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Commensals such as\n                      <jats:italic toggle=\"yes\">Enterococcus faecium<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Staphylococcus epidermidis<\/jats:italic>\n                      can transition into opportunistic pathogens when host defenses are compromised, underscoring the complexity of chronic wound microbiology.\n                      <jats:italic toggle=\"yes\">E. faecium<\/jats:italic>\n                      , particularly vancomycin-resistant strains, is an understudied, clinically important cause of chronic diabetic wound infections. Using a low-dose streptozocin-induced diabetic mouse model, we characterized\n                      <jats:italic toggle=\"yes\">E. faecium<\/jats:italic>\n                      wound infection dynamics and identified differences in colonization and clearance compared to non-diabetic animals. At 8 h post-infection (hpi), control mice exhibited higher\n                      <jats:italic toggle=\"yes\">E. faecium<\/jats:italic>\n                      wound colony-forming units (CFUs) than diabetic mice but cleared the infection more efficiently, resulting in similar CFU by 24 hpi. By contrast, diabetic mice showed impaired clearance, with elevated CFU persisting through 72 hpi. In mixed species infection with\n                      <jats:italic toggle=\"yes\">S. epidermidis<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">S. epidermidis<\/jats:italic>\n                      CFU increased at 72 hpi, while\n                      <jats:italic toggle=\"yes\">E. faecium<\/jats:italic>\n                      CFU remained comparable to single species infection. Despite strong initial cytokine and neutrophil responses,\n                      <jats:italic toggle=\"yes\">E. faecium<\/jats:italic>\n                      persisted in all wounds. Sustained neutrophil recruitment at 72 hpi occurred only in diabetic mice, whereas macrophage accumulation increased from 24 to 72 hpi in all wounds, including sterile controls. Histological analysis showed epithelial hyper thickening in both groups, indicating that diabetes and\n                      <jats:italic toggle=\"yes\">E. faecium<\/jats:italic>\n                      each contribute to impaired wound healing. This study establishes a diabetic mouse model of\n                      <jats:italic toggle=\"yes\">E. faecium<\/jats:italic>\n                      wound infection and suggests that\n                      <jats:italic toggle=\"yes\">E. faecium<\/jats:italic>\n                      modulates innate immune responses to persist in the wound bed.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/iai.00652-25","type":"journal-article","created":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T17:56:29Z","timestamp":1777571789000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["<i>Enterococcus faecium<\/i>\n                    colonization and persistence in a model of diabetic wound infection"],"prefix":"10.1128","volume":"94","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2661-1905","authenticated-orcid":true,"given":"Navin","family":"Jeyabalan","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02e7b5302","id-type":"ROR","asserted-by":"publisher"}],"name":"Singapore Center for Environmental Life Sciences Engineering and School of Biological Sciences, Nanyang Technological University","place":["Singapore, Singapore"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9289-4811","authenticated-orcid":true,"given":"Frederick Reinhart","family":"Tanoto","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02e7b5302","id-type":"ROR","asserted-by":"publisher"}],"name":"Singapore Center for Environmental Life Sciences Engineering and School of Biological Sciences, Nanyang Technological University","place":["Singapore, 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