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Opioids Trigger ₅₁ Integrin-Mediated Monocyte Adhesion¹

Oscar M. Pello^*, Béatrice Duthey^*, David García-Bernal, José Miguel Rodríguez-Frade^*, Jens V. Stein, Joaquín Teixido, Carlos Martínez-A.^* and Mario Mellado^2,*

^* Department of Immunology and Oncology, Centro Nacional de Biotecnología/Consejo Superior de Investigaciones Científicas, and Centro de Investigaciones Biologícas/Consejo Superior de Investigaciones Científicas, Madrid, Spain; and Theodor-Kocher-Institut, Universität Bern, Bern, Switzerland

Inflammatory reactions involve a network of chemical and molecular signals that initiate and maintain host response. In inflamed tissue, immune system cells generate opioid peptides that contribute to potent analgesia by acting on specific peripheral sensory neurons. In this study, we show that opioids also modulate immune cell function in vitro and in vivo. By binding to its specific receptor, the opioid receptor-specific ligand DPDPE triggers monocyte adhesion. Integrins have a key role in this process, as adhesion is abrogated in cells treated with specific neutralizing anti-₅₁ integrin mAb. We found that DPDPE-triggered monocyte adhesion requires PI3K activation and involves Src kinases, the guanine nucleotide exchange factor Vav-1, and the small GTPase Rac1. DPDPE also induces adhesion of pertussis toxin-treated cells, indicating involvement of G proteins other than G_i. These data show that opioids have important implications in regulating leukocyte trafficking, adding a new function to their known effects as immune response modulators.

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