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However, a primary vertebrate reservoir in the United States, the white-footed deermouse\n                      <jats:italic>Peromyscus leucopus<\/jats:italic>\n                      , is reported not to have reduced fitness following infection. Although laboratory strains of\n                      <jats:italic>Mus musculus<\/jats:italic>\n                      mice have successfully been leveraged to model acute human Lyme disease, the ability of these rodents to model\n                      <jats:italic>B. burgdorferi-P. leucopus<\/jats:italic>\n                      interactions remains understudied. Here, we compared infection of\n                      <jats:italic>P. leucopus<\/jats:italic>\n                      with\n                      <jats:italic>B. burgdorferi<\/jats:italic>\n                      B31 with infection of the traditional\n                      <jats:italic>B. burgdorferi<\/jats:italic>\n                      murine models\u2014C57BL\/6J and C3H\/HeN\n                      <jats:italic>Mus musculus<\/jats:italic>\n                      , which develop signs of inflammation akin to human disease. We find that\n                      <jats:italic>B. burgdorferi<\/jats:italic>\n                      was able to reach much higher burdens (10- to 30-times higher) in multiple\n                      <jats:italic>M. musculus<\/jats:italic>\n                      skin sites and that the overall dynamics of infection differed between the two rodent species. We also found that\n                      <jats:italic>P. leucopus<\/jats:italic>\n                      remained transmissive to larval\n                      <jats:italic>Ixodes scapularis<\/jats:italic>\n                      for a far shorter period than either\n                      <jats:italic>M. musculus<\/jats:italic>\n                      strain. In line with these observations, we found that\n                      <jats:italic>P. leucopus<\/jats:italic>\n                      does launch a modest but sustained inflammatory response against\n                      <jats:italic>B. burgdorferi<\/jats:italic>\n                      in the skin, which we hypothesize leads to reduced bacterial viability and rodent-to-tick transmission in these hosts. Similarly, we also observe evidence of inflammation in infected\n                      <jats:italic>P. leucopus<\/jats:italic>\n                      hearts. These observations provide new insight into reservoir species and the\n                      <jats:italic>B. burgdorferi<\/jats:italic>\n                      enzootic cycle.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        A Lyme disease-causing bacteria,\n                        <jats:italic>Borrelia burgdorferi<\/jats:italic>\n                        , must alternate between infecting a vertebrate host\u2014usually rodents or birds\u2014and ticks. In order to be successful in that endeavor, the bacteria must avoid being killed by the vertebrate host before it can infect a new larval tick. In this work, we examine how\n                        <jats:italic>B. burgdorferi<\/jats:italic>\n                        and one of its primary vertebrate reservoirs,\n                        <jats:italic>Peromyscus leucopus<\/jats:italic>\n                        , interact during an experimental infection. We find that\n                        <jats:italic>B. burgdorferi<\/jats:italic>\n                        appears to colonize its natural host less successfully than conventional laboratory mouse models, which aligns with a sustained seemingly anti-bacterial response by\n                        <jats:italic>P. leucopus<\/jats:italic>\n                        against the microbe. These data enhance our understanding of\n                        <jats:italic>P. leucopus<\/jats:italic>\n                        host-pathogen interactions and could potentially serve as a foundation to uncover ways to disrupt the spread of\n                        <jats:italic>B. burgdorferi<\/jats:italic>\n                        in nature.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/aem.00822-24","type":"journal-article","created":{"date-parts":[[2024,6,20]],"date-time":"2024-06-20T09:00:22Z","timestamp":1718874022000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":16,"title":["Comparative reservoir competence of\n                    <i>Peromyscus leucopus<\/i>\n                    , C57BL\/6J, and C3H\/HeN for\n                    <i>Borrelia burgdorferi<\/i>\n                    B31"],"prefix":"10.1128","volume":"90","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9037-8418","authenticated-orcid":false,"given":"Jeffrey S.","family":"Bourgeois","sequence":"first","affiliation":[{"name":"Department of Molecular Biology and Microbiology, Tufts University, Boston, Massachusetts, USA"},{"name":"Tufts University, Tufts Lyme Disease Initiative, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephanie S.","family":"You","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Microbiology, Tufts University, Boston, Massachusetts, USA"},{"name":"Tufts University, Tufts Lyme Disease Initiative, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luke H.","family":"Clendenen","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Microbiology, Tufts University, Boston, Massachusetts, USA"},{"name":"Tufts University, Tufts Lyme Disease Initiative, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muskan","family":"Shrestha","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Microbiology, Tufts University, Boston, Massachusetts, USA"},{"name":"Tufts University, Tufts Lyme Disease Initiative, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanja","family":"Petnicki-Ocwieja","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Microbiology, Tufts University, Boston, Massachusetts, USA"},{"name":"Tufts University, Tufts Lyme Disease Initiative, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4548-8663","authenticated-orcid":true,"suffix":"III","given":"Sam R.","family":"Telford","sequence":"additional","affiliation":[{"name":"Tufts University, Tufts Lyme Disease Initiative, Boston, Massachusetts, USA"},{"name":"Department of Infectious Disease and Global Health, Tufts University, North Grafton, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1659-5558","authenticated-orcid":true,"given":"Linden T.","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Microbiology, Tufts University, Boston, Massachusetts, USA"},{"name":"Tufts University, Tufts Lyme Disease Initiative, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_5_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.aje.a112625"},{"key":"e_1_3_5_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.aje.a112626"},{"key":"e_1_3_5_4_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.7043737"},{"key":"e_1_3_5_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2714"},{"key":"e_1_3_5_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.51.2.394-396.1986"},{"key":"e_1_3_5_7_2","first-page":"960","article-title":"Arthritis caused by Borrelia burgdorferi in dogs","volume":"186","author":"Kornblatt AN","year":"1985","unstructured":"Kornblatt AN, Urband PH, Steere AC. 1985. 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