Journal
IMMUNOLOGIC RESEARCH
Volume 37, Issue 2, Pages 147-159Publisher
HUMANA PRESS INC
DOI: 10.1007/BF02685896
Keywords
allergy; asthma; Flt3-L; mouse model of asthma; pUMVC3-hFLex plasmid; T(H)1/T(H)2 cells
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL070885, R01HL073349] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01HL073349, R01HL070885] Funding Source: Medline
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Airway inflammation and remodeling are primary characteristics of long-standing asthma. A balance between the T,1/T,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 IgG I 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.
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