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Cytokines in asthma

Johan Kips (2001) EUROPEAN RESPIRATORY JOURNAL. 18(34). p.24S-33S
abstract
The airway inflammation underlying asthma is regulated by a network of mutually interacting cytokines. The exact functional role of each individual cytokine in the pathogenesis of the disease remains to be fully established. Type 2 T-helper cells are currently considered to play a crucial role in this process. In giro animal data suggest a sequential involvement of interleukin (IL)-4 and IL-5 in the induction of allergen-induced airway changes. The potential role of other type 2 T-helper cell-like cytokines in asthma is increasingly being recognized. In particular, IL-4 and -13 display a large degree of redundancy. Whereas IL-4 seems to be crucial in the primary allergen sensitization process, IL-13 might be more important during secondary exposure to aerosolized allergen. Animal models also indicate that T-cell-derived cytokine production, rather than eosinophil influx or immunoglobulin-E synthesis, is causally related to altered airway behaviour. An important aspect when evaluating the functional role of cytokines in a complex disease such as asthma is the interaction with other cytokines in the microenvironment. Increased expression of pro-inflammatory cytokines such as tumour necrosis factor-alpha can further enhance the inflammatory process, and is increasingly linked to disease severity. In addition, decreased expression of immunoregulatory cytokines, including interleukin-12, interleukin-18 or interferon gamma could also strengthen the type 2 T-helper cell-driven inflammatory process.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (proceedingsPaper)
publication status
published
subject
keyword
pathogenesis, tumour necrosis factor-alpha, interleukin, cytokine, asthma, IFN-GAMMA, T-HELPER CELL, CELL-DEFICIENT MICE, MESSENGER-RIBONUCLEIC-ACID, BRONCHIAL BIOPSY SPECIMENS, PULMONARY ALLERGIC RESPONSES, RECOMBINANT INTERFERON-GAMMA, NECROSIS-FACTOR-ALPHA, COLONY-STIMULATING FACTOR, INDUCED AIRWAY HYPERRESPONSIVENESS
journal title
EUROPEAN RESPIRATORY JOURNAL
Eur. Resp. J.
volume
18
issue
34
pages
24S - 33S
conference name
Symposium on Cytokines and Obstructive Lung Disease
conference location
Barcelona, Spain
conference start
2001-01-21
conference end
2001-01-21
Web of Science type
Proceedings Paper
Web of Science id
000176754700004
JCR category
RESPIRATORY SYSTEM
JCR impact factor
2.989 (2001)
JCR rank
5/29 (2001)
JCR quartile
1 (2001)
ISSN
0903-1936
DOI
10.1183/09031936.01.00229601
language
English
UGent publication?
yes
classification
A1
id
140509
handle
http://hdl.handle.net/1854/LU-140509
date created
2004-01-14 13:37:00
date last changed
2016-12-19 15:38:05
@article{140509,
  abstract     = {The airway inflammation underlying asthma is regulated by a network of mutually interacting cytokines. The exact functional role of each individual cytokine in the pathogenesis of the disease remains to be fully established. Type 2 T-helper cells are currently considered to play a crucial role in this process. In giro animal data suggest a sequential involvement of interleukin (IL)-4 and IL-5 in the induction of allergen-induced airway changes. The potential role of other type 2 T-helper cell-like cytokines in asthma is increasingly being recognized. In particular, IL-4 and -13 display a large degree of redundancy. Whereas IL-4 seems to be crucial in the primary allergen sensitization process, IL-13 might be more important during secondary exposure to aerosolized allergen. Animal models also indicate that T-cell-derived cytokine production, rather than eosinophil influx or immunoglobulin-E synthesis, is causally related to altered airway behaviour. An important aspect when evaluating the functional role of cytokines in a complex disease such as asthma is the interaction with other cytokines in the microenvironment. Increased expression of pro-inflammatory cytokines such as tumour necrosis factor-alpha can further enhance the inflammatory process, and is increasingly linked to disease severity. In addition, decreased expression of immunoregulatory cytokines, including interleukin-12, interleukin-18 or interferon gamma could also strengthen the type 2 T-helper cell-driven inflammatory process.},
  author       = {Kips, Johan},
  issn         = {0903-1936},
  journal      = {EUROPEAN RESPIRATORY JOURNAL},
  keyword      = {pathogenesis,tumour necrosis factor-alpha,interleukin,cytokine,asthma,IFN-GAMMA,T-HELPER CELL,CELL-DEFICIENT MICE,MESSENGER-RIBONUCLEIC-ACID,BRONCHIAL BIOPSY SPECIMENS,PULMONARY ALLERGIC RESPONSES,RECOMBINANT INTERFERON-GAMMA,NECROSIS-FACTOR-ALPHA,COLONY-STIMULATING FACTOR,INDUCED AIRWAY HYPERRESPONSIVENESS},
  language     = {eng},
  location     = {Barcelona, Spain},
  number       = {34},
  pages        = {24S--33S},
  title        = {Cytokines in asthma},
  url          = {http://dx.doi.org/10.1183/09031936.01.00229601},
  volume       = {18},
  year         = {2001},
}

Chicago
Kips, Johan. 2001. “Cytokines in Asthma.” European Respiratory Journal 18 (34): 24S–33S.
APA
Kips, Johan. (2001). Cytokines in asthma. EUROPEAN RESPIRATORY JOURNAL, 18(34), 24S–33S. Presented at the Symposium on Cytokines and Obstructive Lung Disease.
Vancouver
1.
Kips J. Cytokines in asthma. EUROPEAN RESPIRATORY JOURNAL. 2001;18(34):24S–33S.
MLA
Kips, Johan. “Cytokines in Asthma.” EUROPEAN RESPIRATORY JOURNAL 18.34 (2001): 24S–33S. Print.