Exposure to 17α-ethinylestradiol results in differential susceptibility of largemouth bass (Micropterus salmoides) to bacterial infection

Abstract

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 LD 40 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.