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

Jehad H. Edwan, Devendra K. Agrawal

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Airway inflammation and remodeling are primary characteristics of long-standing asthma. A balance between the TH1/TH2 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

Original languageEnglish
Pages (from-to)147-159
Number of pages13
JournalImmunologic Research
Volume37
Issue number2
DOIs
StatePublished - Feb 2007

Fingerprint

Plasmids
Asthma
Inflammation
Airway Remodeling
Ovalbumin
Eosinophils
Mast Cells
Cytokines
Muscles
Injections
flt3 ligand protein
Therapeutics

All Science Journal Classification (ASJC) codes

  • Immunology

Cite this

Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model. / Edwan, Jehad H.; Agrawal, Devendra K.

In: Immunologic Research, Vol. 37, No. 2, 02.2007, p. 147-159.

Research output: Contribution to journalArticle

@article{ee342bbc4a2a41ba9058316f78d93f97,
title = "Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model",
abstract = "Airway inflammation and remodeling are primary characteristics of long-standing asthma. A balance between the TH1/TH2 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",
author = "Edwan, {Jehad H.} and Agrawal, {Devendra K.}",
year = "2007",
month = "2",
doi = "10.1007/BF02685896",
language = "English",
volume = "37",
pages = "147--159",
journal = "Immunologic Research",
issn = "0257-277X",
publisher = "Humana Press",
number = "2",

}

TY - JOUR

T1 - Flt3-ligand plasmid prevents the development of pathophysiological features of chronic asthma in a mouse model

AU - Edwan, Jehad H.

AU - Agrawal, Devendra K.

PY - 2007/2

Y1 - 2007/2

N2 - Airway inflammation and remodeling are primary characteristics of long-standing asthma. A balance between the TH1/TH2 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

AB - Airway inflammation and remodeling are primary characteristics of long-standing asthma. A balance between the TH1/TH2 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

UR - http://www.scopus.com/inward/record.url?scp=34548324794&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34548324794&partnerID=8YFLogxK

U2 - 10.1007/BF02685896

DO - 10.1007/BF02685896

M3 - Article

VL - 37

SP - 147

EP - 159

JO - Immunologic Research

JF - Immunologic Research

SN - 0257-277X

IS - 2

ER -