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Anisakis pegreffii Extract Induces Airway Inflammation with Airway Remodeling in a Murine Model System

 Jun Ho Choi  ;  Ju Yeong Kim  ;  Myung-Hee Yi  ;  Myungjun Kim  ;  Tai-Soon Yong 
 BIOMED RESEARCH INTERNATIONAL, Vol.2021 : 2522305, 2021-09 
Journal Title
Issue Date
Airway Remodeling* / drug effects ; Animals ; Anisakis / physiology* ; Antibody Specificity / immunology ; Biomarkers / metabolism ; Bronchial Hyperreactivity / blood ; Bronchial Hyperreactivity / complications ; Bronchial Hyperreactivity / physiopathology ; Cytokines / metabolism ; Disease Models, Animal ; Inflammation Mediators / metabolism ; Lung / drug effects ; Lung / physiopathology ; Methacholine Chloride / pharmacology ; Mice, Inbred BALB C ; Pneumonia / blood ; Pneumonia / complications ; Pneumonia / parasitology* ; Pneumonia / physiopathology* ; Th2 Cells / metabolism
Exposure of the respiratory system to the Anisakis pegreffii L3 crude extract (AE) induces airway inflammation; however, the mechanism underlying this inflammatory response remains unknown. AE contains allergens that promote allergic inflammation; exposure to AE may potentially lead to asthma. In this study, we aimed to establish a murine model to assess the effects of AE on characteristic features of chronic asthma, including airway hypersensitivity (AHR), airway inflammation, and airway remodeling. Mice were sensitized for five consecutive days each week for 4 weeks. AHR, lung inflammation, and airway remodeling were evaluated 24 h after the last exposure. Lung inflammation and airway remodeling were assessed from the bronchoalveolar lavage fluid (BALF). To confirm the immune response in the lungs, changes in gene expression in the lung tissue were assessed with reverse transcription-quantitative PCR. The levels of IgE, IgG1, and IgG2a in blood and cytokine levels in the BALF, splenocyte, and lung lymph node (LLN) culture supernatant were measured with ELISA. An increase in AHR was prominently observed in AE-exposed mice. Epithelial proliferation and infiltration of inflammatory cells were observed in the BALF and lung tissue sections. Collagen deposition was detected in lung tissues. AE exposure increased IL-4, IL-5, and IL-13 expression in the lung, as well as the levels of antibodies specific to AE. IL-4, IL-5, and IL-13 were upregulated only in LLN. These findings indicate that an increase in IL-4+ CD4+ T cells in the LLN and splenocyte resulted in increased Th2 response to AE exposure. Exposure of the respiratory system to AE resulted in an increased allergen-induced Th2 inflammatory response and AHR through accumulation of inflammatory and IL-4+ CD4+ T cells and collagen deposition. It was confirmed that A. pegreffii plays an essential role in causing asthma in mouse models and has the potential to cause similar effects in humans.
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1. College of Medicine (의과대학) > Dept. of Tropica Medicine (열대의학교실) > 1. Journal Papers
Yonsei Authors
Kim, Ju Young(김주영) ORCID logo https://orcid.org/0000-0003-2456-6298
Yong, Tai Soon(용태순) ORCID logo https://orcid.org/0000-0002-3445-0769
Yi, Myung Hee(이명희) ORCID logo https://orcid.org/0000-0001-9537-5726
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