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 language | English |
|---|---|
| Pages (from-to) | 147-159 |
| Number of pages | 13 |
| Journal | Immunologic Research |
| Volume | 37 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 2007 |
Fingerprint
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 journal › Article
}
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 -