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However, the effects of\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      blooms on the host in the context of AUD or AUD-related phenotypes, such as ethanol preference, have been unstudied. In this work, we report a reduction in ethanol consumption and preference in mice colonized with\n                      <jats:italic toggle=\"yes\">C. albicans. C. albicans-<\/jats:italic>\n                      colonized mice exhibited elevated levels of serum prostaglandin E\n                      <jats:sub>2<\/jats:sub>\n                      (PGE\n                      <jats:sub>2<\/jats:sub>\n                      ), and the reduced ethanol preference was reversed by injection with antagonists of PGE\n                      <jats:sub>2<\/jats:sub>\n                      receptors. Furthermore, injection of mice with a PGE\n                      <jats:sub>2<\/jats:sub>\n                      derivative decreased their ethanol preference. These results show that PGE\n                      <jats:sub>2<\/jats:sub>\n                      acting on its receptors prostaglandin E receptor 1 (EP1) and prostaglandin E receptor 2 (EP2) drives reduced ethanol preference in\n                      <jats:italic toggle=\"yes\">C. albicans-<\/jats:italic>\n                      colonized mice. We also showed altered transcription of dopamine receptors in the dorsal striatum of\n                      <jats:italic toggle=\"yes\">C. albicans-<\/jats:italic>\n                      colonized mice and more rapid acquisition of ethanol-conditioned taste aversion, suggesting alterations to reinforcement or aversion learning. Finally,\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      -colonized mice were more susceptible to ethanol-induced motor coordination impairment, showing significant alterations to the behavioral effects of ethanol. This study identifies a member of the fungal microbiome that alters ethanol preference and demonstrates a role for PGE\n                      <jats:sub>2<\/jats:sub>\n                      signaling in these phenotypes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Candida albicans<\/jats:italic>\n                      is a commensal yeast that is found in the gut of most individuals.\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      has been shown to contribute to alcoholic liver disease. Outside of this, the impact of intestinal fungi on alcohol use disorder (AUD) had been unstudied. As AUD is a complex disorder characterized by high relapse rates and there are only three FDA-approved therapies for the maintenance of abstinence, it is important to study novel AUD contributors to find new therapeutic targets. Here, we show that an intestinal fungus,\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      , can alter mammalian ethanol consumption through an immune modulator, prostaglandin E\n                      <jats:sub>2<\/jats:sub>\n                      . The results highlight novel contributors to AUD-related phenotypes and further implicate the gut-brain axis in AUD. Future studies could lead to new therapeutic avenues for the treatment of AUD.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.02239-25","type":"journal-article","created":{"date-parts":[[2025,10,16]],"date-time":"2025-10-16T13:00:25Z","timestamp":1760619625000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":3,"title":["<i>Candida albicans<\/i>\n                    colonization modulates murine ethanol consumption and behavioral responses through elevation of serum prostaglandin E\n                    <sub>2<\/sub>\n                    and impact on the striatal dopamine system"],"prefix":"10.1128","volume":"16","author":[{"given":"Andrew W.","family":"Day","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Graduate School of Biomedical Sciences, Tufts University","place":["Boston, USA"]},{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular Biology and Microbiology, Tufts University","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emma","family":"Hayes","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular Biology and Microbiology, Tufts University","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeyra","family":"Perez-Lozada","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular Biology and Microbiology, Tufts University","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alyssa","family":"DiLeo","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Graduate School of Biomedical Sciences, Tufts University","place":["Boston, USA"]},{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Neuroscience, Tufts University","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katrina","family":"Blandino","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Graduate School of Biomedical Sciences, Tufts University","place":["Boston, USA"]},{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Neuroscience, Tufts University","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamie","family":"Maguire","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Neuroscience, Tufts University","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6352-4918","authenticated-orcid":true,"given":"Carol A.","family":"Kumamoto","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05wvpxv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular Biology and Microbiology, Tufts University","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1186\/s40168-017-0373-4"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.3390\/jof7040269"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/ijcp.13655"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1093\/cid\/ciab1057"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-020-60792-y"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/mBio.00915-18"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/mBio.02878-21"},{"key":"e_1_3_4_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41572-022-00406-1"},{"key":"e_1_3_4_10_2","unstructured":"World Health Organization. 2018. 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