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The role of ChemR23 in the induction and resolution of cigarette smoke-induced inflammation

Tine Demoor, Ken Bracke UGent, Lisa Dupont, Maud Plantinga, Benjamin Bondue, Marie-Odile Roy, Vincent Lannoy, Bart Lambrecht UGent, Guy Brusselle UGent and Guy Joos UGent (2011) JOURNAL OF IMMUNOLOGY. 186(9). p.5457-5467
abstract
Chronic obstructive pulmonary disease is mainly triggered by cigarette smoke (CS) and progresses even after smoking cessation. CS induces an exaggerated influx of inflammatory cells to the bronchoalveolar space and lung parenchyma, likely resulting from a complex interplay between chemoattractants and their respective receptors. In a murine CS model of chronic obstructive pulmonary disease, we studied the importance of chemokine-like receptor ChemR23 for the induction and resolution of inflammation in CS-exposed lungs. Subacute and chronic CS exposure increased protein levels of the ChemR23 ligand and chemoattractant, chemerin, in bronchoalveolar lavage (BAL) fluid of wild-type (WT) mice. Moreover, the proinflammatory chemokines CXCL1, CCL2, and CCL20 were increased in the airways of CS-exposed WT mice, accompanied by a massive accumulation of inflammatory neutrophils and monocytes, CD11b(hi)CD103(-) and CD11b(lo)CD103(+) dendritic cells (DCs), and CD4(+) and CD8(+) T cells. The lung parenchyma of WT mice was infiltrated with inflammatory neutrophils, CD11b(hi)CD103(-) DCs, and activated CD4(+) T cells after CS exposure. CS-induced inflammation was severely attenuated in BAL fluid and lungs of ChemR23 knockout mice with regard to the induction of inflammatory chemokines and the recruitment of inflammatory cells. Neutrophils and CD8(+) T cells persisted in the airways of WT mice, as did the airway-derived conventional DCs in the mediastinal lymph nodes, for at least 14 d after smoking cessation. In the BAL fluid of CS-exposed ChemR23 knockout mice, there was a remarkable delayed accumulation of T cells 14 d after the final exposure. Our data support a role for ChemR23 in directing innate and adaptive immune cells to CS-exposed lungs. The Journal of Immunology, 2011, 186: 5457-5467.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
PLASMACYTOID DENDRITIC CELLS, NDUCED PULMONARY INFLAMMATION, LUNG INFLAMMATION, INDUCED EMPHYSEMA, EPITHELIAL-CELLS, RESOLVIN E1, IN-VIVO, CHEMERIN, MICE, RECEPTOR
journal title
JOURNAL OF IMMUNOLOGY
J. Immunol.
volume
186
issue
9
pages
5457 - 5467
Web of Science type
Article
Web of Science id
000289679600048
JCR category
IMMUNOLOGY
JCR impact factor
5.788 (2011)
JCR rank
20/138 (2011)
JCR quartile
1 (2011)
ISSN
0022-1767
DOI
10.4049/jimmunol.1003862
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1234780
handle
http://hdl.handle.net/1854/LU-1234780
date created
2011-05-24 17:51:33
date last changed
2016-12-19 15:44:49
@article{1234780,
  abstract     = {Chronic obstructive pulmonary disease is mainly triggered by cigarette smoke (CS) and progresses even after smoking cessation. CS induces an exaggerated influx of inflammatory cells to the bronchoalveolar space and lung parenchyma, likely resulting from a complex interplay between chemoattractants and their respective receptors. In a murine CS model of chronic obstructive pulmonary disease, we studied the importance of chemokine-like receptor ChemR23 for the induction and resolution of inflammation in CS-exposed lungs. Subacute and chronic CS exposure increased protein levels of the ChemR23 ligand and chemoattractant, chemerin, in bronchoalveolar lavage (BAL) fluid of wild-type (WT) mice. Moreover, the proinflammatory chemokines CXCL1, CCL2, and CCL20 were increased in the airways of CS-exposed WT mice, accompanied by a massive accumulation of inflammatory neutrophils and monocytes, CD11b(hi)CD103(-) and CD11b(lo)CD103(+) dendritic cells (DCs), and CD4(+) and CD8(+) T cells. The lung parenchyma of WT mice was infiltrated with inflammatory neutrophils, CD11b(hi)CD103(-) DCs, and activated CD4(+) T cells after CS exposure. CS-induced inflammation was severely attenuated in BAL fluid and lungs of ChemR23 knockout mice with regard to the induction of inflammatory chemokines and the recruitment of inflammatory cells. Neutrophils and CD8(+) T cells persisted in the airways of WT mice, as did the airway-derived conventional DCs in the mediastinal lymph nodes, for at least 14 d after smoking cessation. In the BAL fluid of CS-exposed ChemR23 knockout mice, there was a remarkable delayed accumulation of T cells 14 d after the final exposure. Our data support a role for ChemR23 in directing innate and adaptive immune cells to CS-exposed lungs. The Journal of Immunology, 2011, 186: 5457-5467.},
  author       = {Demoor, Tine and Bracke, Ken and Dupont, Lisa and Plantinga, Maud and Bondue, Benjamin  and Roy, Marie-Odile  and Lannoy, Vincent and Lambrecht, Bart and Brusselle, Guy and Joos, Guy},
  issn         = {0022-1767},
  journal      = {JOURNAL OF IMMUNOLOGY},
  keyword      = {PLASMACYTOID DENDRITIC CELLS,NDUCED PULMONARY INFLAMMATION,LUNG INFLAMMATION,INDUCED EMPHYSEMA,EPITHELIAL-CELLS,RESOLVIN E1,IN-VIVO,CHEMERIN,MICE,RECEPTOR},
  language     = {eng},
  number       = {9},
  pages        = {5457--5467},
  title        = {The role of ChemR23 in the induction and resolution of cigarette smoke-induced inflammation},
  url          = {http://dx.doi.org/10.4049/jimmunol.1003862},
  volume       = {186},
  year         = {2011},
}

Chicago
Demoor, Tine, Ken Bracke, Lisa Dupont, Maud Plantinga, Benjamin Bondue, Marie-Odile Roy, Vincent Lannoy, Bart Lambrecht, Guy Brusselle, and Guy Joos. 2011. “The Role of ChemR23 in the Induction and Resolution of Cigarette Smoke-induced Inflammation.” Journal of Immunology 186 (9): 5457–5467.
APA
Demoor, Tine, Bracke, K., Dupont, L., Plantinga, M., Bondue, B., Roy, M.-O., Lannoy, V., et al. (2011). The role of ChemR23 in the induction and resolution of cigarette smoke-induced inflammation. JOURNAL OF IMMUNOLOGY, 186(9), 5457–5467.
Vancouver
1.
Demoor T, Bracke K, Dupont L, Plantinga M, Bondue B, Roy M-O, et al. The role of ChemR23 in the induction and resolution of cigarette smoke-induced inflammation. JOURNAL OF IMMUNOLOGY. 2011;186(9):5457–67.
MLA
Demoor, Tine, Ken Bracke, Lisa Dupont, et al. “The Role of ChemR23 in the Induction and Resolution of Cigarette Smoke-induced Inflammation.” JOURNAL OF IMMUNOLOGY 186.9 (2011): 5457–5467. Print.