Abstract:
:Escherichia coli 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 E. coli K1 neonatal isolates carried clbA and clbP, genes contained within the pks 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 clbA and clbP in E. coli 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 clbA, which encodes a pleiotropic enzyme also involved in siderophore synthesis, impacted virulence to a greater extent than mutation of clbP, 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 E. coli K1 to colonize the neonatal gastrointestinal tract and to cause invasive disease in the susceptible neonate.
journal_name
Infect Immunjournal_title
Infection and immunityauthors
McCarthy AJ,Martin P,Cloup E,Stabler RA,Oswald E,Taylor PWdoi
10.1128/IAI.00716-15subject
Has Abstractpub_date
2015-09-01 00:00:00pages
3704-11issue
9eissn
0019-9567issn
1098-5522pii
IAI.00716-15journal_volume
83pub_type
杂志文章abstract::We identified a T-cell determinant of the 35-kDa antigen of Mycobacterium leprae which is discriminatory against cross-sensitization by its closely related homologue in Mycobacterium avium. From synthetic peptides covering the entire sequence, those with the highest affinity and permissive binding to purified HLA-DR m...
journal_title:Infection and immunity
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journal_title:Infection and immunity
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doi:10.1128/IAI.60.12.5197-5203.1992
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journal_title:Infection and immunity
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doi:10.1128/IAI.21.1.333-336.1978
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journal_title:Infection and immunity
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