<?xml version='1.0' encoding='utf-8'?>
<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:contributor>Justin Greer</dc:contributor>
  <dc:contributor>Cathy A. Richter</dc:contributor>
  <dc:contributor>Luke R. Iwanowicz</dc:contributor>
  <dc:contributor>Edward Spinard</dc:contributor>
  <dc:contributor>Jacquelyn McDonald</dc:contributor>
  <dc:contributor>Carla M. Conway</dc:contributor>
  <dc:contributor>Robert W. Gale</dc:contributor>
  <dc:contributor>Donald E. Tillitt</dc:contributor>
  <dc:contributor>John D. Hansen</dc:contributor>
  <dc:creator>Jessica Kristin Leet</dc:creator>
  <dc:date>2022</dc:date>
  <dc:description>&lt;p&gt;&lt;span&gt;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 (&lt;/span&gt;&lt;i&gt;Micropterus salmoides&lt;/i&gt;&lt;span&gt;) exposed to a potent synthetic estrogen (17α-ethinylestradiol, EE2) at a low (EE2&lt;/span&gt;&lt;sub&gt;Low&lt;/sub&gt;&lt;span&gt;, 0.87 ng/L) or high (EE2&lt;/span&gt;&lt;sub&gt;High&lt;/sub&gt;&lt;span&gt;, 9.08 ng/L) dose for 4 weeks, followed by transfer to clean water and injection with an LD&lt;/span&gt;&lt;sub&gt;40&lt;/sub&gt;&lt;span&gt;&amp;nbsp;dose of the Gram-negative bacteria&amp;nbsp;&lt;/span&gt;&lt;i&gt;Edwardsiella piscicida&lt;/i&gt;&lt;span&gt;. Unexpectedly, this prior exposure to EE2&lt;/span&gt;&lt;sub&gt;High&lt;/sub&gt;&lt;span&gt;&amp;nbsp;significantly increased survivorship at 10 d post-infection compared to solvent control or EE2&lt;/span&gt;&lt;sub&gt;Low&lt;/sub&gt;&lt;span&gt;-exposed, infected fish. Both prior exposure and infection with&amp;nbsp;&lt;/span&gt;&lt;i&gt;E. piscicida&lt;/i&gt;&lt;span&gt;&amp;nbsp;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&lt;/span&gt;&lt;sub&gt;High&lt;/sub&gt;&lt;span&gt;&amp;nbsp;treatment that could underlie the observed protective effect and metabolic shift in EE2&lt;/span&gt;&lt;sub&gt;High&lt;/sub&gt;&lt;span&gt;-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.&lt;/span&gt;&lt;/p&gt;</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>10.1021/acs.est.2c02250</dc:identifier>
  <dc:language>en</dc:language>
  <dc:publisher>ACS Publications</dc:publisher>
  <dc:title>Exposure to 17α-ethinylestradiol results in differential susceptibility of largemouth bass (Micropterus salmoides) to bacterial infection</dc:title>
  <dc:type>article</dc:type>
</oai_dc:dc>