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Published on: April 29, 2015
Methyl palmitate inhibits lipopolysaccharide-stimulated phagocytic activity of rat peritoneal macrophages
Swapna Sarkar1, M Firoze Khan, Bhupendra S Kaphalia
1Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Abstract:
Macrophages, in general, are critical effectors of body's immune system. Chemical inhibition of phagocytic activity of such macrophages as Kupffer cells has been extensively studied. We have earlier shown that methyl palmitate (MP) inhibits the activation of Kupffer cells. To evaluate the potential of MP to inhibit the activation of other macrophages, we treated rat peritoneal macrophages with varying concentrations of MP. Its treatment led to a dose-dependent inhibition of phagocytic activity, which was found to be 34%, 47%, and 66% at 0.25, 0.50, and 1.0 mM MP, respectively, as measured by latex bead uptake. When MP-treated peritoneal macrophages were stimulated with lipopolysaccharide (LPS), the nitric oxide (.NO) release was inhibited at 6 h, while cyclooxygenase-2 expression decreased after 24 h. The treatment with MP increased the release of interleukin (IL)-10 in the LPS-treated cells at 6 h, while IL-6 and tumor necrosis factor-alpha were significantly increased both at 6 and 24 h. Our data suggest that MP inhibits phagocytic activity and .NO production similar to that observed in isolated Kupffer cells. Therefore, inhibition of phagocytosis by MP may be a general phenomenon, and it could be used as an inhibitor of macrophage function.
Insights
Methyl palmitate (MP) inhibits macrophage phagocytic activity in a dose-dependent manner. This compound also suppresses nitric oxide production, suggesting MP is a general inhibitor of macrophage function.
Area of Science:
- Immunology
- Cell Biology
Background:
- Macrophages are key immune cells, with Kupffer cells being a focus of study.
- Methyl palmitate (MP) has previously demonstrated inhibitory effects on Kupffer cell activation.
Purpose of the Study:
- To investigate the potential of methyl palmitate (MP) to inhibit the function of other macrophage types.
- To determine if MP's inhibitory effect on phagocytosis is a general phenomenon.
Main Methods:
- Rat peritoneal macrophages were treated with varying concentrations of MP.
- Phagocytic activity was measured using latex bead uptake.
- Nitric oxide (NO) release, cyclooxygenase-2 (COX-2) expression, and cytokine release (IL-10, IL-6, TNF-alpha) were assessed after lipopolysaccharide (LPS) stimulation.
Main Results:
- MP demonstrated a dose-dependent inhibition of macrophage phagocytic activity (34-66%).
- MP treatment inhibited nitric oxide (NO) release and decreased cyclooxygenase-2 (COX-2) expression.
- MP modulated the release of interleukin-10 (IL-10), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) following LPS stimulation.
Conclusions:
- Methyl palmitate (MP) inhibits phagocytic activity and nitric oxide (NO) production in peritoneal macrophages, similar to its effects on Kupffer cells.
- MP's inhibitory effect on macrophage phagocytosis appears to be a general phenomenon.
- MP shows potential as an inhibitor of general macrophage function.
