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Updated: May 8, 2026

An IL-8 Transiently Transgenized Mouse Model for the In Vivo Long-term Monitoring of Inflammatory Responses
Published on: July 7, 2017
IL-13 and STAT6 signaling involve in low dose lipopolysaccharide induced murine model of asthma
Bo-Ram Bang1, Hyun-Seung Lee, Soo-Yeon Lee
1Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-799, Korea. ; Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul 110-799, Korea.
Background:
We reported that level of lipopolysaccharide (LPS) exposure determined the type of airway inflammation in a murine model of asthma.
Objective:
The purpose of this study is to evaluated the role of IL-13 in low dose LPS induced murine model of asthma using IL-13 and signal transducer and activator of transcription 6 (STAT6) deficient mice.
Methods:
Mice were sensitized with an intranasal application of LPS-depleted ovalbumin (OA) and different doses of LPS (0.1 and 10 µg), and then challenged intranasally with OA alone. The phenotype changes between wild type (WT) and IL-13(-/-) mice and between WT and STAT6(-/-) mice were evaluated.
Results:
We confirmed again that low and high dose LPS resulted in different phenotypes of murine asthma. In the present study, we observed that phenotypes of murine asthma induced by low dose LPS were abolished in the homozygous null mutation of the IL-13 and STAT6 gene. However, those changes were not shown in mice sensitized OA plus high dose LPS.
Conclusion:
IL-13 plays an important role in low dose LPS induced murine model of asthma. Our results provided a new insight in understanding of the potential role of IL-13 in innate immunity in human allergic asthma.
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