Asia Pac Allergy.  2013 Jul;3(3):194-199. 10.5415/apallergy.2013.3.3.194.

IL-13 and STAT6 signaling involve in low dose lipopolysaccharide induced murine model of asthma

• Bang BR
• Lee HS
• Lee SY
• Chun E
• Kim YK
• Cho SH
• Min KU
• Kim YY
• Park HW

• KMID: 2397313
• DOI: http://doi.org/10.5415/apallergy.2013.3.3.194

Abstract

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.

Keyword

Asthma; Animal model; IL-13; STAT6; Lipopolysaccharide

MeSH Terms

Animals
Asthma*
Humans
Immunity, Innate
Inflammation
Interleukin-13*
Mice
Models, Animal
Ovalbumin
Phenotype
STAT6 Transcription Factor
Interleukin-13
Ovalbumin
STAT6 Transcription Factor

Figure

• 

  Fig. 1 Protocol for a murine model of asthma. AHR, airway hyperresponsiveness; Def, gene deficient mice; IN, intranasally; LPS, lipopolysaccharide; OA, ovalbumin; WT, wild type mice.

• 

  Fig. 2 Lung inflammation, airway hyperresponsiveness and serum OA-specific IgE in IL-13 deficient mice. (A) Lung inflammation. *p < 0.05 vs. WT_OA and IL-13-/-_OA groups; **p < 0.05 vs. WT_LPS0.1/OA groups. (B) Methacholine airway hyperesponsiveness. (C) Serum OA-specific IgE. *p < 0.05 vs. WT_OA and IL-13-/-_OA groups; **p < 0.05 vs. WT_LPS0.1/OA groups. BAL, bronchoalveolar lavage; OA, ovalbumin; Penh, enhanced pause; WT, wild type. One experiment representative of three is shown.

• 

  Fig. 3 Lung inflammation, AHR and serum OA-specific IgE in STAT6 deficient mice. (A) Lung inflammation. *p < 0.05 vs. WT_OA and STAT6-/-_OA groups; **p < 0.05 vs. WT_LPS0.1/OA groups. (B) Methacholine airway hyperesponsiveness. (C) Serum OA-specific IgE. *p < 0.05 vs. WT_OA and STAT6-/-_OA groups; **p < 0.05 vs. WT_LPS0.1/OA groups. STAT6, signal transducer and activator of transcription 6; BAL, bronchoalveolar lavage; OA, ovalbumin; Penh, enhanced pause; WT, wild type. One experiment representative of three is shown.

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