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Studies using transgenic ApoE human replacement mice (APOE) expressing one of three different allelic variants suggest that there is a hierarchy in terms of responsiveness to proinflammatory stimuli such as APOE4\/E4 &gt; APOE3\/E3 &gt; APOE2\/E2. In this study, we test the hypothesis that\n            <jats:italic>APOE<\/jats:italic>\n            genotype can also predict susceptibility to infection with the facultative intracellular gram-positive bacterium\n            <jats:italic>Listeria monocytogenes<\/jats:italic>\n            . We found that bone-marrow-derived macrophages isolated from aged APOE4\/E4 mice expressed elevated levels of nitric oxide synthase 2 and were highly resistant to\n            <jats:italic>in vitro<\/jats:italic>\n            infection with\n            <jats:italic>L. monocytogenes<\/jats:italic>\n            compared to APOE3\/E3 and APOE2\/E2 mice. However, we did not find statistically significant differences in cytokine or chemokine output from either macrophages or whole splenocytes isolated from APOE2\/E2, APOE3\/E3, or APOE4\/E4 mice following\n            <jats:italic>L. monocytogenes<\/jats:italic>\n            infection.\n            <jats:italic>In vivo<\/jats:italic>\n            , overall susceptibility to foodborne listeriosis also did not differ by\n            <jats:italic>APOE<\/jats:italic>\n            genotype in either young (2 mo old) or aged (15 mo old) C57BL\/6 mice. However, we observed a sex-dependent susceptibility to infection in aged APOE2\/E2 male mice and a sex-dependent resistance to infection in aged APOE4\/E4 male mice that was not present in female mice. Thus, these results suggest that\n            <jats:italic>APOE<\/jats:italic>\n            genotype does not play an important role in innate resistance to infection with\n            <jats:italic>L. monocytogenes<\/jats:italic>\n            but may be linked to sex-dependent changes that occur during immune senescence.\n          <\/jats:p>","DOI":"10.1128\/iai.00251-23","type":"journal-article","created":{"date-parts":[[2023,8,18]],"date-time":"2023-08-18T13:00:26Z","timestamp":1692363626000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["Apolipoprotein E genotype affects innate susceptibility to\n            <i>Listeria monocytogenes<\/i>\n            infection in aged male mice"],"prefix":"10.1128","volume":"91","author":[{"given":"Jooyoung","family":"Cho","sequence":"first","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky College of Medicine , Lexington, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katie L.","family":"Alexander","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky College of Medicine , Lexington, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica L.","family":"Ferrell","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky College of Medicine , Lexington, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lance A.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Kentucky College of Medicine , Lexington, Kentucky, USA"},{"name":"Sanders Brown Center on Aging, University of Kentucky College of Medicine , Lexington, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven","family":"Estus","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Kentucky College of Medicine , Lexington, Kentucky, USA"},{"name":"Sanders Brown Center on Aging, University of Kentucky College of Medicine , Lexington, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0716-3518","authenticated-orcid":true,"given":"Sarah E. 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