{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,7,14]],"date-time":"2024-07-14T05:20:11Z","timestamp":1720934411395},"reference-count":34,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"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":[[2012,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The ability of viridans group streptococci to bind human plasminogen and its subsequent activation into plasmin may contribute to the pathogenesis of infective endocarditis (IE) by leading to a decreased stability of the streptococcal vegetation and facilitating dehiscence of emboli. At levels greater than or equal to their MICs, penicillin, vancomycin, and linezolid are efficacious in the treatment of streptococcal endocarditis. However, at sub-MICs, antibiotics can modulate the expression of bacterial genes, including virulence-associated genes, which can have counterproductive effects on the treatment of endocarditis. The effects of 1\/8\u00d7 and 1\/4\u00d7 MICs of penicillin, vancomycin, and linezolid on the plasminogen binding ability of IE isolates\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Streptococcus mitis<\/jats:named-content>\n            881\/956,\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Streptococcus oralis<\/jats:named-content>\n            12601, and\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Streptococcus sanguinis<\/jats:named-content>\n            12403 were assessed phenotypically and the expression of plasminogen receptors \u03b1-enolase and glyceraldehyde 3-phosphate dehydrogenase of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. oralis<\/jats:named-content>\n            12601 when exposed to 1\/4\u00d7 MIC of penicillin, was analyzed through quantitative reverse transcription (qRT)-PCR. The plasminogen binding ability of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. mitis<\/jats:named-content>\n            881\/956 and\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. sanguinis<\/jats:named-content>\n            12403 remained unaffected by exposure to sub-MICs of all of the antibiotics tested, while that of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. oralis<\/jats:named-content>\n            12601 was significantly enhanced by all of the antibiotics tested at sub-MICs. qRT-PCR analysis of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. oralis<\/jats:named-content>\n            12601 demonstrated an upregulation of the\n            <jats:italic>eno<\/jats:italic>\n            and\n            <jats:italic>gapdh<\/jats:italic>\n            genes, indicating an overexpression of plasminogen receptors. These findings suggest that for some endocarditis isolates, the effect of antibiotic sub-MICs, in addition to a reduced antibacterial effect, may influence the clinical response to nonsurgical therapy. It remains difficult to accurately predict isolate responses to sub-MIC antimicrobials since there appears to be interspecies variation.\n          <\/jats:p>","DOI":"10.1128\/aac.00452-11","type":"journal-article","created":{"date-parts":[[2011,10,29]],"date-time":"2011-10-29T03:20:13Z","timestamp":1319858413000},"page":"458-463","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["Antibiotic Modulation of the Plasminogen Binding Ability of Viridans Group Streptococci"],"prefix":"10.1128","volume":"56","author":[{"given":"Cristina","family":"Teles","sequence":"first","affiliation":[{"name":"Department of Biological and Biomedical Sciences, Glasgow Caledonian University, Glasgow, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew","family":"Smith","sequence":"additional","affiliation":[{"name":"College of Medical, Veterinary &amp; Life Sciences, Glasgow Dental Hospital &amp; School, University of Glasgow, Glasgow, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sue","family":"Lang","sequence":"additional","affiliation":[{"name":"Department of Biological and Biomedical Sciences, Glasgow Caledonian University, Glasgow, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.00546-09"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/48.suppl_1.5"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-695X.2007.00330.x"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00184-08"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cpcardiol.2005.12.001"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200320430"},{"key":"e_1_3_1_8_2","doi-asserted-by":"crossref","first-page":"1069","DOI":"10.1016\/S0735-1097(00)01206-7","article-title":"Echocardiography predicts embolic events in infective endocarditis","volume":"37","author":"Di Salvo G","year":"2001","unstructured":"Di SalvoG. 2001. 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