{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,15]],"date-time":"2026-06-15T11:05:34Z","timestamp":1781521534302,"version":"3.54.1"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2025,5,13]],"date-time":"2025-05-13T00:00:00Z","timestamp":1747094400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01 AI145310"],"award-info":[{"award-number":["R01 AI145310"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["K08 AI151253"],"award-info":[{"award-number":["K08 AI151253"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["UM1TR004927"],"award-info":[{"award-number":["UM1TR004927"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100020360","name":"Infectious Diseases Society of America Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100020360","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000867","name":"Robert Wood Johnson Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000867","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,5,31]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>The emergence of antibiotic-tolerant staphylococcal strains, such as vancomycin-intermediate Staphylococcus aureus (VISA), poses a significant healthcare challenge and complicates treatment regimens. VISA often exhibits mutations in Krebs cycle enzymes, promoting anaerobic metabolism under physiological conditions and reducing susceptibility to antibiotics and innate immune defenses\u2014factors not typically captured in standard susceptibility testing. Building on these findings, we investigated ethylenediaminetetraacetic acid (EDTA), a chelator that enhances reactive oxygen species (ROS) production, as an adjunct to vancomycin for combating VISA infections.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>RNA sequencing analysis compared gene expression of a well-characterized VISA strain (D712) under physiological versus nutrient-rich conditions. Hydrogen peroxide (H2O2) killing assays were conducted with and without the hydroxyl radical quencher thiourea, while neutrophil killing assays used ROS scavenger butylated hydroxyanisole (BHA). A murine bacteremia model assessed the effects of vancomycin, EDTA, or their combination on VISA.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>VISA exhibited downregulation of Krebs cycle enzymes and other genes associated with resistance to iron and ROS-mediated killing under physiological conditions. EDTA, alone or with vancomycin, improved H2O2-mediated killing compared to vancomycin alone, a response counteracted by thiourea. The combination of EDTA and vancomycin enhanced neutrophil killing of VISA more effectively than either treatment alone, an effect negated by BHA. In vivo, EDTA enhanced vancomycin activity against VISA.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>EDTA potentiates vancomycin efficacy against VISA in vivo and enhances susceptibility to H2O2 and neutrophil killing. Reduced expression of Krebs cycle enzymes in VISA suggests that EDTA promotes ROS-mediated bacterial killing, targeting a key mechanism by which persistent staphylococci evade host defenses.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ofid\/ofaf291","type":"journal-article","created":{"date-parts":[[2025,5,13]],"date-time":"2025-05-13T17:50:23Z","timestamp":1747158623000},"source":"Crossref","is-referenced-by-count":2,"title":["Ethylenediaminetetraacetic Acid Enhances Vancomycin and Reactive Oxygen Species\u2013Mediated Killing of Vancomycin-Intermediate <i>Staphylococcus aureus<\/i>"],"prefix":"10.1093","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1733-0431","authenticated-orcid":false,"given":"Joshua","family":"Olson","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of California, San Diego School of Medicine , La Jolla, California 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,","place":["USA"]},{"name":"Department of Pediatrics, Collaborative to Halt Antibiotic-Resistant Microbes, University of California, San Diego School of Medicine , La Jolla, California ,","place":["USA"]},{"name":"Division of Infectious Diseases, Sharp Rees Stealy Medical Group , San Diego, California ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0330-278X","authenticated-orcid":false,"given":"Erlinda R","family":"Ulloa","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of California, Irvine School of Medicine , Irvine, California ,","place":["USA"]},{"name":"Division of Infectious Diseases, Children's Hospital of Orange County , Orange, California 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