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The immunostimulatory peptide WKYMVm-NH activates bone marrow mouse neutrophils via multiple signal transduction pathways.

Abstract：

:G-protein-coupled receptors play a major role in the activation of the innate immune system, such as polymorphonuclear neutrophils. Members of the formyl peptide receptor family recognize chemotactic peptides as well the amyloïd-beta peptide and fragments of the human immunodeficiency virus envelope and may thus be implicated in major pathologies. The peptide WKYMVm-NH2 probably activates the receptor FPRL1 and its mouse orthologues Fpr-rs1 and Fpr-rs2. We examined the stimulation of C57BL6 mouse neutrophils by WKYMVm-NH2 and the effects of several inhibitors for intracellular signalling pathways (wortmannin, LY 294002, staurosporin, H-89, U 73122, thapsigargin and SKF 96365). We show here that WKYMVm-NH2 is a powerful stimulator of primary and secondary granule exocytosis as well as superoxide production. The signalling pathway involves phosphoinositide 3-kinase, protein kinase C, phospholipase C and store-operated calcium influx. Studies with peptide antagonists suggest that WKYMVm-NH2 preferentially activates exocytosis via FPRL1 and not FPR, the major receptor for N-formylated peptides such as fMLF. However, the signalling pathways activated by WKYMVm-NH2 in mouse neutrophils are similar to those activated by fMLF in human neutrophils. Thus, the effect and the signalling pathways of the two agonists and their receptors are at least partially overlapping.

journal_name

Scand J Immunol

journal_title

Scandinavian journal of immunology

authors

Boxio R,Bossenmeyer-Pourié C,Vanderesse R,Dournon C,Nüsse O

doi

10.1111/j.1365-3083.2005.01651.x

keywords:

subject

Has Abstract

pub_date

2005-08-01 00:00:00

pages

140-7

issue

2

eissn

0300-9475

issn

1365-3083

pii

SJI1651

journal_volume

62

pub_type

杂志文章

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