The Role of IL-17 in a Lipopolysaccharide-Induced Rhinitis Model.
10.4168/aair.2017.9.2.169
- Author:
Jun Sang BAE
1
;
Ji Hye KIM
;
Eun Hee KIM
;
Ji Hun MO
Author Information
1. Department of Otorhinolaryngology, Dankook University College of Medicine, Cheonan, Korea. jihunmo@gmail.com
- Publication Type:Original Article
- Keywords:
Rhinitis;
lipopolysaccharide;
interleukin-17;
vascular endothelial growth factor
- MeSH:
Animals;
Cell Culture Techniques;
Cell Wall;
Eosinophils;
Gram-Negative Bacteria;
Inflammation;
Interferon-gamma;
Interleukin-17*;
Interleukins;
Mice;
Mice, Knockout;
Nasal Mucosa;
Neutrophil Infiltration;
Ovalbumin;
Ovum;
Phenotype;
Rhinitis*;
Rhinitis, Allergic;
RNA, Messenger;
Spleen;
Vascular Endothelial Growth Factor A
- From:Allergy, Asthma & Immunology Research
2017;9(2):169-176
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
