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.

中文翻译：

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Anisakis pegreffii 提取物通过小鼠模型系统中的气道重塑诱导气道炎症

呼吸系统暴露于异尖线虫L3 粗提物 (AE) 诱导气道炎症；然而，这种炎症反应背后的机制仍然未知。AE含有促进过敏性炎症的过敏原；暴露于 AE 可能会导致哮喘。在这项研究中，我们旨在建立一个小鼠模型来评估 AE 对慢性哮喘特征的影响，包括气道过敏 (AHR)、气道炎症和气道重塑。小鼠每周连续 5 天致敏，持续 4 周。在最后一次暴露后 24 小时评估 AHR、肺部炎症和气道重塑。从支气管肺泡灌洗液 (BALF) 评估肺部炎症和气道重塑。为了确认肺部的免疫反应，用逆转录定量 PCR 评估了肺组织中基因表达的变化。用ELISA测量血液中IgE、IgG1和IgG2a的水平以及BALF、脾细胞和肺淋巴结（LLN）培养上清液中的细胞因子水平。在暴露于 AE 的小鼠中明显观察到 AHR 的增加。在BALF和肺组织切片中观察到上皮细胞增殖和炎性细胞浸润。在肺组织中检测到胶原蛋白沉积。AE 曝光增加IL-4、IL-5和IL-13在肺中的表达，以及对 AE 特异的抗体水平。IL-4、IL-5 和 IL-13 仅在 LLN 中上调。这些发现表明，LLN 和脾细胞中 IL-4 ⁺ CD4 ⁺ T 细胞的增加导致 Th2 对 AE 暴露的反应增加。呼吸系统暴露于 AE 导致过敏原诱导的 Th2 炎症反应和 AHR 通过炎症和 IL-4 ⁺ CD4 ⁺ T 细胞的积累和胶原沉积增加。已证实，A. pegreffii在小鼠模型中引起哮喘的过程中起着重要作用，并有可能在人类中引起类似的影响。