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Updated: Sep 26, 2026
Culture of Macrophage Colony-stimulating Factor Differentiated Human Monocyte-derived Macrophages
Published on: June 30, 2016
Carvedilol modulates in-vitro granulocyte-macrophage colony-stimulating factor-induced interleukin-10 production in
Shu-Meng Cheng1, Shih-Ping Yang, Ling-Jun Ho
1Division of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, Taipei, Taiwan, ROC.
Insights
Carvedilol, a medication, was found to inhibit the production of interleukin-10 (IL-10) induced by granulocyte-macrophage colony-stimulating factor (GM-CSF) in human cells. This suggests carvedilol may help regulate inflammatory responses involved in conditions like atherosclerosis.
Area of Science:
- Immunology
- Pharmacology
- Cardiovascular Research
Background:
- Granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-10 (IL-10) are key regulators of inflammatory responses.
- Inflammation plays a significant role in the development of atherosclerosis.
Purpose of the Study:
- To investigate the effects of carvedilol on GM-CSF-induced IL-10 production in human monocytic cells (U937) and primary human monocytes.
- To determine the concentration-dependent effects and cytotoxicity of carvedilol.
Main Methods:
- U937 cells and purified human monocytes were pretreated with varying concentrations of carvedilol.
- GM-CSF was used to induce IL-10 production.
- IL-10 levels and mRNA expression were measured.
- Cytotoxicity assays were performed to assess cell viability.
Main Results:
- Carvedilol pretreatment (0.3-10 microM) dose-dependently inhibited GM-CSF-induced IL-10 production in U937 cells and human monocytes.
- Carvedilol was non-cytotoxic at concentrations up to 10 microM but induced apoptosis at higher concentrations.
- Inhibition of IL-10 production was confirmed at the mRNA expression level.
- Long-term (2 months) carvedilol pretreatment (1.0 microM) mildly enhanced IL-10 production.
Conclusions:
- Carvedilol modulates GM-CSF-induced IL-10 production, suggesting a role in regulating inflammatory processes.
- These findings may contribute to understanding the anti-inflammatory mechanisms of carvedilol in conditions like atherosclerosis.
Abstract:
Both granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-10 (IL-10) are important mediators regulating inflammatory responses. Inflammatory processes have an important role in atherogenesis. In this paper, the effects of carvedilol on GM-CSF-induced IL-10 production were examined on human monocytic cell line, U937, and purified human monocytes. First, we showed that one-time carvedilol pretreatment at concentrations 0.3-10 microM dose-dependently inhibited GM-CSF-induced IL-10 production in U937 cells. In addition, we found carvedilol to be non-cytotoxic at concentrations equal to or less than 10 microM. However, at concentrations higher than 10 microM, carvedilol induced programmed cell death in U937 cells. The inhibition of GM-CSF-induced IL-10 production by carvedilol was also observed at the expression of mRNA. Furthermore, the inhibition of IL-10 production was demonstrated in GM-CSF-activated purified human peripheral blood monocytes. Finally, long-term carvedilol pretreatment of U937 cells up to 2 months at concentrations of 1.0 microM mildly enhanced the IL-10 production. Our observations that carvedilol modulated GM-CSF-induced IL-10 production may have some implication in understanding the broad-spectrum effects of carvedilol in regulating inflammatory reactions.
