| Adenovirus-mediated overexpression of soluble ST2 provides a protective effect on lipopolysaccharide-induced acute lung injury in mice. | |
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MedLine Citation:
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PMID: 21352201 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Acute lung injury is characterized by a diffuse inflammatory parenchymal process, implicated in the context of significant morbidity and mortality. Previously, we have reported that soluble ST2 (sST2), a member of the Toll-interleukin (IL)-1 receptor (TIR) superfamily, represses proinflammatory cytokine production of macrophage exposed to lipopolysaccharide (LPS). In this study, we examined the possibility of modulating LPS-induced murine inflammatory pulmonary damage by recombinant adenovirus-mediated sST2-Fc (Ad-sST2-Fc) gene transfer. Single intranasal administration of Ad-sST2-Fc led to a profound decrease in LPS-induced bronchoalveolar lavage leucocyte exudation and lung tissue myeloperoxidase activity (reflecting phagocyte infiltration). Histological examination revealed alveolitis with inflammatory cell infiltration and alveolar haemorrhage in the alveolar airspace was less severe in Ad-sST2-Fc-treated mice when compared with control groups. In addition, high levels of sST2-Fc in vivo reduced the transcription of tumour necrosis factor-α, IL-6 and Toll-like receptor-4 gene remarkably, and suppressed the nuclear translocation of nuclear factor-κB in lung tissues in response to LPS challenge. Taken together, these results suggested that administration of Ad-sST2-Fc gene transfer may have therapeutic potential for the immunomodulatory treatment of LPS-mediated inflammatory lung injury. |
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Authors:
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H Yin; X Y Li; B H Yuan; B B Zhang; S L Hu; H B Gu; X B Jin; J Y Zhu |
Publication Detail:
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Type: Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't Date: 2011-02-24 |
Journal Detail:
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Title: Clinical and experimental immunology Volume: 164 ISSN: 1365-2249 ISO Abbreviation: Clin. Exp. Immunol. Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-04-11 Completed Date: 2011-06-14 Revised Date: 2012-05-01 |
Medline Journal Info:
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Nlm Unique ID: 0057202 Medline TA: Clin Exp Immunol Country: England |
Other Details:
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Languages: eng Pagination: 248-55 Citation Subset: IM |
Copyright Information:
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© 2011 The Authors; Clinical and Experimental Immunology © 2011 British Society for Immunology. |
Affiliation:
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Department of Microbiology and Immunology, Guangzhou, China. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acute Lung Injury
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chemically induced,
complications,
pathology,
therapy* Adenoviridae / genetics* Administration, Intranasal Animals Anti-Inflammatory Agents / therapeutic use Bronchoalveolar Lavage Fluid / cytology Gene Therapy* Genetic Vectors / therapeutic use* Hemorrhage / etiology, prevention & control Immunologic Factors / genetics, physiology, therapeutic use* Interleukin-6 / biosynthesis, genetics Leukocytes / immunology Lipopolysaccharides / toxicity Male Mice Mice, Inbred BALB C NF-kappa B / metabolism Receptors, Interleukin / genetics, physiology, therapeutic use* Recombinant Fusion Proteins / genetics, physiology, therapeutic use Solubility Toll-Like Receptor 4 / biosynthesis, genetics Transgenes Tumor Necrosis Factor-alpha / biosynthesis, genetics |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents; 0/Il1rl1 protein, mouse; 0/Immunologic Factors; 0/Interleukin-6; 0/Lipopolysaccharides; 0/NF-kappa B; 0/Receptors, Interleukin; 0/Recombinant Fusion Proteins; 0/Tlr4 protein, mouse; 0/Toll-Like Receptor 4; 0/Tumor Necrosis Factor-alpha; 0/lipopolysaccharide, Escherichia coli 0111 B4 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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