{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T22:28:05Z","timestamp":1792794485681,"version":"4.5.0"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2020,3,3]],"date-time":"2020-03-03T00:00:00Z","timestamp":1583193600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Hospices Civils de Lyon for \u2018Young Investigator\u2019","id":[{"id":"https:\/\/ror.org\/01502ca60","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Targeting biofilm-embedded and intraosteoblastic Staphylococcus aureus, rifampicin gained a pivotal role in bone and joint infection (BJI) treatment. Two other rifamycins, rifabutin and rifapentine, may represent better-tolerated alternatives, but their activity against bacterial reservoirs associated with BJI chronicity has never been evaluated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To evaluate the activities of rifampicin, rifabutin and rifapentine in osteoblast infection models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using three S. aureus isolates, rifamycins were compared regarding: (i) their intracellular activity in \u2018acute\u2019 (24\u2009h) and \u2018chronic\u2019 (7\u2009days) osteoblast infection models at 0.1\u00d7 MIC, 1\u00d7 MIC, 10\u00d7 MIC and 100\u00d7 MIC, while impacting infection-induced cytotoxicity (MTT assay), intracellular phenol-soluble modulin (PSM) secretion (RT\u2013PCR), resistance selection and small colony variant (SCV) emergence; and (ii) their minimal biofilm eradication concentration (MBEC) and their MIC to prevent biofilm formation (bMIC).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>At 0.1\u00d7 MIC, only rifabutin significantly reduced intracellular inoculum and PSM secretion. All rifamycins allowed a 50% reduction of intraosteoblastic inoculum at higher concentrations, with no difference between acute and chronic infection models, while reducing infection-induced cytotoxicity and PSM secretion. Dose-dependent emergence of intracellular SCVs was observed for all molecules. No intracellular emergence of resistance was detected. bMICs were equivalent for all molecules, but MBEC90s of rifapentine and rifabutin were 10- to 100-fold lower than those of rifampicin, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>All rifamycins are efficient in reducing the S. aureus intraosteoblastic reservoir while limiting infection-induced cytotoxicity, with a higher activity of rifabutin at low concentrations. All molecules prevent biofilm formation, but only rifapentine and rifabutin consistently reduce formed biofilm-embedded bacteria for all isolates. The activity of rifabutin at lower doses highlights its therapeutic potential.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/jac\/dkaa061","type":"journal-article","created":{"date-parts":[[2020,2,5]],"date-time":"2020-02-05T07:09:19Z","timestamp":1580886559000},"page":"1466-1473","source":"Crossref","is-referenced-by-count":39,"title":["Antibiofilm and intraosteoblastic activities of rifamycins against Staphylococcus aureus: promising in vitro profile of rifabutin"],"prefix":"10.1093","volume":"75","author":[{"given":"L\u00e9lia","family":"Abad","sequence":"first","affiliation":[{"name":"CIRI \u2013 Centre International de Recherche en Infectiologie, Inserm, U1111, Universit\u00e9\u00b4 Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Sup\u00e9rieure de Lyon, Univ Lyon, F-69007 Lyon, France"},{"name":"Universit\u00e9 Claude Bernard Lyon 1, Lyon, France"},{"name":"Laboratoire de bact\u00e9riologie, Institut des Agents Infectieux, French National Reference Center for 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