Iron acquisition by Pseudomonas aeruginosa in the lungs of patients with cystic fibrosis

Lamont, Iain L.; Konings, Anna F.; Reid, David W.

doi:10.1007/s10534-008-9197-9

Cited by 69 publications

(71 citation statements)

References 86 publications

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“…For example, Pseudomonas siderophores have been detected in the sputum of infected cystic fibrosis patients. In addition, mutations in the siderophore receptor LbtU in Legionella and the Ybt siderophore system of Y. pestis cause a significant loss of virulence during pneumonic infections (17,28,51). Thus, it would appear that in Y. pestis, ferric iron transport via the Ybt system plays a more important role than ferrous iron transport in a pneumonic mouse model of plague.…”

Section: Discussionmentioning

confidence: 99%

The Yfe and Feo Transporters Are Involved in Microaerobic Growth and Virulence of Yersinia pestis in Bubonic Plague

et al. 2012

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The Yfe/Sit and Feo transport systems are important for the growth of a variety of bacteria. In Yersinia pestis, single mutations in either yfe or feo result in reduced growth under static (limited aeration), iron-chelated conditions, while a yfe feo double mutant has a more severe growth defect. These growth defects were not observed when bacteria were grown under aerobic conditions or in strains capable of producing the siderophore yersiniabactin (Ybt) and the putative ferrous transporter FetMP. Both fetP and a downstream locus (flp for fet linked phenotype) were required for growth of a yfe feo ybt mutant under static, ironlimiting conditions. An feoB mutation alone had no effect on the virulence of Y. pestis in either bubonic or pneumonic plague models. An feo yfe double mutant was still fully virulent in a pneumonic plague model but had an ϳ90-fold increase in the 50% lethal dose (LD 50 ) relative to the Yfe ؉ Feo ؉ parent strain in a bubonic plague model. Thus, Yfe and Feo, in addition to Ybt, play an important role in the progression of bubonic plague. Finally, we examined the factors affecting the expression of the feo operon in Y. pestis. Under static growth conditions, the Y. pestis feo::lacZ fusion was repressed by iron in a Fur-dependent manner but not in cells grown aerobically. Mutations in feoC, fnr, arcA, oxyR, or rstAB had no significant effect on transcription of the Y. pestis feo promoter. Thus, the factor(s) that prevents repression by Fur under aerobic growth conditions remains to be identified.

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Section: Discussionmentioning

confidence: 99%

The Yfe and Feo Transporters Are Involved in Microaerobic Growth and Virulence of Yersinia pestis in Bubonic Plague

et al. 2012

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“…In two separate studies of chronic isolates from CF patients, P. aeruginosa lost the ability to make pyoverdine, but retained the ability to take up ferripyoverdine (De Vos et al, 2001;Smith et al, 2006). A review by Lamont et al (2009) describes the multifaceted and adaptive nature of iron acquisition by P. aeruginosa in the CF lung. More recently, Martin et al (2011) showed that although pyoverdine was detectable in most P. aeruginosa infected CF sputa, some sputa were pyoverdine-negative (Martin et al, 2011).…”

Section: Pathogen Interactions and Competition For Iron In Cfmentioning

confidence: 99%

Iron acquisition in the cystic fibrosis lung and potential for novel therapeutic strategies

Tyrrell¹,

Callaghan²

2016

Microbiology

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Iron acquisition is vital to microbial survival and is implicated in the virulence of many of the pathogens that reside in the cystic fibrosis (CF) lung. The multifaceted nature of iron acquisition by both bacterial and fungal pathogens encompasses a range of conserved and speciesspecific mechanisms, including secretion of iron-binding siderophores, utilization of siderophores from other species, release of iron from host iron-binding proteins and haemoproteins, and ferrous iron uptake. Pathogens adapt and deploy specific systems depending on iron availability, bioavailability of the iron pool, stage of infection and presence of competing pathogens. Understanding the dynamics of pathogen iron acquisition has the potential to unveil new avenues for therapeutic intervention to treat both acute and chronic CF infections. Here, we examine the range of strategies utilized by the primary CF pathogens to acquire iron and discuss the different approaches to targeting iron acquisition systems as an antimicrobial strategy.

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“…Haem is an uncommon iron source in the natural environment and P. aeruginosa must also be capable of scavenging nonhaem iron, which under aerobic conditions is most probably present in the poorly soluble ferric (Fe 3+ ) form. P. aeruginosa (and other bacteria and fungi) therefore produces high-affinity iron chelating siderophores [53]. Siderophores are secreted by P. aeruginosa into the local environment to chelate free iron and ''strip'' iron from host iron-binding proteins.…”

Section: The Susceptibility Of the Cf Airway To Infectionmentioning

confidence: 99%

“…Pyochelin is considered a secondary siderophore in P. aeruginosa, having a much lower iron binding affinity than pyoverdine [52,53]. Pyochelin appears to have less influence on the biofilm forming capacity of P. aeruginosa than pyoverdine, and its importance for iron acquisition during clinical airway infections is unclear [36,53].…”

Section: The Susceptibility Of the Cf Airway To Infectionmentioning

confidence: 99%

“…Pyochelin appears to have less influence on the biofilm forming capacity of P. aeruginosa than pyoverdine, and its importance for iron acquisition during clinical airway infections is unclear [36,53]. In addition to acquiring iron using autologous siderophores, P. aeruginosa has a high capacity to take up iron-laden siderophores produced by other bacteria and fungi [52].…”

Section: The Susceptibility Of the Cf Airway To Infectionmentioning

confidence: 99%

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Targeting iron uptake to controlPseudomonas aeruginosainfections in cystic fibrosis

et al. 2012

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The aerobic Gram-negative bacterium Pseudomonas aeruginosa is an opportunistic pathogen responsible for life-threatening acute and chronic infections in humans. As part of chronic infection P. aeruginosa forms biofilms, which shield the encased bacteria from host immune clearance and provide an impermeable and protective barrier against currently available antimicrobial agents.P. aeruginosa has an absolute requirement for iron for infection success. By influencing cell-cell communication (quorum sensing) and virulence factor expression, iron is a powerful regulator of P. aeruginosa behaviour. Consequently, the imposed perturbation of iron acquisition systems has been proposed as a novel therapeutic approach to the treatment of P. aeruginosa biofilm infection.In this review, we explore the influence of iron availability on P. aeruginosa infection in the lungs of the people with the autosomal recessive condition cystic fibrosis as an archetypal model of chronic P. aeruginosa biofilm infection. Novel therapeutics aimed at disrupting P. aeruginosa are discussed, with an emphasis placed on identifying the barriers that need to be overcome in order to translate these promising in vitro agents into effective therapies in human pulmonary infections. @ERSpublications Can targeting iron uptake be utilised to control Pseudomonas aeruginosa infections in cystic fibrosis patients?

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Iron acquisition by Pseudomonas aeruginosa in the lungs of patients with cystic fibrosis

Cited by 69 publications

References 86 publications

The Yfe and Feo Transporters Are Involved in Microaerobic Growth and Virulence of Yersinia pestis in Bubonic Plague

The Yfe and Feo Transporters Are Involved in Microaerobic Growth and Virulence of Yersinia pestis in Bubonic Plague

Iron acquisition in the cystic fibrosis lung and potential for novel therapeutic strategies

Targeting iron uptake to controlPseudomonas aeruginosainfections in cystic fibrosis

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