Differential expression of Bordetella pertussis iron transport system genes during infection.
Temporal expression patterns of the Bordetella pertussis alcaligin, enterobactin and haem iron acquisition systems were examined using alcA-, bfeA- and bhuR-tnpR recombinase fusion strains in a mouse respiratory infection model. The iron systems were differentially expressed in vivo, showing early induction of the alcaligin and enterobactin siderophore systems, and delayed induction of the haem system in a manner consistent with predicted changes in host iron source availability during infection. Previous mixed infection competition studies established the importance of alcaligin and haem utilization for B. pertussis in vivo growth and survival. In this study, the contribution of the enterobactin system to the fitness of B. pertussis was confirmed using wild-type and enterobactin receptor mutant strains in similar competition infection experiments. As a correlate to the in vivo expression studies of B. pertussis iron systems in mice, sera from uninfected and B. pertussis-infected human donors were screened for antibody reactivity with Bordetella iron-repressible cell envelope proteins. Pertussis patient sera recognized multiple iron-repressible proteins including the known outer membrane receptors for alcaligin, enterobactin and haem, supporting the hypothesis that B. pertussis is iron-starved and responds to the presence of diverse iron sources during natural infection.
Department of Microbiology, University of Minnesota Medical School, 925 Mayo Memorial Building, 420 Delaware Street, S.E., Minneapolis, MN 55455-0312, USA.
Timothy J
TJ
Brickman
Tomoko
T
Hanawa
Mark T
MT
Anderson
Ryan J
RJ
Suhadolc
Sandra K
SK
Armstrong
D000293:Adolescent; D000328:Adult; D000818:Animals; D001425:Bacterial Outer Membrane Proteins / Q000235:genetics*; D001426:Bacterial Proteins / Q000235:genetics; D001886:Bordetella pertussis / Q000235:genetics* / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics*; D002648:Child; D003001:Cloning, Molecular; D004758:Enterobactin / Q000378:metabolism; D005260:Female; D015964:Gene Expression Regulation, Bacterial; D005798:Genes, Bacterial; D006418:Heme / Q000378:metabolism; D006801:Humans; D006877:Hydroxamic Acids / Q000378:metabolism; D007501:Iron / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D010957:Plasmids; D016133:Polymerase Chain Reaction; D011401:Promoter Regions, Genetic; D011956:Receptors, Cell Surface / Q000235:genetics*; D017262:Siderophores / Q000378:metabolism; D014917:Whooping Cough / Q000382:microbiology*
D001425:Bacterial Outer Membrane Proteins; D001426:Bacterial Proteins; C431916:BhuR protein, Bordetella pertussis; D002352:Carrier Proteins; D006877:Hydroxamic Acids; D011956:Receptors, Cell Surface; D017262:Siderophores; C092056:alcaligin; C029489:enterobactin receptor; D004758:Enterobactin; D006418:Heme; D007501:Iron