[The effect of opioid peptides on peripheral blood granulocytes].

Some neuropeptides may influence various functions of immunocompetent cells. Endogenous opioids have been implicated in the correlation of the immune, endocrine and nervous system. The object of our study was to evaluate the effects induced by some agonist and antagonist endogenous peptides to opioid receptors on granulocytes (PMNs) functions in vitro. We used these drugs: D-Ala2-D-Leu6-enkephalin (DADL-Sigma-Chemical-Usa); D-Ala2-N-ME-Phe4-Gly-ol5-enkephalin (DAGO-Sigma-Chemical-Usa); Dynorphin 1-9 (Sigma Chemical-Usa); naloxone (Sigma Chemical-Usa) and morphine (Sifac-Italy). Morphine was able to inhibiting neutrophil granulocyte chemotaxis induced by serum activated with E. Coli (p < 0.01), by casein (p < 0.01 and <fMLP (p < 0.01). Furthermore morphine and 1-9 dynorphin inhibited spontaneous migration of PMNs both when added to the upper compartment together with cells. Naloxone was able to inhibit PMNs chemotaxis induced by serum, casein and fMLP, this drug was not able to behave on chemokinesis or random migration activity. Morphine was found to inhibit PMNs aggregation induced by PHA (0.01), PMA (0.01), fMLP (0.01) and Ca++ ionophore (p < 0.01), ATP release (p < 0.01), thromboxane B2 (TxB2) and leukotriene B4 (LTB4) secretion during cell aggregation. Dynorphin 1-9, per sé, induced TxB2 and LTB4 secretion from PMNs. Morphine inhibition of both cell aggregation and ATP release, but not arachidonic acid metabolism product secretion, was prevented by naloxone. The naloxone sensitive impairment by morphine of CD 11/CD 18 complex surface expression observed could play a role in opioid inhibition of PMNs activation.