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Mast cell-derived tumour necrosis factor-alpha mediates macrophage inflammatory protein-2-induced recruitment of neutrophils in mice.

Wang, Yusheng LU and Thorlacius, Henrik LU (2005) In British Journal of Pharmacology 145(8). p.1062-1068
Abstract
1 Recent studies have indicated that mast cells play an intermediate role in chemokine-induced neutrophil recruitment in vivo. 2 The aim of the present investigation was to determine the role of tumour necrosis factor-alpha (TNF-alpha) in neutrophil recruitment provoked by the CXC chemokine macrophage inflammatory protein-2 (MIP-2). For this purpose, we used mast cell- and TNF-alpha-deficient mice and studied neutrophil adhesion to endothelial cells in vitro and neutrophil recruitment in the mouse cremaster muscle in vivo. 3 In contrast to the classical chemoattractant formyl-methionine-leucine-phenylalanin ( fMLP), MIP-2 dose dependently increased neutrophil accumulation in vivo. This MIP-2-regulated neutrophil recruitment was abolished... (More)
1 Recent studies have indicated that mast cells play an intermediate role in chemokine-induced neutrophil recruitment in vivo. 2 The aim of the present investigation was to determine the role of tumour necrosis factor-alpha (TNF-alpha) in neutrophil recruitment provoked by the CXC chemokine macrophage inflammatory protein-2 (MIP-2). For this purpose, we used mast cell- and TNF-alpha-deficient mice and studied neutrophil adhesion to endothelial cells in vitro and neutrophil recruitment in the mouse cremaster muscle in vivo. 3 In contrast to the classical chemoattractant formyl-methionine-leucine-phenylalanin ( fMLP), MIP-2 dose dependently increased neutrophil accumulation in vivo. This MIP-2-regulated neutrophil recruitment was abolished in mast cell- deficient mice. 4 TNF-alpha increased E-selectin mRNA expression in both wild-type (WT) and mast cell-deficient mice. In contrast, MIP-2 challenge increased gene expression of E-selectin in WT but not in mast cell-deficient animals. Moreover, MIP-2-provoked extravascular accumulation of neutrophils was reduced by 78% in mice lacking TNF-alpha. 5 In order to better define the role of mast cell-derived TNF-alpha in neutrophil responses to MIP-2, we used an in vitro endothelial cell adhesion assay with and without mast cells. Interestingly, MIP-2-induced neutrophil adhesion to endothelial cells was decreased by 58% using TNF-alpha-deficient compared to WT mast cells. Moreover, mast cell secretion of TNF-alpha increased by more than 71% in response to challenge with MIP-2. 6 Taken together, our results suggest that MIP-2-induced neutrophil recruitment is mediated by TNF-alpha released from local mast cells. These findings help to explain the complex molecular interactions between chemokines, mast cell activation and neutrophil infiltration in vivo. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
mast cells, adhesion, chemokines, migration, leukocytes
in
British Journal of Pharmacology
volume
145
issue
8
pages
1062 - 1068
publisher
The British Pharmacological Society
external identifiers
  • wos:000231722000007
  • pmid:15937521
  • scopus:30544448930
ISSN
1476-5381
DOI
10.1038/sj.bjp.0706274
language
English
LU publication?
yes
id
9ec79dfd-993f-443a-a90c-f4ac9520541d (old id 140231)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15937521&query_hl=25
date added to LUP
2007-07-30 14:39:42
date last changed
2017-01-01 06:55:21
@article{9ec79dfd-993f-443a-a90c-f4ac9520541d,
  abstract     = {1 Recent studies have indicated that mast cells play an intermediate role in chemokine-induced neutrophil recruitment in vivo. 2 The aim of the present investigation was to determine the role of tumour necrosis factor-alpha (TNF-alpha) in neutrophil recruitment provoked by the CXC chemokine macrophage inflammatory protein-2 (MIP-2). For this purpose, we used mast cell- and TNF-alpha-deficient mice and studied neutrophil adhesion to endothelial cells in vitro and neutrophil recruitment in the mouse cremaster muscle in vivo. 3 In contrast to the classical chemoattractant formyl-methionine-leucine-phenylalanin ( fMLP), MIP-2 dose dependently increased neutrophil accumulation in vivo. This MIP-2-regulated neutrophil recruitment was abolished in mast cell- deficient mice. 4 TNF-alpha increased E-selectin mRNA expression in both wild-type (WT) and mast cell-deficient mice. In contrast, MIP-2 challenge increased gene expression of E-selectin in WT but not in mast cell-deficient animals. Moreover, MIP-2-provoked extravascular accumulation of neutrophils was reduced by 78% in mice lacking TNF-alpha. 5 In order to better define the role of mast cell-derived TNF-alpha in neutrophil responses to MIP-2, we used an in vitro endothelial cell adhesion assay with and without mast cells. Interestingly, MIP-2-induced neutrophil adhesion to endothelial cells was decreased by 58% using TNF-alpha-deficient compared to WT mast cells. Moreover, mast cell secretion of TNF-alpha increased by more than 71% in response to challenge with MIP-2. 6 Taken together, our results suggest that MIP-2-induced neutrophil recruitment is mediated by TNF-alpha released from local mast cells. These findings help to explain the complex molecular interactions between chemokines, mast cell activation and neutrophil infiltration in vivo.},
  author       = {Wang, Yusheng and Thorlacius, Henrik},
  issn         = {1476-5381},
  keyword      = {mast cells,adhesion,chemokines,migration,leukocytes},
  language     = {eng},
  number       = {8},
  pages        = {1062--1068},
  publisher    = {The British Pharmacological Society},
  series       = {British Journal of Pharmacology},
  title        = {Mast cell-derived tumour necrosis factor-alpha mediates macrophage inflammatory protein-2-induced recruitment of neutrophils in mice.},
  url          = {http://dx.doi.org/10.1038/sj.bjp.0706274},
  volume       = {145},
  year         = {2005},
}