Characterization of the ferrous iron uptake system of Escherichia coli

Kammler, M; Schön, Chris‐Carolin; Hantke, Klaus

doi:10.1128/jb.175.19.6212-6219.1993

Cited by 394 publications

(421 citation statements)

References 37 publications

Supporting

Mentioning

404

Contrasting

Unclassified

Order By: Relevance

“…FeoAB is a well-conserved system that is involved in the transport of ferrous iron (Marlovits et al, 2002). Previous studies have shown that FeoB mutants of Escherichia coli (Boyer et al, 2002;Kammler et al, 1993) and Helicobacter pylori (Velayudhan et al, 2000) demonstrate reduced virulence and/or colonization activity, yet in our study the equivalent P. aeruginosa mutants demonstrated normal wild-type virulence in rat chronic lung infections (data not shown).…”

Section: Com)contrasting

confidence: 35%

The sensor kinase PhoQ mediates virulence in Pseudomonas aeruginosa

et al. 2009

View full text Add to dashboard Cite

Pseudomonas aeruginosa is a ubiquitous environmental Gram-negative bacterium that is also a major opportunistic human pathogen in nosocomial infections and cystic fibrosis chronic lung infections. PhoP-PhoQ is a two-component regulatory system that has been identified as essential for virulence and cationic antimicrobial peptide resistance in several other Gram-negative bacteria. This study demonstrated that mutation of phoQ caused reduced twitching motility, biofilm formation and rapid attachment to surfaces, 2.2-fold reduced cytotoxicity to human lung epithelial cells, substantially reduced lettuce leaf virulence, and a major, 10 000-fold reduction in competitiveness in chronic rat lung infections. Microarray analysis revealed that PhoQ controlled the expression of many genes consistent with these phenotypes and with its known role in polymyxin B resistance. It was also demonstrated that PhoQ controls the expression of many genes outside the known PhoP regulon.

show abstract

Section: Com)contrasting

confidence: 35%

The sensor kinase PhoQ mediates virulence in Pseudomonas aeruginosa

et al. 2009

View full text Add to dashboard Cite

show abstract

“…6B). Of note, FNR has been shown to positively regulate transcription of metal transporters, such as nikABCDE nickel transport genes and feoABC iron uptake genes of E. coli (34,73) and feoABC, sitABCD, and fhuA iron uptake genes of Shigella flexneri (10,74). To our knowledge, FNR-mediated regulation of genes involved in zinc acquisition or homeostasis has not previously been demonstrated.…”

Section: Discussionmentioning

confidence: 90%

A Novel Zinc Binding System, ZevAB, Is Critical for Survival of Nontypeable Haemophilus influenzae in a Murine Lung Infection Model

et al. 2011

View full text Add to dashboard Cite

Nontypeable Haemophilus influenzae (NTHI) is a Gram-negative bacterial pathogen that causes upper and lower respiratory infections. Factors required for pulmonary infection by NTHI are not well understood. Previously, using high-throughput insertion tracking by deep sequencing (HITS), putative lung colonization factors were identified. Also, previous research indicates that secreted disulfide-dependent factors are important for virulence of H. influenzae. In the present study, HITS data were compared with an informatics-based list of putative substrates of the periplasmic oxidoreductase DsbA to find and characterize secreted virulence factors. This analysis resulted in identification of the "zinc binding essential for virulence" (zev) locus consisting of zevA (HI1249) and zevB (HI1248). NTHI mutants of zevA and zevB grew normally in rich medium but were defective for colonization in a mouse lung model. Mutants also exhibited severe growth defects in medium containing EDTA and were rescued by supplementation with zinc. Additionally, purified recombinant ZevA was found to bind to zinc with high affinity. Together, these data demonstrate that zevAB is a novel virulence factor important for zinc utilization of H. influenzae under conditions where zinc is limiting. Furthermore, evidence presented here suggests that zinc limitation is likely an important mechanism for host defense against pathogens during lung infection.

show abstract

“…One system for iron uptake present in H. pylori appears to be similar to the ferrous (feo) iron uptake system present in Escherichia coli. The feoAB operon encodes proteins which contribute significantly to the iron supply of E. coli cells under anaerobic conditions [38]. An feoB-like gene (HP0687), coding for a putative cytoplasmic protein with homology to ATPase, was identified in H. pylori, whereas no feoA orthologue seems to be present.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori adherence to gastric epithelial cells: a role for non-adhesin virulence genes

Zhang¹,

Dorrell

Wren

et al. 2002

Journal of Medical Microbiology

View full text Add to dashboard Cite

Helicobacter pylori is a major aetiological agent in gastroduodenal disorders and adherence of the bacteria to the gastric mucosa is one of the initial stages of infection. Although a number of specific adhesins has been identified, other H. pylori virulence factors may play a role in adherence to gastric epithelial cells directly or through interaction with other adhesins. This study assessed the effect of 16 H. pylori virulence factors on the adherence of the bacteria to gastric AGS cells and on gastric epithelial cell cycle distribution. Defined isogenic H. pylori SS1 mutants were used. After coincubation of gastric AGS cells and bacteria, adherence of H. pylori to AGS cells was visualised by immunofluorescence microscopy and quantified by flow cytometry. Cell cycle phase distribution was analysed by flow cytometry with propidium iodide staining. Mutants were tested for their ability to adhere to AGS cells and compared with the wild-type SS1 strain. Mutations in genes in the cag pathogenicity island showed that cagP and cagE mutants adhered less than the wild-type strain to AGS cells, whereas a cagF mutant showed no reduction in adherence. Mutations in genes involved in flagellar biosynthesis showed that the adherence ability of fliQ, f liM and fliS mutants was reduced, but a flhB mutant possessed wild-type levels of adherence. Mutations in genes coding for the urease (ureB) and phospholipase (pldA) enzymes did not affect adherence, but mutation of the tlyA gene encoding an H. pylori haemolysin resulted in a reduced adherence. A fliQ mutant, with reduced adherence to AGS cells, was less able to induce AGS cell apoptosis than SS1. The ability to induce G 0 G 1 cell cycle arrest was also abolished in the fliQ mutant. However, an increased cell number in S phase was observed when AGS cells were exposed to the fliQ mutant compared with SS1, suggesting that unattached bacteria may still be able to stimulate cell proliferation. In addition to known adhesins, other bacterial virulence factors such as CagE, CagP, FliQ, FliM, FliS and TlyA appear to play a role in H. pylori adherence to gastric epithelial cells. Mutations in these genes may affect H. pylori pathogenicity by reducing either the ability of the bacteria to attach to gastric epithelial cells or the intensity of bacteriahost cell interactions.

show abstract

Characterization of the ferrous iron uptake system of Escherichia coli

Cited by 394 publications

References 37 publications

The sensor kinase PhoQ mediates virulence in Pseudomonas aeruginosa

The sensor kinase PhoQ mediates virulence in Pseudomonas aeruginosa

A Novel Zinc Binding System, ZevAB, Is Critical for Survival of Nontypeable Haemophilus influenzae in a Murine Lung Infection Model

Helicobacter pylori adherence to gastric epithelial cells: a role for non-adhesin virulence genes

Contact Info

Product

Resources

About