Inhibitory effect of vasoactive intestinal peptide (VIP) on phagocytosis in mouse peritoneal macrophages.
Ichinose. M M; Sawada. M M; Maeno. T T
Key Findings
- VIP suppresses macrophage phagocytosis in a dose‑dependent way.
- The C‑terminal fragment of VIP (amino acids 10‑28) is required for the suppression; the N‑terminal fragment (1‑12) does not work.
- A VIP‑antagonist peptide (N‑Ac‑Tyr1,D‑Phe2‑GRF‑1‑29‑NH2) reduces phagocytosis, but far less than VIP itself.
Practical Outcomes
- For biohackers, the data suggest that using GRF‑1‑29 is unlikely to boost immune‑cell “eating” functions and may even slightly dampen them. There is no clear protocol or dosage recommendation for health or performance benefits, and the findings are mainly of mechanistic interest rather than actionable guidance.
Summary
The study shows that the brain‑gut peptide VIP can dial down the ability of mouse immune cells (macrophages) to eat foreign particles, and that a short piece of VIP (the C‑terminal part) is needed for this effect. A related peptide, GRF‑1‑29, which blocks VIP, only weakly reduces this eating activity.
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.
Study Information
pubmed
1994
1994-12-15T00:00:00.000Z
10.1016/0167-0115(94)90543-6
15
31