{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T09:33:33Z","timestamp":1791192813259,"version":"4.1.0"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2013,2,1]],"date-time":"2013-02-01T00:00:00Z","timestamp":1359676800000},"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":[[2013,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\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 pneumococcus) is a major human pathogen that is carried asymptomatically in the nasopharynx by up to 70% of the human population. Translocation of the bacteria into internal sites can cause a range of diseases, such as pneumonia, otitis media, meningitis, and bacteremia. This transition from nasopharynx to growth at systemic sites means that the pneumococcus needs to adjust to a variety of environmental conditions, including transition metal ion availability. Although it is an important nutrient, iron potentiates oxidative stress, and it is established that in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. pneumoniae<\/jats:named-content>\n            , expression of iron transport systems and proteins that protect against oxidative stress are regulated by an orphan response regulator, RitR. In this study, we investigated the effect of iron and manganese ion availability on the growth of a\n            <jats:italic>ritR<\/jats:italic>\n            mutant. Deletion of\n            <jats:italic>ritR<\/jats:italic>\n            led to impaired growth of bacteria in high-iron medium, but this phenotype could be suppressed with the addition of manganese. Measurement of metal ion accumulation indicated that manganese prevents iron accumulation. Furthermore, the addition of manganese also led to a reduction in the amount of hydrogen peroxide produced by bacterial cells. Studies of virulence in a murine model of infection indicated that RitR was not essential for pneumococcal survival and suggested that derepression of iron uptake systems may enhance the survival of pneumococci in some niches.\n          <\/jats:p>","DOI":"10.1128\/iai.00805-12","type":"journal-article","created":{"date-parts":[[2012,11,27]],"date-time":"2012-11-27T05:57:04Z","timestamp":1353995824000},"page":"421-429","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":38,"title":["Interplay between Manganese and Iron in Pneumococcal Pathogenesis: Role of the Orphan Response Regulator RitR"],"prefix":"10.1128","volume":"81","author":[{"given":"Cheryl-Lynn Y.","family":"Ong","sequence":"first","affiliation":[{"name":"School of Chemistry and Molecular Biosciences and Australian Infectious Diseases Research Centre, University of Queensland, Brisbane, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam J.","family":"Potter","sequence":"additional","affiliation":[{"name":"Research Centre for Infectious Diseases, School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia","family":"Trappetti","sequence":"additional","affiliation":[{"name":"Research Centre for Infectious Diseases, School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark J.","family":"Walker","sequence":"additional","affiliation":[{"name":"School of Chemistry and Molecular Biosciences and Australian Infectious Diseases Research Centre, University of Queensland, Brisbane, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael P.","family":"Jennings","sequence":"additional","affiliation":[{"name":"Institute for Glycomics, Griffith University, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James C.","family":"Paton","sequence":"additional","affiliation":[{"name":"Research Centre for Infectious Diseases, School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alastair G.","family":"McEwan","sequence":"additional","affiliation":[{"name":"School of Chemistry and Molecular Biosciences and Australian Infectious Diseases Research Centre, University of Queensland, Brisbane, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"89","article-title":"Pneumococcal disease in Australia","volume":"24","author":"Forrest JM","year":"2000","unstructured":"ForrestJMMcIntyrePBBurgessMA. 2000. 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