{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T23:49:32Z","timestamp":1793836172725,"version":"4.6.1"},"reference-count":66,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2022,6,1]],"date-time":"2022-06-01T00:00:00Z","timestamp":1654041600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["T90DE021989-11"],"award-info":[{"award-number":["T90DE021989-11"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DP2GM146456-01"],"award-info":[{"award-number":["DP2GM146456-01"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["T90DE021989-11"],"award-info":[{"award-number":["T90DE021989-11"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007710","name":"University of Connecticut","doi-asserted-by":"publisher","award":["Start-Up Fund"],"award-info":[{"award-number":["Start-Up Fund"]}],"id":[{"id":"10.13039\/100007710","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007710","name":"University of Connecticut","doi-asserted-by":"publisher","award":["UConn Summer Undergraduate Research Fund"],"award-info":[{"award-number":["UConn Summer Undergraduate Research Fund"]}],"id":[{"id":"10.13039\/100007710","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Bacterial persisters are rare phenotypic variants in clonal bacterial cultures that can endure antimicrobial therapy and potentially contribute to infection relapse. Here, we investigate the potential of leveraging microbial interactions to disrupt persisters as they resuscitate during the post-antibiotic treatment recovery period.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and Results<\/jats:title>\n                  <jats:p>We treated stationary-phase E. coli MG1655 with a DNA-damaging fluoroquinolone and co-cultured the cells with probiotic E. coli Nissle following antibiotic removal. We found that E. coli Nissle reduced the survival of fluoroquinolone persisters and their progeny by over three orders of magnitude within 24 h. Using a bespoke H-diffusion cell apparatus that we developed, we showed that E. coli Nissle antagonized the fluoroquinolone-treated cells in a contact-dependent manner. We further demonstrated that the fluoroquinolone-treated cells can still activate the SOS response as they recover from antibiotic treatment in the presence of E. coli Nissle and that the persisters depend on TolC-associated efflux systems to defend themselves against the action of E. coli Nissle.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Our results demonstrate that probiotic bacteria, such as E. coli Nissle, have the potential to inhibit persisters as they resuscitate following antibiotic treatment.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Significance and Impact of the Study<\/jats:title>\n                  <jats:p>Bacterial persisters are thought to underlie chronic infections and they can lead to an increase in antibiotic-resistant mutants in their progenies. Our data suggest that we can leverage the knowledge we gain on the interactions between microbial strains\/species that interfere with persister resuscitation, such as those involving probiotic E. coli Nissle and E. coli MG1655 (a K-12 strain), to bolster the activity of our existing antibiotics.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1111\/jam.15541","type":"journal-article","created":{"date-parts":[[2022,3,25]],"date-time":"2022-03-25T10:08:32Z","timestamp":1648202912000},"page":"4020-4032","source":"Crossref","is-referenced-by-count":17,"title":["Probiotic Escherichia coli Nissle 1917 inhibits bacterial persisters that survive fluoroquinolone treatment"],"prefix":"10.1093","volume":"132","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5014-6161","authenticated-orcid":false,"given":"Patricia J.","family":"Hare","sequence":"first","affiliation":[{"name":"Department of Molecular Biology & Biophysics UCONN Health Farmington Connecticut USA"},{"name":"School of Dental Medicine UCONN Health Farmington Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanna E.","family":"Englander","sequence":"additional","affiliation":[{"name":"Cutaneous Microbiome & Inflammation Section National Institute of Arthritis and Musculoskeletal and Skin Diseases Bethesda Maryland USA"},{"name":"Department of Molecular Biology & Biophysics UCONN Health Farmington Connecticut USA"},{"name":"Department of Physiology & Neurobiology University of Connecticut Storrs Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6638-2959","authenticated-orcid":false,"given":"Wendy W. K.","family":"Mok","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology & Biophysics UCONN Health Farmington Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2022,6,1]]},"reference":[{"key":"2023011712024520400_jam15541-bib-0001","doi-asserted-by":"crossref","first-page":"1245","DOI":"10.1126\/science.1115109","article-title":"Contact-dependent inhibition of growth in Escherichia coli","volume":"309","author":"Aoki","year":"2005","journal-title":"Science"},{"key":"2023011712024520400_jam15541-bib-0002","doi-asserted-by":"crossref","first-page":"323","DOI":"10.1111\/j.1365-2958.2008.06404.x","article-title":"Contact-dependent growth inhibition requires the essential outer membrane protein BamA (YaeT) as the receptor and the inner membrane transport protein AcrB","volume":"70","author":"Aoki","year":"2008","journal-title":"Molecular Microbiology"},{"issue":"2006","key":"2023011712024520400_jam15541-bib-0003","first-page":"8","article-title":"Construction of Escherichia coli K-12 in-frame, single-gene knockout mutants: the Keio collection","volume":"2","author":"Baba","year":"2006","journal-title":"Molecular Systems Biology"},{"key":"2023011712024520400_jam15541-bib-0004","doi-asserted-by":"crossref","first-page":"441","DOI":"10.1038\/s41579-019-0196-3","article-title":"Definitions and guidelines for research on antibiotic persistence","volume":"17","author":"Balaban","year":"2019","journal-title":"Nature Reviews. 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