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Updated: Aug 18, 2026
Depletion and Reconstitution of Macrophages in Mice
Published on: August 1, 2012
Modulation of Fc tau receptor expression and function in mouse peritoneal macrophages by ammonium metavanadate
1Food Science and Human Nutrition Department, University of Florida, Gainesville 32611-0163.
Abstract:
Resident peritoneal macrophages (PEM) harvested from female B6C3F1 mice given an intraperitoneal injection of ammonium metavanadate (2.5 or 10 mg V/kg), an equivalent amount of ammonium in the form of ammonium chloride, or sodium phosphate buffer (0.1 M, pH 7.2) every third day for 6 weeks, were subjected to flow cytometric analysis of Fc tau 2a and Fc tau 2b receptor expression, and photometric microassay to measure receptor mediated binding and phagocytosis of sheep red blood cells (SRBC). The NH4Cl and 10V groups showed 21.7 and 17.2% lower mean fluorescence channel (MFC) values and 7.1 and 5.9% lower values in percentage fluorescence-positive cells than the phosphate buffer control with respect to Fc tau 2a expression. For Fc tau 2b expression, the 10V group showed significantly (P less than 0.05) lower MFC (31.2%) and percentage fluorescence-positive cells (15.7%) than the phosphate buffer control. Though the four groups did not show a significant difference in Fc tau 2a mediated binding and phagocytosis of SRBC, the 10V group showed a significantly lower Fc tau 2b mediated binding and phagocytosis. The results indicate that the reduction in Fc tau 2b expression and function could contribute toward the previously observed depression in phagocytosis, NADPH-oxidase and superoxide generation in peritoneal macrophages obtained from vanadate-treated animals.
Insights
Ammonium metavanadate exposure in mice reduced Fc gamma RIIb (Fc tau 2b) expression and function on peritoneal macrophages. This impaired receptor function may explain previously observed decreases in macrophage phagocytosis and oxidative activity.
Area of Science:
- Immunology
- Toxicology
- Cell Biology
Background:
- Peritoneal macrophages (PEM) play a crucial role in immune responses.
- Vanadium compounds, like ammonium metavanadate, are environmental toxins with known biological effects.
- Previous studies suggest vanadium exposure can impair macrophage function.
Purpose of the Study:
- To investigate the effect of ammonium metavanadate on Fc gamma receptor (Fc gamma R) expression and function in mouse peritoneal macrophages.
- To determine if altered Fc gamma R expression and function correlate with impaired phagocytosis.
Main Methods:
- Mice were treated with ammonium metavanadate, ammonium chloride, or phosphate buffer for 6 weeks.
- Peritoneal macrophages were isolated and analyzed for Fc gamma RIIa (Fc tau 2a) and Fc gamma RIIb (Fc tau 2b) expression using flow cytometry.
- Receptor-mediated binding and phagocytosis of sheep red blood cells (SRBC) were measured.
Main Results:
- Ammonium metavanadate exposure (10 mg V/kg) significantly reduced Fc gamma RIIb expression (mean fluorescence channel and percentage of positive cells).
- While Fc gamma RIIa expression was slightly reduced, Fc gamma RIIb-mediated binding and phagocytosis of SRBC were significantly impaired in vanadate-treated mice.
- No significant differences in Fc gamma RIIa-mediated phagocytosis were observed across groups.
Conclusions:
- Vanadium exposure, specifically ammonium metavanadate, downregulates Fc gamma RIIb expression on peritoneal macrophages.
- The reduction in Fc gamma RIIb expression and function likely contributes to the impaired phagocytic capacity observed in vanadate-treated animals.
- These findings highlight a specific mechanism by which vanadium may compromise immune function.
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