=0.001). The re-stimulated secretion of TNF-α was significantly lower in rosuvastatin recipients (p=0.031); the effect of statins on re-stimulated secretion IL-1β wasn't revealed. The correlation analysis revealed the association of total cholesterol and LDL serum levels with basal secretion of TNF-α and IL-1β.
Conclusions:
Thus, the study demonstrated the significant decrease of inflammatory cytokines secretion by cultured monocytes of patients with coronary atherosclerosis receiving statin therapy. The most prominent effect was observed in rosuvastatin recipients. The reduction of the TNF-α and IL-1β secretion by monocytes correlated with low levels of total cholesterol and LDL.
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