Neurotensin modulates human neutrophil locomotion and phagocytic capability

Rachel Goldman; Zvi Bar-Shavit; Domenico Romeo

doi:10.1016/0014-5793(83)80417-7

Neurotensin modulates human neutrophil locomotion and phagocytic capability

Rachel Goldman, Zvi Bar-Shavit, Domenico Romeo^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

42 Scopus citations

Abstract

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 permeability, mast cell degranulation and the enhancement of directional migration and phagocytosis of neutrophils described here, classify NT as a typical mediator of inflammation.

Original language	English
Pages (from-to)	63-67
Number of pages	5
Journal	FEBS Letters
Volume	159
Issue number	1-2
DOIs	https://doi.org/10.1016/0014-5793(83)80417-7
State	Published - 8 Aug 1983
Externally published	Yes

Keywords

Ca extrusion
Chemotaxis
Inflammation
Neurotensin
Neutrophil
Phagocytosis

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10.1016/0014-5793(83)80417-7

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abstract = "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 permeability, mast cell degranulation and the enhancement of directional migration and phagocytosis of neutrophils described here, classify NT as a typical mediator of inflammation.",

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N2 - 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 permeability, mast cell degranulation and the enhancement of directional migration and phagocytosis of neutrophils described here, classify NT as a typical mediator of inflammation.

AB - 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 permeability, mast cell degranulation and the enhancement of directional migration and phagocytosis of neutrophils described here, classify NT as a typical mediator of inflammation.

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KW - Chemotaxis

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Neurotensin modulates human neutrophil locomotion and phagocytic capability

Abstract

Keywords

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