微塑料 (MP) 几乎存在于地球上的每个环境中，并成为世界各地的污染源。微塑料对免疫的毒理学是一个新兴的研究领域，需要更多的研究来充分了解微塑料暴露对动物健康的影响。因此，我们试图通过使用动物模型——日本鹌鹑（Coturnix japonica）来确定微塑料对禽类脾脏的免疫毒性作用。一周龄雏鸡在饲料中接触环境相关浓度为 0.02 毫克/千克、0.4 毫克/千克和 8 毫克/千克的聚苯乙烯微塑料 5 周。结果表明，微塑料会引起微结构损伤，其特征是细胞紊乱和空泡形成，表明脾脏炎症。包括膜溶解和线粒体空泡化在内的超微结构损伤也表明微塑料暴露导致脾脏发生炎症反应。同时，活性氧（ROS）和丙二醛（MDA）增加，而超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽S-转移酶（GST）失活表明脾脏存在氧化应激。此外，促炎细胞因子水平升高，包括肿瘤坏死因子α（TNF-α）、干扰素γ（IFN-γ）、白介素-1β（IL-1β）、白细胞介素-6（IL-6）水平，以及抗-细胞因子水平下降。炎症细胞因子白介素 10 (IL-10) 提示脾脏炎症。此外，转录组分析表明，微塑料通过 p38 丝裂原激活蛋白激酶 (p38 MAPK) 通路激活和肿瘤坏死因子 (TNF) 信号刺激诱导脾脏炎症反应。信号刺激还加剧了脾脏中的细胞凋亡。本研究可能有助于了解微塑料发育免疫毒理学的潜在机制。版权所有 © 2023。由 Elsevier Ltd 出版。

Microplastics (MPs) have been found in virtually every environment on earth and become a source of pollution around the world. The toxicology of microplastics on immunity is an emerging area of research, and more studies are needed to fully understand the effects of microplastics exposure on animal health. Therefore, we tried to determine the immunotoxic effects of microplastics on avian spleen by using an animal model- Japanese quail (Coturnix japonica). One-week chicks were exposed to environmentally relevant concentrations of 0.02 mg/kg, 0.4 mg/kg and 8 mg/kg polystyrene microplastics in the feed for 5 weeks. The results demonstrated that microplastics induced microstructural injuries featured by cell disarrangement and vacuolation indicating splenic inflammation. Ultrastructural damages including membrane lysis and mitochondrial vacuolation also suggested inflammatory responses in the spleen by microplastics exposure. Meanwhile, increasing reactive oxygen species (ROS) and Malondialdehyde (MDA) while the inactivation of superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST) indicated oxidative stress in the spleen. Moreover, the increasing level of proinflammatory cytokines including Tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin-1β (IL-1β), interleukin-6 (IL-6) and decreasing level of anti-inflammatory cytokine interleukin-10 (IL-10) implied splenic inflammation. Furthermore, transcriptomic analysis showed that microplastics induced inflammatory responses in the spleen through p38 mitogen-activated protein kinases (p38 MAPK) pathway activation and tumor necrosis factor (TNF) signaling stimulation. The signaling stimulation also aggravated cell apoptosis in the spleen. The present study may benefit to understand potential mechanisms of developmental immunotoxicology of microplastics.Copyright © 2023. Published by Elsevier Ltd.