Impact of Microplastic Exposure on Airway Inflammation in an Acute Asthma Murine Model.

IF 3.6 Q2 RESPIRATORY SYSTEM
Tuberculosis and Respiratory Diseases Pub Date : 2026-01-01 Epub Date: 2025-10-23 DOI:10.4046/trd.2025.0091
Joon Young Choi, Jung Hur, Yong Suk Jo, Chin Kook Rhee
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引用次数: 0

Abstract

Background: Widely distributed in the environment, microplastics (MPs) are increasingly recognized as potential respiratory hazards. While several studies suggest their role in worsening allergic airway diseases, findings remain inconsistent. This study aimed to investigate the immunologic effects of repeated MP exposure in an acute murine model of ovalbumin (OVA)-induced asthma.

Methods: Female BALB/c mice were assigned to four groups: control with vehicle, control with MPs, OVA-sensitized with vehicle, and OVA-sensitized with MPs. An acute asthma model was established by sensitizing and challenging mice with OVA. Spherical polystyrene MPs of 1-5 μm were administered intranasally at 300 μg daily from day 0 to 21. Lung inflammation was assessed via bronchoalveolar lavage fluid (BALF) analysis, histopathology, cytokine measurements, and macrophage polarization by immunofluorescence.

Results: MP exposure did not exacerbate allergic inflammation in OVA-sensitized mice. Instead, it led to reduced eosinophilic infiltration and lower levels of interleukin 5 (IL-5) and IL-13, compared to vehicle-treated OVA mice. In contrast, MP exposure in control mice increased tumor necrosis factor-α and decreased interferon-γ levels, upregulated epithelial alarmins (IL-25 and IL-33), and elevated inflammation scores. Alarmin levels, including IL-25 and IL-33, were elevated by MP exposure in control mice, whereas no significant differences were observed between vehicle- and MP-treated mice in the OVA-sensitized group. Macrophage analysis showed a shift toward M1 polarization only in control mice.

Conclusion: While MP exposure aggravated inflammatory responses in healthy lungs, it did not exacerbate airway inflammation in asthmatic mice.

微塑料暴露对急性哮喘小鼠模型气道炎症的影响。
背景:微塑料(MPs)广泛分布于环境中,越来越被认为是潜在的呼吸危害。虽然有几项研究表明它们在加重过敏性气道疾病中的作用,但研究结果仍不一致。本研究旨在探讨反复暴露MP对急性卵清蛋白(OVA)诱发哮喘小鼠模型的免疫影响。方法:将雌性BALB/c小鼠分为四组:载药对照组、MPs对照组、载药致敏ova组和MPs致敏ova组。用卵清蛋白(OVA)致敏攻毒小鼠,建立急性哮喘模型。从第0天至第21天,给予球形聚苯乙烯MPs (1-5 μm),每日300 μg。通过支气管肺泡灌洗液(BALF)分析、组织病理学、细胞因子测量和免疫荧光巨噬细胞极化来评估肺部炎症。结果:MP暴露不会加重ova致敏小鼠的变应性炎症。相反,与载体处理的卵子小鼠相比,它导致嗜酸性粒细胞浸润减少,IL-5和IL-13水平降低。相比之下,MP暴露在对照小鼠中,TNF-α升高,IFN-γ水平降低,上皮报警因子(IL-25和IL-33)上调,炎症评分升高。对照组小鼠暴露于MP后,警示素(包括IL-25和IL-33)水平升高,而ova致敏组小鼠与MP处理小鼠之间无显著差异。巨噬细胞分析显示,仅在对照组小鼠中,巨噬细胞向M1极化方向转移。结论:MP暴露虽然加重了健康肺部的炎症反应,但并未加重哮喘小鼠的气道炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
5.30
自引率
0.00%
发文量
42
审稿时长
12 weeks
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