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.