Linked Life Data

16495546

Source:http://linkedlifedata.com/resource/pubmed/id/16495546

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-2-23
pubmed:abstractText
Bordetella pertussis, the causative agent of whooping cough or pertussis, is an obligate human pathogen with multiple high-affinity iron transport systems. Maximal expression of the dedicated heme utilization functions encoded by the hurIR bhuRSTUV genes requires an iron starvation signal to relieve Fur repression at the hurIR promoter-operator and an inducing signal supplied by heme for HurI-mediated transcriptional activation at the bhuRSTUV promoter. The BhuR outer membrane receptor protein is required for heme uptake and for heme sensing for induction of bhuRSTUV transcription. It was hypothesized that heme utilization contributed to the success of B. pertussis as a pathogen. In this study, virulence attenuation resulting from inactivation of the B. pertussis heme system was assessed using mixed infection competition experiments in a mouse model. As a measure of in vivo fitness, the ability of a B. pertussis heme utilization mutant to colonize and persist was determined relative to that of an isogenic coinfecting wild-type strain. Relative fitness of the mutant strain declined significantly after 7 days postinfection and continued to decline throughout the remainder of the 28-day infection time course. In parallel infections using inocula supplemented with an inducing 2 microM concentration of hemin chloride, hemin coadministration augmented the competitive advantage of the wild-type strain over the mutant. The results confirm that heme utilization contributes to the pathogenesis of B. pertussis in the mouse infection model and indicate that heme utilization may be most important for adaptation to host conditions existing during the later stages of infection.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-11092824, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-11418569, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-11755424, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-12533466, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-13481312, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-14761988, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-15667299, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-2883655, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-6292105, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-7298186, http://linkedlifedata.com/resource/pubmed/commentcorrection/16495546-8550442
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0019-9567
pubmed:author
pubmed:issnType
Print
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1741-4
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Heme transport contributes to in vivo fitness of Bordetella pertussis during primary infection in mice.
pubmed:affiliation
Department of Microbiology, University of Minnesota, MMC 196, 420 Delaware Street S.E., Minneapolis, MN 55455-0312, USA. brick011@umn.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural