{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T19:09:38Z","timestamp":1791227378312,"version":"4.1.0"},"reference-count":69,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2011,7,1]],"date-time":"2011-07-01T00:00:00Z","timestamp":1309478400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2011,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Previous articles reported that beta-lactam antibiotics increase the expression of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Staphylococcus aureus<\/jats:named-content>\n            Panton-Valentine leukocidin (PVL) by activating its transcription. We investigated the mechanisms underlying the inductor effect of beta-lactams on PVL expression by determining targets and regulatory pathways possibly implicated in this process. We measured PVL production in the presence of oxacillin (nonselective), imipenem (penicillin-binding protein 1 [PBP1] selective), cefotaxime (PBP2 selective), cefaclore (PBP3 selective), and cefoxitin (PBP4 selective).\n            <jats:italic>In vitro<\/jats:italic>\n            , we observed increased PVL production consistent with\n            <jats:italic>luk<\/jats:italic>\n            -PV mRNA levels that were 20 to 25 times higher for community-acquired methicillin-resistant\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. aureus<\/jats:named-content>\n            (CA-MRSA) cultures treated with PBP1-binding oxacillin and imipenem than for cultures treated with other beta-lactams or no antibiotic at all. This effect was also observed\n            <jats:italic>in vivo<\/jats:italic>\n            , with increased PVL mRNA levels in lung tissues from CA-MRSA-infected mice treated with imipenem but not cefoxitin. To confirm the involvement of PBP1 inhibition in this pathway, PBP1 depletion by use of an inducible\n            <jats:italic>pbp1<\/jats:italic>\n            antisense RNA showed a dose-dependent relationship between the level of\n            <jats:italic>pbp1<\/jats:italic>\n            antisense RNA and the\n            <jats:italic>luk<\/jats:italic>\n            -PV mRNA level. Upon imipenem treatment of exponential-phase cultures, we observed an increased\n            <jats:italic>sarA<\/jats:italic>\n            mRNA level after 30 min of incubation followed by a decreased\n            <jats:italic>rot<\/jats:italic>\n            mRNA level after 1 to 4 h of incubation. Unlike the\n            <jats:italic>agr<\/jats:italic>\n            and\n            <jats:italic>saeRS<\/jats:italic>\n            positive regulators, which were nonessential for PVL induction by beta-lactams, the\n            <jats:italic>sarA<\/jats:italic>\n            (positive) and\n            <jats:italic>rot<\/jats:italic>\n            (negative) PVL regulators were necessary for PVL induction by imipenem. Our results suggest that antibiotics binding to PBP1 increase PVL expression by modulating\n            <jats:italic>sarA<\/jats:italic>\n            and\n            <jats:italic>rot<\/jats:italic>\n            , which are essential mediators of the inductor effect of beta-lactams on PVL expression.\n          <\/jats:p>","DOI":"10.1128\/aac.01401-10","type":"journal-article","created":{"date-parts":[[2011,4,19]],"date-time":"2011-04-19T04:25:10Z","timestamp":1303187110000},"page":"3261-3271","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":77,"title":["\u03b2-Lactams Interfering with PBP1 Induce Panton-Valentine Leukocidin Expression by Triggering\n            <i>sarA<\/i>\n            and\n            <i>rot<\/i>\n            Global Regulators of Staphylococcus aureus"],"prefix":"10.1128","volume":"55","author":[{"given":"Oana","family":"Dumitrescu","sequence":"first","affiliation":[{"name":"INSERM, U851, and Universit\u00e9 de Lyon, Centre National de R\u00e9f\u00e9rence des Staphylocoques, Facult\u00e9 Lyon Est, Lyon F-69008, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Priya","family":"Choudhury","sequence":"additional","affiliation":[{"name":"Center for Infectious and Inflammatory Diseases, Institute of Biosciences and Technology, Texas A&amp;M Health Science Center, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandrine","family":"Boisset","sequence":"additional","affiliation":[{"name":"INSERM, U851, and Universit\u00e9 de Lyon, Centre National de R\u00e9f\u00e9rence des Staphylocoques, Facult\u00e9 Lyon Est, Lyon F-69008, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00e9dric","family":"Badiou","sequence":"additional","affiliation":[{"name":"INSERM, U851, and Universit\u00e9 de Lyon, Centre National de R\u00e9f\u00e9rence des Staphylocoques, Facult\u00e9 Lyon Est, Lyon F-69008, 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