Disease outbreaks, skin lesions, mortality events, and reproductive abnormalities have been observed in wild populations of centrarchids. The presence of estrogenic endocrine disrupting compounds (EEDCs) has been implicated as a potential causal factor for these effects. The effects of prior EEDC exposure on immune response were examined in juvenile largemouth bass (Micropterus salmoides) exposed to a potent synthetic estrogen (17α-ethinylestradiol, EE2) at a low (EE2_Low, 0.87 ng/L) or high (EE2_High, 9.08 ng/L) dose for 4 weeks, followed by transfer to clean water and injection with an LD₄₀ dose of the Gram-negative bacteria Edwardsiella piscicida. Unexpectedly, this prior exposure to EE2_High significantly increased survivorship at 10 d post-infection compared to solvent control or EE2_Low-exposed, infected fish. Both prior exposure and infection with E. piscicida led to significantly reduced hepatic glycogen levels, indicating a stress response resulting in depletion of energy stores. Additionally, pathway analysis for liver and spleen indicated differentially expressed genes associated with immunometabolic processes in the mock-injected EE2_High treatment that could underlie the observed protective effect and metabolic shift in EE2_High-infected fish. Our results demonstrate that exposure to a model EEDC alters metabolism and immune function in a fish species that is ecologically and economically important in North America.

中文翻译：

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暴露于 17α-炔雌醇导致大口黑鲈 (Micropterus salmoides) 对细菌感染的不同易感性

已在野生食心虫种群中观察到疾病爆发、皮肤损伤、死亡事件和生殖异常。雌激素内分泌干扰化合物 (EEDCs) 的存在被认为是这些影响的潜在原因。在暴露于低（EE2低_， 0.87 ng/L）或高（EE2_高， 9.08 ng/L) 剂量持续 4 周，然后转移到干净的水中并注射 LD ₄₀剂量的革兰氏阴性细菌Edwardsiella piscicida。出乎意料的是，之前接触过 EE2 _High与溶剂控制或 EE2_低暴露的感染鱼相比，感染后 10 天的存活率显着提高。先前接触和感染E. pisciciida导致肝糖原水平显着降低，表明压力反应导致能量储存耗尽。此外，肝脏和脾脏的通路分析表明，在模拟注射 EE2 _{High治疗中与免疫代谢过程相关的差异表达基因可能是 EE2 High}观察到的保护作用和代谢转变的基础-受感染的鱼。我们的研究结果表明，暴露于模型 EEDC 会改变鱼类的新陈代谢和免疫功能，这在北美具有重要的生态和经济意义。