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Effects of Atorvastatin on Th polarization in patients with acute myocardial infarction
Xiang Cheng1, Yu-Hua Liao, Jinying Zhang
1The Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.
Insights
Atorvastatin reduces T helper 1 cell development in acute myocardial infarction patients, potentially improving heart function. This study investigated atorvastatin
Area of Science:
- Immunology
- Cardiology
- Pharmacology
Background:
- Inflammation, regulated by T helper (Th) 1 and Th2 lymphocytes, influences heart failure post-acute myocardial infarction (AMI).
- Statins are known to potentially improve cardiac function following AMI.
Purpose of the Study:
- To investigate the impact of atorvastatin on T helper cell polarization in patients diagnosed with AMI.
Main Methods:
- Peripheral blood mononuclear cells from AMI patients with and without atorvastatin treatment were analyzed.
- Flow cytometry quantified cytokine-producing Th lymphocytes before and after in vitro atorvastatin exposure.
Main Results:
- Atorvastatin treatment significantly decreased the ratio of IFN-gamma-producing T cells (Th1) in AMI patients.
- In vitro atorvastatin exposure reduced Th1 development in the AMI-C group.
- No significant changes were observed in interleukin-4-producing T cells (Th2) frequencies.
Conclusions:
- Atorvastatin modulates Th1/Th2 polarization by reducing Th1 cell development without affecting Th2 cell function in AMI patients.
- This regulation of T helper cell polarization may represent a mechanism by which atorvastatin enhances cardiac recovery after AMI.
Background:
The development of heart failure after acute myocardial infarction (AMI) has been shown to be associated with inflammation, which is positively and negatively regulated by T helper (Th) 1 and Th2 lymphocytes, respectively. Several studies have indicated that statins can improve heart function after AMI.
Aims:
To study the effects of atorvastatin on Th polarization in patients with AMI.
Methods:
Peripheral blood mononuclear cells were collected from 20 patients with AMI treated with oral atorvastatin (10 mg/d, group AMI-A) and 18 patients with AMI (group AMI-C) who did not receive treatment with statins. Cytokine-producing Th lymphocytes were quantified by 3-color flow cytometry. After in vitro culturing in the presence or absence of atorvastatin (0, 0.3, 1 and 3 micromol/L) for 6 days, cytokine-producing Th lymphocytes were quantified again in AMI-C group.
Results:
The ratio of IFN-gamma-producing T cells was significantly higher in AMI-C group (17.8% +/- 6.4%) than in the AMI patients treated with oral atorvastatin (AMI-A, 13.1% +/- 4.6%). In vitro culturing with atorvastatin significantly reduced Th1 development in the AMI-C group. There was no significant difference on the frequencies of interleukin (IL)-4-producing T cells between each group.
Conclusions:
Atorvastatin can reduce Th1 development but has no effect on Th2 cell-functions in AMI patients. Our findings suggest that atorvastatin can regulate the polarization of Th1/Th2, this may be one of the mechanisms through which atorvastatin improves heart function after AMI.
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