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TLR4 signalling in pulmonary stromal cells is critical for inflammation and immunity in the airways

Frédèric Perros UGent, Bart Lambrecht UGent and Hamida Hammad UGent (2011) RESPIRATORY RESEARCH. 12.
abstract
Inflammation of the airways, which is often associated with life-threatening infection by Gram-negative bacteria or presence of endotoxin in the bioaerosol, is still a major cause of severe airway diseases. Moreover, inhaled endotoxin may play an important role in the development and progression of airway inflammation in asthma. Pathologic changes induced by endotoxin inhalation include bronchospasm, airflow obstruction, recruitment of inflammatory cells, injury of the alveolar epithelium, and disruption of pulmonary capillary integrity leading to protein rich fluid leak in the alveolar space. Mammalian Toll-like receptors (TLRs) are important signalling receptors in innate host defense. Among these receptors, TLR4 plays a critical role in the response to endotoxin. Lungs are a complex compartmentalized organ with separate barriers, namely the alveolar-capillary barrier, the microvascular endothelium, and the alveolar epithelium. An emerging theme in the field of lung immunology is that structural cells (SCs) of the airways such as epithelial cells (ECs), endothelial cells, fibroblasts and other stromal cells produce activating cytokines that determine the quantity and quality of the lung immune response. This review focuses on the role of TLR4 in the innate and adaptive immune functions of the pulmonary SCs.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
pulmonary stromal cells, TLR4, dendritic cells, epithelial cell, Airway diseases, TOLL-LIKE RECEPTORS, NF-KAPPA-B, DOMAIN-CONTAINING ADAPTER, LPS-INDUCED ACTIVATION, MARROW-DERIVED CELLS, ACUTE LUNG INJURY, EPITHELIAL-CELLS, DENDRITIC CELLS, NEUTROPHIL SEQUESTRATION, INHALED ENDOTOXIN
journal title
RESPIRATORY RESEARCH
Respir. Res.
volume
12
article number
125
pages
8 pages
Web of Science type
Review
Web of Science id
000295598900001
JCR category
RESPIRATORY SYSTEM
JCR impact factor
3.36 (2011)
JCR rank
13/48 (2011)
JCR quartile
2 (2011)
ISSN
1465-993X
DOI
10.1186/1465-9921-12-125
language
English
UGent publication?
yes
classification
A1
copyright statement
I have retained and own the full copyright for this publication
id
1996929
handle
http://hdl.handle.net/1854/LU-1996929
date created
2012-01-19 14:49:39
date last changed
2017-05-08 13:24:07
@article{1996929,
  abstract     = {Inflammation of the airways, which is often associated with life-threatening infection by Gram-negative bacteria or presence of endotoxin in the bioaerosol, is still a major cause of severe airway diseases. Moreover, inhaled endotoxin may play an important role in the development and progression of airway inflammation in asthma. Pathologic changes induced by endotoxin inhalation include bronchospasm, airflow obstruction, recruitment of inflammatory cells, injury of the alveolar epithelium, and disruption of pulmonary capillary integrity leading to protein rich fluid leak in the alveolar space. Mammalian Toll-like receptors (TLRs) are important signalling receptors in innate host defense. Among these receptors, TLR4 plays a critical role in the response to endotoxin. Lungs are a complex compartmentalized organ with separate barriers, namely the alveolar-capillary barrier, the microvascular endothelium, and the alveolar epithelium. An emerging theme in the field of lung immunology is that structural cells (SCs) of the airways such as epithelial cells (ECs), endothelial cells, fibroblasts and other stromal cells produce activating cytokines that determine the quantity and quality of the lung immune response. This review focuses on the role of TLR4 in the innate and adaptive immune functions of the pulmonary SCs.},
  articleno    = {125},
  author       = {Perros, Fr{\'e}d{\`e}ric and Lambrecht, Bart and Hammad, Hamida},
  issn         = {1465-993X},
  journal      = {RESPIRATORY RESEARCH},
  keyword      = {pulmonary stromal cells,TLR4,dendritic cells,epithelial cell,Airway diseases,TOLL-LIKE RECEPTORS,NF-KAPPA-B,DOMAIN-CONTAINING ADAPTER,LPS-INDUCED ACTIVATION,MARROW-DERIVED CELLS,ACUTE LUNG INJURY,EPITHELIAL-CELLS,DENDRITIC CELLS,NEUTROPHIL SEQUESTRATION,INHALED ENDOTOXIN},
  language     = {eng},
  pages        = {8},
  title        = {TLR4 signalling in pulmonary stromal cells is critical for inflammation and immunity in the airways},
  url          = {http://dx.doi.org/10.1186/1465-9921-12-125},
  volume       = {12},
  year         = {2011},
}

Chicago
Perros, Frédèric, Bart Lambrecht, and Hamida Hammad. 2011. “TLR4 Signalling in Pulmonary Stromal Cells Is Critical for Inflammation and Immunity in the Airways.” Respiratory Research 12.
APA
Perros, F., Lambrecht, B., & Hammad, H. (2011). TLR4 signalling in pulmonary stromal cells is critical for inflammation and immunity in the airways. RESPIRATORY RESEARCH, 12.
Vancouver
1.
Perros F, Lambrecht B, Hammad H. TLR4 signalling in pulmonary stromal cells is critical for inflammation and immunity in the airways. RESPIRATORY RESEARCH. 2011;12.
MLA
Perros, Frédèric, Bart Lambrecht, and Hamida Hammad. “TLR4 Signalling in Pulmonary Stromal Cells Is Critical for Inflammation and Immunity in the Airways.” RESPIRATORY RESEARCH 12 (2011): n. pag. Print.