Aquatic environments face escalating challenges from multiple stressors like hypoxia and nanoparticle exposure, with impact of these combined stressors on mussel immunity being poorly understood. We investigated the individual and combined effects of short-term and long-term hypoxia and exposure to zinc oxide nanoparticles (nZnO) on immune system of the mussels (). Hemocyte functional traits (mortality, adhesion capacity, phagocytosis, lysosomal abundance, and oxidative burst), and transcript levels of immune-related genes involved in pathogen recognition (the Toll-like receptors, the complement system components, and the adaptor proteins MyD88) were assessed. Short-term hypoxia minimally affected hemocyte parameters, while prolonged exposure led to immunosuppression, impacting hemocyte abundance, viability, phagocytosis, and gene expression. Under normoxia, nZnO stimulated immune responses of mussel hemocytes. However, combined nZnO and hypoxia induced more pronounced and rapid immunosuppression than hypoxia alone, indicating a synergistic interaction. nZnO exposure hindered immune parameter recovery during post-hypoxic reoxygenation, suggesting persistent impact. Opposing trends were observed in pathogen-sensing and pathogen-elimination mechanisms, with a positive correlation between pathogen-recognition system activation and hemocyte mortality. These findings underscore a complex relationship and potential conflict between pathogen-recognition ability, immune function, and cell survival in mussel hemocytes under hypoxia and nanopollutant stress, and emphasize the importance of considering multiple stressors in assessing the vulnerability and adaptability of mussel immune system under complex environmental conditions of anthropogenically modified coastal ecosystems.

中文翻译：

---

接触纳米污染物（nZnO）会增强缺氧的负面影响并延迟贻贝免疫系统的恢复


水生环境面临着缺氧和纳米颗粒暴露等多种应激源带来的不断升级的挑战，而这些组合应激源对贻贝免疫力的影响知之甚少。我们研究了短期和长期缺氧以及接触氧化锌纳米颗粒 (nZnO) 对贻贝免疫系统的单独和综合影响 ()。血细胞功能特征（死亡率、粘附能力、吞噬作用、溶酶体丰度和氧化爆发）以及参与病原体识别的免疫相关基因（Toll 样受体、补体系统组件和接头蛋白 MyD88）的转录水平评估。短期缺氧对血细胞参数的影响最小，而长期缺氧会导致免疫抑制，影响血细胞丰度、活力、吞噬作用和基因表达。在常氧条件下，nZnO 刺激贻贝血细胞的免疫反应。然而，nZnO 和缺氧组合比单独缺氧诱导更明显和更快速的免疫抑制，表明存在协同相互作用。 nZnO 暴露阻碍了缺氧后复氧过程中免疫参数的恢复，表明影响持续存在。在病原体感知和病原体消除机制中观察到相反的趋势，病原体识别系统激活与血细胞死亡率之间呈正相关。这些发现强调了缺氧和纳米污染物胁迫下贻贝血细胞的病原体识别能力、免疫功能和细胞存活之间的复杂关系和潜在冲突，并强调在评估复杂环境下贻贝免疫系统的脆弱性和适应性时考虑多种应激源的重要性。人为改变的沿海生态系统的环境条件。