{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T01:28:39Z","timestamp":1790386119626,"version":"4.1.0"},"reference-count":65,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2013,10,1]],"date-time":"2013-10-01T00:00:00Z","timestamp":1380585600000},"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":["Infect Immun"],"published-print":{"date-parts":[[2013,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The arginine deiminase system (ADS) is associated with arginine catabolism and plays a role in virulence of several pathogenic bacteria. In\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Streptococcus pneumoniae<\/jats:named-content>\n            , the ADS genes exist as a locus consisting of\n            <jats:italic>arcABCDT<\/jats:italic>\n            . A recent genome-wide mutagenesis approach revealed that both\n            <jats:italic>arcD<\/jats:italic>\n            and\n            <jats:italic>arcT<\/jats:italic>\n            are potentially essential in a chinchilla otitis media (OM) model. In the present study, we generated \u0394\n            <jats:italic>arcD<\/jats:italic>\n            , \u0394\n            <jats:italic>arcT<\/jats:italic>\n            , and \u0394\n            <jats:italic>arcDT<\/jats:italic>\n            mutants by homologous recombination and evaluated their infectivity. Our results showed that only\n            <jats:italic>arcD<\/jats:italic>\n            , and not\n            <jats:italic>arcT<\/jats:italic>\n            , of an OM isolate is required during chinchilla middle ear infection. Additionally, D39 \u0394\n            <jats:italic>arcD<\/jats:italic>\n            exhibited enhanced nasopharyngeal colonization and was attenuated in both mouse pneumonia and bacteremia models.\n            <jats:italic>In vitro<\/jats:italic>\n            , D39 \u0394\n            <jats:italic>arcD<\/jats:italic>\n            displayed enhanced adherence to A549 epithelial cells and increased phagocytosis by J774A.1 macrophages compared to those with the parental strain. This mutant also exhibited an impaired capsule, as detected using electron microscopy, immunofluorescence, and a capsule assay. We demonstrated that the capsule defect in the D39 \u0394\n            <jats:italic>arcD<\/jats:italic>\n            mutant may not be associated with a deficiency in arginine but rather is likely caused by a loss of interaction between the capsule and the transmembrane protein ArcD.\n          <\/jats:p>","DOI":"10.1128\/iai.00778-13","type":"journal-article","created":{"date-parts":[[2013,8,6]],"date-time":"2013-08-06T05:35:49Z","timestamp":1375767349000},"page":"3903-3911","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":30,"title":["Deletion of\n            <i>arcD<\/i>\n            in Streptococcus pneumoniae D39 Impairs Its Capsule and Attenuates Virulence"],"prefix":"10.1128","volume":"81","author":[{"given":"Radha","family":"Gupta","sequence":"first","affiliation":[{"name":"Center for Immunology and Microbial Disease, Albany Medical College, Albany, New York, 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