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KMID : 0361020080510010051
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Korean Journal of Otolaryngology - Head and Neck Surgery
2008 Volume.51 No. 1 p.51 ~ p.57
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The Differential Expression of Upper and Lower Airway after Lipopolysaccharide Administration in a Murine Allergy Model
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Park Su-Kyoung
Rhee Chae-Seo
Kim Yoon-Keun
Cho Sang-Heon
Min Kyung-Up
Kim You-Young
Oh Seung-Ha
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Abstract
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Background & Objectives: It is well recognized that respiratory infection modulates allergic airway inflammation. However, there is apparent controversy about the role for exposure site of bacterial components such as lipopolysaccharide (LPS) in allergic inflammation. This study investigated allergic airway inflammation after the administration of the same amount of LPS in the ovalbumin (OVA) induced murine allergy model.
Materials & Method: Six-week-old BALB/c mice were sensitized with OVA at day 0 and 7 of the start of experiment via intraperitoneal route and challenged with OVA or OVA and LPS at day 14, 15, 16, 21, 22 and 23 with or without anesthesia via intranasal route. After the last challenge, parameters for airway hyperresponsiveness were measured, followed by evaluation of airway histology, serum OVA specific antibodies, inflammatory cells and cytokines of bronchoalveolar lavage fluid (BALF) and nasal cavity lavage fluid (NALF).
Results: Airway hyperresponsiveness significantly increased not only in the groups of asthma (ASM) and asthma with LPS (ASM+LPS) but also in the allergic rhinitis with LPS (AR+LPS) group. In the lung, infiltration of inflammatory cells including eosinophils and lymphocytes were prominent only in the groups of ASM and ASM+LPS. When compared with the control, in the nasal cavity, the infiltration of inflammatory cells was prominent in all of the groups, whereas in BALF, IL-5 and IL-13 were significantly increased in the groups of ASM+LPS and ASM, and OVA specific IgE and IgG2a were significantly increased in all of the groups.
Conclusions: These results support the concept that the systemic mechanism linking allergic rhinitis to asthma depends on the location and extent of airway allergen exposure.
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KEYWORD
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Allergy, Lipopolysaccharide, Airway, Inflammation
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