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Effect of angiotensin II on macrophage functions
Abstract:
Angiotensin II (At II) has been shown to inhibit in vitro the IgG2a-mediated rosette formation of 51Cr-sheep red blood cells (SRBC) by provoked peritoneal macrophages (PM) at 10(-5)-10(-6) M concentrations. The decreased rosette formation was associated with an increased phagocytosis. It was found that the enhanced rosette formation at 10(-7) M hormone concentration was followed by diminished phagocytosis via Fc gamma receptors (R). Processes mediated through Fc microR were affected only after incubation with 10(-5) M of At II. The attachment and subsequent phagocytosis through C3bR was markedly enhanced by At II in a dose-dependent way. Thus, the relative phagocytosis (RP) through both FcRs was significantly enhanced by 10(-5), i.e. by 10(-5)-10(-6) M of At II, but lowered at 10(-7) M hormone concentration. In addition, there was no RP enhancing effect of At II after preincubation with 10(-5) M of indomethacin (IM), indicating the significance of prostaglandins (PG) in the hormone effect. The medium containing 5 mM of EGTA diminished both the RP enhancing and inhibiting effects of At II. The RP mediated by C3b was not affected by At II, IM or EGTA. The intracellular killing capability, measured by chromium release from Candida albicans, was not altered or even slightly diminished after At II treatment of PMs.
Insights
Angiotensin II (At II) affects macrophage phagocytosis through different receptors. It enhances C3bR-mediated uptake while inhibiting Fc gamma receptor activity, with prostaglandin involvement.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Angiotensin II (At II) is a key hormone in the renin-angiotensin system.
- Macrophages play a crucial role in innate and adaptive immunity.
- Phagocytosis is a primary mechanism for pathogen clearance and immune regulation.
Purpose of the Study:
- To investigate the in vitro effects of Angiotensin II on macrophage phagocytosis via different receptor pathways.
- To elucidate the role of prostaglandins and complement in Angiotensin II-mediated modulation of phagocytosis.
Main Methods:
- In vitro experiments using provoked peritoneal macrophages (PM).
- Measurement of rosette formation and phagocytosis of 51Cr-sheep red blood cells (SRBC).
- Assessment of phagocytosis mediated by Fc gamma receptors (Fc gamma R), Fc micro receptors (Fc mu R), and complement C3b receptors (C3bR).
- Evaluation of the effects of indomethacin (IM) and EGTA on Angiotensin II's action.
- Measurement of intracellular killing capability using Candida albicans.
Main Results:
- Angiotensin II inhibited IgG2a-mediated rosette formation (Fc gamma R) at 10(-5)-10(-6) M, correlating with increased phagocytosis.
- At 10(-7) M, Angiotensin II enhanced Fc gamma R rosette formation but diminished phagocytosis.
- Fc mu R-mediated processes were affected only at 10(-5) M Angiotensin II.
- C3bR-mediated attachment and phagocytosis were markedly enhanced by Angiotensin II in a dose-dependent manner.
- Prostaglandins (via indomethacin) and EGTA significantly modulated Angiotensin II's effects on FcR-mediated phagocytosis.
- Intracellular killing capability was not significantly altered by Angiotensin II treatment.
Conclusions:
- Angiotensin II differentially modulates macrophage phagocytosis depending on the receptor pathway involved.
- Prostaglandins play a significant role in mediating Angiotensin II's effects on Fc receptor-dependent phagocytosis.
- Angiotensin II enhances complement-mediated phagocytosis while having complex inhibitory and enhancing effects on Fc receptor-mediated phagocytosis.