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Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model.

Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model. Research Abstract Details 

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  • Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model. Abstract Text:

    jehad h edwanJehad H Edwan,devendra k agrawalDevendra K Agrawal,

    Airway inflammation and remodeling are primary characteristics of long-standing asthma. A balance between the T(H)1/T(H)2 cytokines regulates the accumulation and activation of inflammatory cells, including mast cells and eosinophils. Recently, we demonstrated that pUMVC3-hFLex, an active plasmid, mammalian expression vector for the secretion of Flt3-L, reversed established airway hyperresponsiveness (AHR) in a murine model of acute allergic airway inflammation. The present experiments were undertaken to examine the effect of pUMVC3-hFLex in a chronic model of allergic airway inflammation that was established in Balb/c mice by sensitization and challenge with ovalbumin (OVA). pUMVC3-hFLex or the control plasmid, pUMVC3, were administered by injection into the muscle interior tibialis. Treatment with pUMVC3-hFLex completely reversed established AHR (p < 0.05), and this effect continued even after several exposures to the allergen (p < 0.05). pUMVC3-hFLex treatment prevented the development of goblet cell hyperplasia and subepithelial fibrosis, and significantly reduced serum levels of IL-4 and IL-5, and increased serum IL-10 levels (p < 0.05) with no effect on serum IL-13. Serum IgE or serum total and anti-OVA IgG1 and IgG2a levels did not change. Total BALF cellularity and BALF IL-5 levels were reduced (p < 0.05), but there was no significant effect on BALF IL-10 and IL-13. These results suggest that pUMVC3-hFLex treatment can prevent the development of airway remodeling and maintain airway protection in chronic experimental asthma model, and might provide a novel approach for treating chronic asthma.

    Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model. Publishing Authors By Initials

    jh edwanJH Edwan,dk agrawalDK Agrawal,

    For similar genetic structures: plasmids research abstracts see: genetic structures: plasmids research

    PUBMED ID PMID:

    MEDLINE DATE:

    Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Immunologic research

    VOLUME: 37

    Page Numbers: 147-59

    Journal Abbreviation: Immunol. Res.

    ISSN: 0257-277X

    DAY: 3

    MONTH: 12

    YEAR: 2007

    Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8611087

    Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model. Keywords Mesh Terms:

    KEYWORDS: Plasmids

    MESH TERMS: immunology

    Chemical & Substance for Abstract: Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model. Information

    Substance Name: Collagen

    Registry Number: 9007-34-5

    Grant and Affiliation Information for Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model.

    AFFILIATION: Department of Biomedical Sciences, Medical Microbiology & Immunology, Creighton University School of Medicine, Omaha, NE 68178, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: R01HL073349

    ACRONYM: HL

    MEDLINETA: Immunol Res

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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