{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T02:50:40Z","timestamp":1791341440922,"version":"4.3.1"},"reference-count":35,"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":["Infect Immun"],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>\n            strains expressing the K1 capsule are a major cause of sepsis and meningitis in human neonates. The development of these diseases is dependent on the expression of a range of virulence factors, many of which remain uncharacterized. Here, we show that all but 1 of 34\n            <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n            K1 neonatal isolates carried\n            <jats:italic>clbA<\/jats:italic>\n            and\n            <jats:italic>clbP<\/jats:italic>\n            , genes contained within the\n            <jats:italic>pks<\/jats:italic>\n            pathogenicity island and required for the synthesis of colibactin, a polyketide-peptide genotoxin that causes genomic instability in eukaryotic cells by induction of double-strand breaks in DNA. Inactivation of\n            <jats:italic>clbA<\/jats:italic>\n            and\n            <jats:italic>clbP<\/jats:italic>\n            in\n            <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n            A192PP, a virulent strain of serotype O18:K1 that colonizes the gastrointestinal tract and translocates to the blood compartment with very high frequency in experimental infection of the neonatal rat, significantly reduced the capacity of A192PP to colonize the gut, engender double-strand breaks in DNA, and cause invasive, lethal disease. Mutation of\n            <jats:italic>clbA<\/jats:italic>\n            , which encodes a pleiotropic enzyme also involved in siderophore synthesis, impacted virulence to a greater extent than mutation of\n            <jats:italic>clbP<\/jats:italic>\n            , encoding an enzyme specific to colibactin synthesis. Restoration of colibactin gene function by complementation reestablished the fully virulent phenotype. We conclude that colibactin contributes to the capacity of\n            <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n            K1 to colonize the neonatal gastrointestinal tract and to cause invasive disease in the susceptible neonate.\n          <\/jats:p>","DOI":"10.1128\/iai.00716-15","type":"journal-article","created":{"date-parts":[[2015,7,7]],"date-time":"2015-07-07T02:30:36Z","timestamp":1436236236000},"page":"3704-3711","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":91,"title":["The Genotoxin Colibactin Is a Determinant of Virulence in Escherichia coli K1 Experimental Neonatal Systemic Infection"],"prefix":"10.1128","volume":"83","author":[{"given":"Alex J.","family":"McCarthy","sequence":"first","affiliation":[{"name":"University College London School of Pharmacy, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricia","family":"Martin","sequence":"additional","affiliation":[{"name":"UMR1043 Inserm, Centre de Physiopathologie de Toulouse Purpan (CPTP), Toulouse, France"},{"name":"USC 1360 INRA, Centre de Physiopathologie de Toulouse Purpan (CPTP), Toulouse, France"},{"name":"UMR 5282 CNRS, Centre de Physiopathologie de Toulouse Purpan (CPTP), Toulouse, France"},{"name":"Universit\u00e9 de Toulouse, UPS, Centre de Physiopathologie de Toulouse Purpan (CPTP), Toulouse, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emilie","family":"Cloup","sequence":"additional","affiliation":[{"name":"UMR1043 Inserm, Centre de Physiopathologie de Toulouse Purpan (CPTP), Toulouse, France"},{"name":"USC 1360 INRA, Centre de Physiopathologie de Toulouse Purpan (CPTP), Toulouse, France"},{"name":"UMR 5282 CNRS, Centre de Physiopathologie de Toulouse Purpan (CPTP), Toulouse, France"},{"name":"Universit\u00e9 de 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