Dissecting the Salmonella response to copper

Espariz, Martín; Checa, Susana K.; Audero, María E. Pérez; Pontel, Lucas B.; Soncini, Fernando C.

doi:10.1099/mic.0.2007/006536-0

Cited by 83 publications

(133 citation statements)

References 36 publications

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“…cholerae was more susceptible to copper in anaerobiosis than in aerobiosis (Table 1 and Fig. 2b), which concurs with previous reports for other bacteria (Espariz et al, 2007;Macomber & Imlay, 2009;Outten et al, 2001). Copper tolerance of V. cholerae strains under different conditions.…”

Section: Resultssupporting

confidence: 82%

“…Under anaerobiosis, when the multicopper oxidases are inactive, E. coli utilizes the CusRSregulated CusCFBA transporter, to expel periplasmic Cu + ions (Outten et al, 2001). In contrast, Salmonella, which contains no CusCFBA orthologues (Espariz et al, 2007), employs the CueR-dependent, copper-binding CueP protein (Osman et al, 2010;Pontel & Soncini, 2009). …”

Section: Introductionmentioning

confidence: 99%

“…In the human digestive tract, copper concentration is not likely to exceed 10 mM (Rensing & Grass, 2003); however, the acidic and anaerobic conditions prevailing there are known enhancers of copper toxicity (Weissman et al, 2000). Thus, intestinal pathogens have evolved systems to manage copper excess and its toxicity to survive these in vivo conditions (Espariz et al, 2007;Rensing & Grass, 2003;Weissman et al, 2000). In enteric Gramnegative bacteria, copper surplus is primarily handled by the cue regulon, which is controlled by the MerR family regulator CueR (Espariz et al, 2007;Outten et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…Thus, intestinal pathogens have evolved systems to manage copper excess and its toxicity to survive these in vivo conditions (Espariz et al, 2007;Rensing & Grass, 2003;Weissman et al, 2000). In enteric Gramnegative bacteria, copper surplus is primarily handled by the cue regulon, which is controlled by the MerR family regulator CueR (Espariz et al, 2007;Outten et al, 2000). CueR activates the expression of copper homeostasis genes, such as those encoding P1B-1-type ATPases, multicopper oxidases and metallochaperones.…”

Section: Introductionmentioning

confidence: 99%

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Periplasmic proteins encoded by VCA0261–0260 and VC2216 genes together with copA and cueR products are required for copper tolerance but not for virulence in Vibrio cholerae

Marrero¹,

Sánchez

González

et al. 2012

Microbiology

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Section: Resultssupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Periplasmic proteins encoded by VCA0261–0260 and VC2216 genes together with copA and cueR products are required for copper tolerance but not for virulence in Vibrio cholerae

Marrero¹,

Sánchez

González

et al. 2012

Microbiology

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“…Bacterial Cu detoxification systems are diverse and are often found in some degree of redundancy, as best exemplified by the dual CueR/CusRS systems in E. coli (51), the CsoR/RicR regulons in Mycobacterium tuberculosis (52,53), and the SctR/GolS systems in S. Typhimurium (54). These redundancies may also be a strategy to fine-tune the response to fluctuating Cu levels in the environment.…”

Section: The Role Of Bacterial Cu and Zn Detoxification Systems In VImentioning

confidence: 99%

The Role of Copper and Zinc Toxicity in Innate Immune Defense against Bacterial Pathogens

Djoko¹,

Ong²,

Walker

et al. 2015

Journal of Biological Chemistry

343

268

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Zinc (Zn) and copper (Cu) are essential for optimal innate immune function, and nutritional deficiency in either metal leads to increased susceptibility to bacterial infection. Recently, the decreased survival of bacterial pathogens with impaired Cu and/or Zn detoxification systems in phagocytes and animal models of infection has been reported. Consequently, a model has emerged in which the host utilizes Cu and/or Zn intoxication to reduce the intracellular survival of pathogens. This review describes and assesses the potential role for Cu and Zn intoxication in innate immune function and their direct bactericidal function.Six first row d-block metal ions, manganese (Mn), iron (Fe), cobalt (Co), nickel (Ni), copper (Cu), and zinc (Zn), are essential micronutrients in living organisms. Investigations and discussions of the roles of these trace metals in biology often relate to their acquisition, storage, and incorporation into enzymes. However, conditions where these metal ions are present in excess or are found in the wrong location, resulting in toxicity, have also been described. Thus, there are also systems that sequester, export, and detoxify excess trace metal ions. Today, the concept of trace metal homeostasis, in which various cellular actions maintain the fine balance between nutrition and toxicity, is well developed.Recently, the concept of "nutritional immunity" has emerged in the context of host defense against pathogens. This envisages a role for mechanisms that protect the host from invading pathogens by restricting their ability to acquire key transition metal ions. One example involves lipocalin, which binds siderophores and thereby prevents Fe acquisition by bacterial pathogens (1). Another is calprotectin, which restricts acquisition of Zn or Mn (2). However, what if the host was able to harness the toxic properties of transition metal ions and use them as bactericides? This review explores the evidence for an antimicrobial role for Cu and Zn in the host defense against bacterial pathogens.

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