Abstract | RATIONALE: OBJECTIVES: METHODS:
Ovalbumin-sensitized and -challenged mice, a model for allergic airway inflammation, were used in conjunction with recombinant adenovirus expressing UGRP1. MEASUREMENTS AND MAIN RESULTS: We demonstrated that intranasal administration of adeno-UGRP1 successfully delivered UGRP1 to the epithelial cells of airways and markedly reduced the number of infiltrating inflammatory cells, particularly eosinophils, in lung tissue as well as the level of proinflammatory cytokines such as interleukin (IL)-4, IL-5, and IL-13 in bronchoalveolar lavage fluids. The healed phase of inflammation was clearly seen in the peripheral areas of adeno-UGRP1-treated mouse lungs. CONCLUSION: These results demonstrate that UGRP1 can suppress inflammation in the mouse model of allergic airway inflammation. Based on this result, we propose UGRP1 as a novel therapeutic candidate for treating lung inflammation such as is found in asthma.
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Authors | Yoshihiko Chiba, Reiko Kurotani, Takashi Kusakabe, Tomiko Miura, Benjamin W Link, Miwa Misawa, Shioko Kimura |
Journal | American journal of respiratory and critical care medicine
(Am J Respir Crit Care Med)
Vol. 173
Issue 9
Pg. 958-64
(May 01 2006)
ISSN: 1073-449X [Print] United States |
PMID | 16456148
(Publication Type: Journal Article, Research Support, N.I.H., Intramural)
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Chemical References |
- Interleukins
- Proteins
- RNA, Messenger
- Scgb3a2 protein, mouse
- Secretoglobins
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Topics |
- Adenoviridae
- Animals
- Bronchoalveolar Lavage Fluid
- Disease Models, Animal
- Female
- Genetic Vectors
- Interleukins
(metabolism)
- Lung Diseases, Obstructive
(metabolism, pathology)
- Mice
- Mice, Inbred BALB C
- Proteins
(genetics, metabolism)
- RNA, Messenger
(metabolism)
- Respiratory Hypersensitivity
(metabolism, pathology)
- Respiratory Mucosa
(metabolism, pathology)
- Secretoglobins
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