Neurotensin modulates human neutrophil locomotion and phagocytic capability.
Neurotensin (NT) was found to induce oriented locomotion and augment the phagocytic capability of human blood neutrophils over 10(-11) - 10(-7) M. The tridecapeptide also causes Ca2+ extrusion from neutrophils, very likely as a result of intracellular Ca2+ mobilization. It is suggested that the NT-mediated functional modulation of neutrophils correlates with the capacity of NT to affect the intracellular compartmentalization of Ca2+. Peripheral NT-elicited phenomena such as vasodilation, enhanced vascular compartmentalization of Ca2+. Peripheral NT-elicited phenomena such as vasodilation, enhanced vascular permeability, mast cell degranulation and the enhancement of directional migration and phagocytosis of neutrophils described here, classify NT as a typical mediator of inflammation.
D002118:Calcium / Q000097:blood; D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D006801:Humans; D007700:Kinetics; D009496:Neurotensin / Q000494:pharmacology*; D009504:Neutrophils / Q000276:immunology*; D010587:Phagocytosis / Q000187:drug effects*
D009496:Neurotensin; D002118:Calcium