TY  - JOUR
A1  - Springer, Jochen
A1  - Scholz, Frank R.
A1  - Peiser, Christian
A1  - Dinh, Q. Thai
A1  - Fischer, Axel
A1  - Quarcoo, David
A1  - Groneberg, Jan David Alexander
T1  - Transcriptional down-regulation of suppressor of cytokine signaling (SOCS)-3 in chronic obstructive pulmonary disease
T2  - Journal of occupational medicine and toxicology
N2  - Background: Tobacco is a leading environmental factor in the initiation of respiratory diseases and causes chronic obstructive pulmonary disease (COPD). Suppressor of cytokine signaling (SOCS) family members are involved in the pathogenesis of many inflammatory diseases and SOCS-3 has been shown to play an important role in the regulation, onset and maintenance of airway allergic inflammation indicating that SOCS-3 displays a potential therapeutic target for anti-inflammatory respiratory drugs development. Since chronic obstructive pulmonary disease (COPD) is also characterized by inflammatory changes and airflow limitation, the present study assessed the transcriptional expression of SOCS-3 in COPD.
Methods: Real-time PCR was performed to assess quantitative changes in bronchial biopsies of COPD patients in comparison to unaffected controls.
Results: SOCS-3 was significantly down-regulated in COPD at the transcriptional level while SOCS-4 and SOCS-5 displayed no change.
Conclusions: It can be concluded that the presently observed inhibition of SOCS-3 mRNA expression may be related to the dysbalance of cytokine signaling observed in COPD.
KW  - Chronic obstructive airway disease
KW  - Lung
KW  - SOCS
KW  - Cytokine
KW  - Airways
Y1  - 2013
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/31966
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-319665
SN  - 1745-6673
N1  - © 2013 Springer et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
VL  - 8
IS  - 29
PB  - BioMed Central
CY  - London
ER  -