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Inhibitory effect of vasoactive intestinal peptide (VIP) on phagocytosis in mouse peritoneal macrophages
M Ichinose1, M Sawada, T Maeno
1Department of Physiology, Shimane Medical University, Izumo, Japan.
Abstract:
The effect of VIP on phagocytosis in peritoneal macrophages was examined by means of flow cytometry (FCM). This assay revealed that VIP suppressed phagocytosis in a dose-dependent manner. VIP(1-12) did not suppress phagocytosis. VIP(10-28) was more suppressive than VIP(1-28). A known VIP-antagonist (N-Ac-Tyr1,D-Phe2)-growth hormone-releasing factor (GRF) (1-29)-NH2 suppressed phagocytosis less than VIP. Control phagocytosis was partially suppressed in Ca(2+)-free solution. Phagocytosis was suppressed by VIP further in Ca(2+)-free solution than in the normal solution. Phagocytosis was suppressed in a known phosphodiesterase inhibitor IBMX-containing solution. The degree of suppression by VIP was the same in the presence or the absence of IBMX. These results suggest that VIP suppresses extracellular Ca(2+)-dependent and -independent phagocytosis, that the C-terminal fragment of VIP is essential for VIP action, that the suppression is mediated by cAMP and that the inhibition of macrophage phagocytosis by VIP is one of the mechanisms which modulates immune responses by the nervous system.
Insights
Vasoactive intestinal peptide (VIP) suppresses macrophage phagocytosis in a dose-dependent way, with the C-terminal fragment being crucial for this immune response modulation.
Area of Science:
- Immunology
- Neuroendocrinology
- Cell Biology
Background:
- Phagocytosis is a critical cellular process for immune defense.
- Vasoactive intestinal peptide (VIP) is a neuropeptide with known immunomodulatory functions.
- The precise mechanisms by which VIP affects macrophage phagocytosis require further elucidation.
Purpose of the Study:
- To investigate the effect of VIP on phagocytosis in peritoneal macrophages.
- To determine the dose-dependency and structural requirements of VIP's action on phagocytosis.
- To explore the role of calcium and cyclic AMP (cAMP) in VIP-mediated suppression of phagocytosis.
Main Methods:
- Flow cytometry (FCM) was employed to quantify phagocytosis.
- Macrophages were treated with varying concentrations of VIP and its fragments.
- Experiments were conducted in the presence or absence of calcium and a phosphodiesterase inhibitor (IBMX).
Main Results:
- VIP significantly suppressed macrophage phagocytosis in a dose-dependent manner.
- The C-terminal fragment of VIP (VIP 10-28) was more potent in suppression than the full-length peptide.
- VIP-induced suppression occurred independently of extracellular calcium and was mediated by cAMP, as indicated by experiments with IBMX.
Conclusions:
- VIP inhibits both extracellular calcium-dependent and -independent phagocytosis.
- The C-terminal portion of VIP is essential for its suppressive activity on phagocytosis.
- VIP modulates immune responses by inhibiting macrophage phagocytosis, likely through a cAMP-dependent pathway, linking the nervous system to immune function.