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KMID : 1225720170090020169
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Allergy, Asthma & Immunology Research : AAIR
2017 Volume.9 No. 2 p.169 ~ p.176
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The Role of IL-17 in a Lipopolysaccharide-Induced Rhinitis Model
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Bae Jun-Sang
Kim Ji-Hye
Kim Eun-Hee
Mo Ji-Hun
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Abstract
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Purpose: Lipopolysaccharide (LPS) is a cell wall component of Gram-negative bacteria and important for pro-inflammatory mediators. This study aimed to establish a rhinitis model using ovalbumin (OVA) and LPS in order to evaluate the role of interleukin (IL)-17 in the pathogenesis of an LPS-induced non-eosionophilic rhinitis model.
Methods: Mice were divided into 4 groups and each group consisted of 10 mice (negative control group, allergic rhinitis model group, 1-μg LPS treatment group, and 10-μg LPS treatment group). BALB/c mice were sensitized with OVA and 1 or 10 μg of LPS, and challenged intranasally with OVA. Multiple parameters of rhinitis were also evaluated to establish the LPS-induced rhinitis model. IL-17 knockout mice were used to check if the LPS-induced rhinitis model were dependent on IL-17. Eosinophil and neutrophil infiltration, and mRNA and protein expression profiles of cytokine in nasal mucosa or spleen cell culture were evaluated using molecular, biochemical, histopathological, and immunohistological methods.
Results: In the LPS-induced rhinitis model, neutrophil infiltration increased in the nasal mucosa, and systemic and nasal IL-17 and interferon-gamma (IFN-γ) levels also increased as compared with the OVA-induced allergic rhinitis model. These findings were LPS-dose-dependent. In IL-17 knockout mice, those phenotypes (neutrophil infiltration, IL-17, and IFN-γ) were reversed, showing IL-17 dependency of LPS-induced rhinitis. The expression of vascular endothelial growth factor (VEGF), an important mediator for inflammation and angiogenesis, decreased in IL-17 knockout mice, showing the relationship between IL-17 and VEGF.
Conclusions: This study established an LPS-induced rhinitis model dependent on IL-17, characterized by neutrophil infiltration and increased expression of IL-17.
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KEYWORD
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Rhinitis, lipopolysaccharide, interleukin-17, vascular endothelial growth factor
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