gene expression profiling in lungs of chronic asthmatic mice treated with galectin-3 downregulation of inflammatory and regulatory genes基因表达分析在慢性哮喘小鼠肺治疗炎性和监管的差别galectin-3对这些基因.pdfVIP

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gene expression profiling in lungs of chronic asthmatic mice treated with galectin-3 downregulation of inflammatory and regulatory genes基因表达分析在慢性哮喘小鼠肺治疗炎性和监管的差别galectin-3对这些基因.pdf

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gene expression profiling in lungs of chronic asthmatic mice treated with galectin-3 downregulation of inflammatory and regulatory genes基因表达分析在慢性哮喘小鼠肺治疗炎性和监管的差别galectin-3对这些基因

Hindawi Publishing Corporation Mediators of Inﬂammation Volume 2011, Article ID 823279, 9 pages doi:10.1155/2011/823279 Research Article Gene Expression Proﬁling in Lungs of Chronic Asthmatic Mice Treated with Galectin-3: Downregulation of Inﬂammatory and Regulatory Genes ´ ´ Esther Lopez, M. Paz Zafra, Beatriz Sastre, Cristina Gamez, Carlos Lahoz, and Victoria del Pozo Immunology Department IIS-Fundacion Jimenez Dıaz, CIBER de Enfermedades Respiratorias (CIBERES), 28040 Madrid, Spain ´ ´ ´ Correspondence should be addressed to Victoria del Pozo, vpozo@fjd.es Received 5 October 2010; Accepted 23 January 2011 Academic Editor: A. Malamitsi-Puchner ´ Copyright © 2011 Esther Lopez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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 ch