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Differential expression of chemokines in inflammatory myopathies

Jan De Bleecker UGent, Boel De Paepe UGent, IRIS VANWALLEGHEM and JM Schröder (2002) NEUROLOGY. 58(12). p.1779-1785
abstract
Background: Chemokines represent a family of small-molecular-weight cytokines that recruit and activate inflammatory cells in response to inflammation. Invasion of cytotoxic memory T cells and macrophages in nonnecrotic muscle fibers characterizes polymyositis and sporadic inclusion body myositis. Dermatomyositis is a complement-mediated endotheliopathy. Elucidation of the mechanisms guiding lymphocyte diapedesis and trafficking could lead to selective therapeutic interventions. Methods: Immunoblots and multistep immunofluoreseence studies with non-cross-reactive antibodies recognizing interleukin-8, monocyte chemoattractant protein-1 (MCP-1), MCP-3, TARC (thymus and activation regulated cytokine), and RANTES (regulated upon activation, normal T-cell expressed and secreted), using appropriate positive and negative controls. In situ hybridization was used to localize MCP-1 mRNA. Results: MCP-1 protein was strongly expressed on T cells and a subset of macrophages actively invading a proportion of the nonnecrotic muscle fibers in polymyositis and inclusion body myositis alike. Capillaries and arterioles in the vicinity of endomysial inflammatory foci were immunoreactive for MCP-1, with faint or no expression in unaffected parts of the tissue. By contrast, widespread and strong endothelial MCP-1 expression occurred on perifascicular and perimysial endothelia in dermatomyositis, also at sites remote from inflammatory infiltrates. In some control specimens, a subset of capillaries also expressed MCP-1, possibly reflecting a role of this chemokine in normal immune surveillance. MCP-1 mRNA was detected in scattered macrophages in each inflammatory myopathy. All other chemokines were absent. Conclusion: Chemokines are differentially expressed in the symptomatic stage of inflammatory myopathies. MCP-1 plays a major role in the myocytotoxicity in polymyositis and inclusion body myositis. MCP-1 may be induced by membranolytic attack complex binding to endothelial cells in dermatomyositis.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (proceedingsPaper)
publication status
published
subject
keyword
MONOCYTE-CHEMOATTRACTANT PROTEIN-1, MEMBRANE ATTACK COMPLEX, NECROSIS-FACTOR-ALPHA, MONOCLONAL-ANTIBODY ANALYSIS, MESSENGER-RNA EXPRESSION, INCLUSION-BODY MYOSITIS, CELL-ADHESION MOLECULES, MEDIATED CYTO-TOXICITY, FACTOR-KAPPA-B, MONONUCLEAR-CELLS
journal title
NEUROLOGY
Neurology
volume
58
issue
12
pages
1779 - 1785
conference name
53rd Annual meeting of the American Academy of Neurology
conference location
Philadelphia, PA, USA
conference start
2001-05-05
conference end
2001-05-12
Web of Science type
Article
Web of Science id
000176429700012
JCR category
CLINICAL NEUROLOGY
JCR impact factor
5.34 (2002)
JCR rank
5/137 (2002)
JCR quartile
1 (2002)
ISSN
0028-3878
DOI
10.1212/WNL.58.12.1779
language
English
UGent publication?
yes
classification
A1
id
318936
handle
http://hdl.handle.net/1854/LU-318936
date created
2005-07-13 15:54:00
date last changed
2018-05-15 12:34:06
@article{318936,
  abstract     = {Background: Chemokines represent a family of small-molecular-weight cytokines that recruit and activate inflammatory cells in response to inflammation. Invasion of cytotoxic memory T cells and macrophages in nonnecrotic muscle fibers characterizes polymyositis and sporadic inclusion body myositis. Dermatomyositis is a complement-mediated endotheliopathy. Elucidation of the mechanisms guiding lymphocyte diapedesis and trafficking could lead to selective therapeutic interventions.
Methods: Immunoblots and multistep immunofluoreseence studies with non-cross-reactive antibodies recognizing interleukin-8, monocyte chemoattractant protein-1 (MCP-1), MCP-3, TARC (thymus and activation regulated cytokine), and RANTES (regulated upon activation, normal T-cell expressed and secreted), using appropriate positive and negative controls. In situ hybridization was used to localize MCP-1 mRNA.
Results: MCP-1 protein was strongly expressed on T cells and a subset of macrophages actively invading a proportion of the nonnecrotic muscle fibers in polymyositis and inclusion body myositis alike. Capillaries and arterioles in the vicinity of endomysial inflammatory foci were immunoreactive for MCP-1, with faint or no expression in unaffected parts of the tissue. By contrast, widespread and strong endothelial MCP-1 expression occurred on perifascicular and perimysial endothelia in dermatomyositis, also at sites remote from inflammatory infiltrates. In some control specimens, a subset of capillaries also expressed MCP-1, possibly reflecting a role of this chemokine in normal immune surveillance. MCP-1 mRNA was detected in scattered macrophages in each inflammatory myopathy. All other chemokines were absent.
Conclusion: Chemokines are differentially expressed in the symptomatic stage of inflammatory myopathies. MCP-1 plays a major role in the myocytotoxicity in polymyositis and inclusion body myositis. MCP-1 may be induced by membranolytic attack complex binding to endothelial cells in dermatomyositis.},
  author       = {De Bleecker, Jan and De Paepe, Boel and VANWALLEGHEM, IRIS and Schr{\"o}der, JM},
  issn         = {0028-3878},
  journal      = {NEUROLOGY},
  keyword      = {MONOCYTE-CHEMOATTRACTANT PROTEIN-1,MEMBRANE ATTACK COMPLEX,NECROSIS-FACTOR-ALPHA,MONOCLONAL-ANTIBODY ANALYSIS,MESSENGER-RNA EXPRESSION,INCLUSION-BODY MYOSITIS,CELL-ADHESION MOLECULES,MEDIATED CYTO-TOXICITY,FACTOR-KAPPA-B,MONONUCLEAR-CELLS},
  language     = {eng},
  location     = {Philadelphia, PA, USA},
  number       = {12},
  pages        = {1779--1785},
  title        = {Differential expression of chemokines in inflammatory myopathies},
  url          = {http://dx.doi.org/10.1212/WNL.58.12.1779},
  volume       = {58},
  year         = {2002},
}

Chicago
De Bleecker, Jan, Boel De Paepe, IRIS VANWALLEGHEM, and JM Schröder. 2002. “Differential Expression of Chemokines in Inflammatory Myopathies.” Neurology 58 (12): 1779–1785.
APA
De Bleecker, J., De Paepe, B., VANWALLEGHEM, I., & Schröder, J. (2002). Differential expression of chemokines in inflammatory myopathies. NEUROLOGY, 58(12), 1779–1785. Presented at the 53rd Annual meeting of the American Academy of Neurology.
Vancouver
1.
De Bleecker J, De Paepe B, VANWALLEGHEM I, Schröder J. Differential expression of chemokines in inflammatory myopathies. NEUROLOGY. 2002;58(12):1779–85.
MLA
De Bleecker, Jan, Boel De Paepe, IRIS VANWALLEGHEM, et al. “Differential Expression of Chemokines in Inflammatory Myopathies.” NEUROLOGY 58.12 (2002): 1779–1785. Print.