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The Journal of Immunology, 2001, 166: 3650-3654.
Copyright © 2001 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: Nociceptin Stimulates Neutrophil Chemotaxis and Recruitment: Inhibition by Aspirin-Triggered-15-Epi-Lipoxin A41

Charles N. Serhan2, Iolanda M. Fierro3, Nan Chiang and Marc Pouliot4

Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115

The nociceptin receptor (Noci-R) is a G protein-coupled receptor present in neural tissues and its activation by nociceptin is involved in the processing of pain signals. Here, we report that Noci-R is present and functional on peripheral blood polymorphonuclear leukocytes (PMN). Human PMN express mRNA for Noci-R, its nucleotide sequence determined, and specific binding with [125I]-labeled nociceptin gave an apparent Kd ~1.5 nM for this PMN opioid receptor. Nociceptin evoked PMN chemotaxis with maximal activity at 100 pM, without intracellular Ca2+ mobilization. When injected in murine air pouches, nociceptin elicited leukocyte infiltration in a concentration-dependent fashion. Nociceptin-stimulated PMN infiltration was inhibited by treating mice with a synthetic analog of the aspirin-triggered lipid mediator 15-epi-lipoxin A4. The present results identify nociceptin as a potent chemoattractant and provide a novel link between the neural and immune systems that are blocked by aspirin-triggered lipid mediators and may be relevant in neurogenic inflammation.




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