{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:02:04Z","timestamp":1791331324034,"version":"4.3.1"},"reference-count":15,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2004,7,1]],"date-time":"2004-07-01T00:00:00Z","timestamp":1088640000000},"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":[[2004,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The Ami-AliA\/AliB oligopeptide permease is an ATP-binding cassette transporter which is found in\n            <jats:italic>Streptococcus pneumoniae<\/jats:italic>\n            and which is involved in nutrient uptake. We investigated the role of the three paralogous oligopeptide-binding lipoproteins AmiA, AliA, and AliB by using murine models of pneumococcal colonization and invasive disease. A series of mutants lacking\n            <jats:italic>aliA<\/jats:italic>\n            ,\n            <jats:italic>aliB<\/jats:italic>\n            , and\n            <jats:italic>amiA<\/jats:italic>\n            either alone or in combination as double or triple mutations were used. Inoculation of the nasopharynx with a mixture of the\n            <jats:italic>obl<\/jats:italic>\n            (oligopeptide-binding lipoprotein-negative) triple-mutant and wild-type (D39) bacteria resulted in significantly smaller numbers of\n            <jats:italic>obl<\/jats:italic>\n            bacteria colonizing the nasopharynx. The use of a mixture of individual mutants and wild-type pneumococci revealed that AmiA, AliA, and AliB were all required for successful colonization of the nasopharynx. The\n            <jats:italic>obl<\/jats:italic>\n            mutant was more attenuated than the\n            <jats:italic>aliB<\/jats:italic>\n            mutant but not the\n            <jats:italic>aliA<\/jats:italic>\n            or\n            <jats:italic>amiA<\/jats:italic>\n            mutant. Therefore, there is some redundancy in the Ami-AliA\/AliB complex in terms of nasopharyngeal colonization, with AliA and AmiA being able to compensate for the removal of AliB. Animals with invasive disease caused by these mutants had survival times, bacterial loads, and inflammatory cytokine production levels similar to those of animals infected with wild-type pneumococci. Our results show that although the Ami-AliA\/AliB complex is not required for virulence during pneumococcal pneumonia, it does play a role in colonization of the nasopharynx.\n          <\/jats:p>","DOI":"10.1128\/iai.72.7.3902-3906.2004","type":"journal-article","created":{"date-parts":[[2004,6,22]],"date-time":"2004-06-22T22:43:13Z","timestamp":1087944193000},"page":"3902-3906","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":75,"title":["The Ami-AliA\/AliB Permease of\n            <i>Streptococcus pneumoniae<\/i>\n            Is Involved in Nasopharyngeal Colonization but Not in Invasive Disease"],"prefix":"10.1128","volume":"72","author":[{"given":"A. R.","family":"Kerr","sequence":"first","affiliation":[{"name":"Division of Infection and Immunity, IBLS, University of Glasgow, Glasgow, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. V.","family":"Adrian","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Erasmus MC-Sophia, Rotterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Esteva\u0303o","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Erasmus MC-Sophia, Rotterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"de Groot","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Erasmus MC-Sophia, Rotterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G.","family":"Alloing","sequence":"additional","affiliation":[{"name":"Laboratoire de Microbiologie et Ge\u0301ne\u0301tique Mole\u0301culaires, CNRS-Universite\u0301 Paul Sabatier, Toulouse, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.-P.","family":"Claverys","sequence":"additional","affiliation":[{"name":"Laboratoire de Microbiologie et Ge\u0301ne\u0301tique Mole\u0301culaires, CNRS-Universite\u0301 Paul Sabatier, Toulouse, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. J.","family":"Mitchell","sequence":"additional","affiliation":[{"name":"Division of Infection and Immunity, IBLS, University of Glasgow, Glasgow, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. W. M.","family":"Hermans","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Erasmus MC-Sophia, Rotterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.62.12.5683-5688.1994"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.1994.1472"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.1990.tb00632.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.71.8.4405-4413.2003"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.71.9.4925-4935.2003"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0923-2508(00)00169-8"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.63.7.2493-2498.1995"},{"key":"e_1_3_2_9_2","first-page":"1389","volume":"45","year":"2002","unstructured":"Hava, D. L., and A. Camilli. 2002. 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