Vasoactive intestinal peptide inhibits the respiratory burst in human monocytes by a cyclic AMP-mediated mechanism.

The neuropeptide vasoactive intestinal peptide (VIP) was shown to inhibit the production of reactive oxygen compounds (respiratory burst) in monocytes activated by serum opsonized zymosan. Reactive oxygen compounds are of importance for host defence against micro-organisms and cancer, but normal tissues are also susceptible to damage from these reactive substances. Maximum inhibition of respiratory burst was 40% by 0.1 microM VIP (ID100), while ID50 for the VIP effect was 0.36 nM VIP. PHM-27, closely related to VIP on the basis of the amino acid sequence, inhibited the respiratory burst with much lower potency (ID50 = 60 nM, ID100 = 1 microM). Secretin, related to VIP and PHM-27, produced no effect on the respiratory burst in monocytes. VIP was also shown to stimulate the cyclic AMP production in monocytes in a dose dependent manner. IBMX and forskolin, as well as the cyclic AMP analogue butyryl cyclic AMP were shown to produce an inhibition of the respiratory burst. In conclusion, this study showed that VIP inhibited the respiratory burst in monocytes by a cyclic AMP-mediated mechanism, and serves to establish still another role for VIP as a mediator in the neuro-immune axis.