{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T05:35:29Z","timestamp":1779255329941,"version":"3.51.4"},"reference-count":22,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"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":[[2015,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The direct or indirect interactions that antifungals have with the host immune response may play a significant role in defining their activity\n            <jats:italic>in vivo<\/jats:italic>\n            . However, the impact that acquired antifungal resistance has on the immunopharmacologic activity of antifungals is not well described. We assessed the immunopharmacologic activity of caspofungin, micafungin, and voriconazole among isolates of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Candida glabrata<\/jats:named-content>\n            with or without FKS-mediated echinocandin resistance. Clinical bloodstream isolates of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">C. glabrata<\/jats:named-content>\n            from patients who did (\n            <jats:italic>n<\/jats:italic>\n            = 5) or did not (\n            <jats:italic>n<\/jats:italic>\n            = 3) develop persistent candidemia and who did (\n            <jats:italic>n<\/jats:italic>\n            = 2) or did not (\n            <jats:italic>n<\/jats:italic>\n            = 11) harbor FKS gene mutations were included. A cell-based assay was used to compare differences in macrophage activation among isolates when grown in the presence or absence of subinhibitory concentrations of caspofungin, micafungin, or voriconazole. In the absence of antifungals, macrophage activation was significantly lower for index\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">C. glabrata<\/jats:named-content>\n            isolates obtained from persistent candidemia patients than for those from nonpersistent patients (33% versus 79% increase over negative controls, respectively;\n            <jats:italic>P<\/jats:italic>\n            &lt; 0.01). Growth of isolates possessing wild-type\n            <jats:italic>FKS<\/jats:italic>\n            genes in subinhibitory concentrations of micafungin or caspofungin, but not voriconazole, significantly increased macrophage inflammatory responses compared to untreated controls (1.25- to 2.75-fold increase,\n            <jats:italic>P<\/jats:italic>\n            &lt; 0.01). For isolates harboring the\n            <jats:italic>FKS2<\/jats:italic>\n            hot spot 1 (HS1) S663P mutation, however, a significant increase was observed only with micafungin treatment (1.75-fold increase versus negative control,\n            <jats:italic>P<\/jats:italic>\n            &lt; 0.01). Macrophage activation correlated with the level of unmasking of \u03b2-glucan in the cell wall. The diminished macrophage inflammatory response to isolates that caused persistent candidemia and differential immunopharmacologic activity of echinocandins among\n            <jats:italic>FKS<\/jats:italic>\n            mutants suggest that certain strains of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">C. glabrata<\/jats:named-content>\n            may have a higher propensity for immunoevasion and development of antifungal resistance during treatment.\n          <\/jats:p>","DOI":"10.1128\/aac.00624-15","type":"journal-article","created":{"date-parts":[[2015,6,23]],"date-time":"2015-06-23T01:45:36Z","timestamp":1435023936000},"page":"5405-5412","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":10,"title":["Innate Inflammatory Response and Immunopharmacologic Activity of Micafungin, Caspofungin, and Voriconazole against Wild-Type and\n            <i>FKS<\/i>\n            Mutant Candida glabrata Isolates"],"prefix":"10.1128","volume":"59","author":[{"given":"Nicholas D.","family":"Beyda","sequence":"first","affiliation":[{"name":"Department of Pharmacy Practice and Translational Research, University of Houston College of Pharmacy, Houston, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guangling","family":"Liao","sequence":"additional","affiliation":[{"name":"Department of Pharmacy Practice and Translational Research, University of Houston College of Pharmacy, Houston, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bradley T.","family":"Endres","sequence":"additional","affiliation":[{"name":"Department of Pharmacy Practice and Translational Research, University of Houston College of Pharmacy, Houston, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Russell E.","family":"Lewis","sequence":"additional","affiliation":[{"name":"Department of Medical Sciences and Surgery, University of Bologna, Bologna, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kevin W.","family":"Garey","sequence":"additional","affiliation":[{"name":"Department of Pharmacy Practice and Translational Research, University of Houston College of Pharmacy, Houston, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1086\/596757"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.02408-13"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1000227"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.0020035"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1086\/589304"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.2165\/11585270-000000000-00000"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.00027-12"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1093\/cid\/ciu407"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1004478"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1002863"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.4161\/viru.20746"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1003730"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1345\/aph.1R020"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/jir351"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.00836-10"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri2939"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.diagmicrobio.2011.11.004"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.48.3.815-823.2004"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1097\/INF.0b013e31824ab9b0"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.01486-12"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.38.8.2862-2869.2000"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/44.1.109"}],"container-title":["Antimicrobial 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