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Neurotensin modulates human neutrophil locomotion and phagocytic capability
Author(s) -
Goldman Rachel,
Bar-Shavit Zvi,
Romeo Domenico
Publication year - 1983
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(83)80417-7
Subject(s) - intracellular , neurotensin , compartmentalization (fire protection) , degranulation , phagocytosis , vasodilation , vascular permeability , microbiology and biotechnology , inflammation , chemistry , biology , immunology , endocrinology , receptor , biochemistry , neuropeptide , enzyme
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 Ca 2+ extrusion from neutrophils, very likely as a result of intracellular Ca 2+ mobilization. It is suggested that the NT‐mediated functional modulation of neutrophils correlates with the capacity of NT to affect the intracellular compartmentalization of Ca 2+ . 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.