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

Jun Ho Choi,Myungjun Kim,Ju Yeong Kim,Tai-Soon Yong,Myung-Hee Yi

doi:10.1155/2021/2522305

Abstract

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.

Highlights

The fish-borne zoonotic parasites Anisakis simplex and A. pegreffii are known to cause anisakiasis or allergies in humans [1]
A. pegreffii and A. simplex allergens are known to contribute to respiratory allergies and contact dermatitis [9, 10]; repeated inhalation of the aerosolized anisakid protein may trigger a respiratory reaction, as suggested by prior studies in humans [6, 11]
Airway remodeling through collagen deposition is usually not observed in mouse models until mice are exposed to allergens for more than 4 weeks [36, 37]

Summary

Introduction

The fish-borne zoonotic parasites Anisakis simplex and A. pegreffii are known to cause anisakiasis or allergies in humans [1]. The gastrointestinal symptoms may be minimal or absent, and the onset of symptoms is usually delayed between 2 and 24 h [2] This delay between consumption of fish and the onset of symptoms can be an important diagnostic clue for the detection of Anisakis allergy. Aerosolization of seafood and cooking fluids during processing is a potential occupational hazard that can cause sensitization through inhalation [6]. A. pegreffii and A. simplex allergens are known to contribute to respiratory allergies and contact dermatitis [9, 10]; repeated inhalation of the aerosolized anisakid protein may trigger a respiratory reaction, as suggested by prior studies in humans [6, 11]. A case of occupational hypersensitivity to Anisakis had previously been reported in a worker in a frozen fish

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