Abstract | BACKGROUND:
Asthma is a disorder characterized by a predominance of Th2 cells and eosinophilic inflammation. Suppressors of cytokine signaling ( SOCS) proteins act as negative regulators of cytokine signaling. In particular, SOCS1 and SOCS3 play an important role in immune response by controlling the balance between Th1 and Th2 cells. In a previous study, we demonstrated that treatment of chronic asthmatic mice with gene therapy using plasmid encoding galectin-3 (Gal-3) led to an improvement in Th2 allergic inflammation. METHODS: Using a microarray approach, this study endeavored to evaluate the changes produced by therapeutic Gal-3 delivered by gene therapy in a well-characterized mouse model of chronic airway inflammation. Results were confirmed by real-time RT-PCR, Western blot and immunohistochemical analysis. RESULTS: We identify a set of genes involved in different pathways whose expression is coordinately decreased/increased in mice treated with Gal-3 gene therapy. We report a correlation between Gal-3 treatment and inhibition of SOCS1 and SOCS3 expression in lungs. CONCLUSION: These results suggest that negative regulation of SOCS1 and 3 following Gal-3 treatment could be a valuable therapeutic approach in allergic disease.
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Authors | Esther López, M Paz Zafra, Beatriz Sastre, Cristina Gámez, Carlos Lahoz, Victoria del Pozo |
Journal | Mediators of inflammation
(Mediators Inflamm)
Vol. 2011
Pg. 823279
( 2011)
ISSN: 1466-1861 [Electronic] United States |
PMID | 21547260
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
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Topics |
- Animals
- Asthma
(genetics, immunology)
- Down-Regulation
- Galectin 3
(pharmacology)
- Gene Expression Profiling
- Gene Expression Regulation
(drug effects)
- Lung
(cytology, drug effects, immunology, physiology)
- Male
- Mice
- Microarray Analysis
- Signal Transduction
(genetics)
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