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Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
Published on: June 25, 2015
TatC-dependent translocation of pyoverdine is responsible for the microbial growth suppression
Yeji Lee1, Yong-Jae Kim1, Jung-Hoon Lee1
1Department of Biotechnology and Bioinformatics, Korea University, Sejong, 339-700, Republic of Korea.
Abstract:
Infections are often not caused by a colonization of Pseudomonas aeruginosa alone but by a consortium of other bacteria. Little is known about the impact of P. aeruginosa on the growth of other bacteria upon coinfection. Here, cell-ree culture supernatants obtained from P. aeruginosa suppressed the growth of a number of bacterial strains such as Corynebacterium glutamicum, Bacillus subtilis, Staphylococcus aureus, and Agrobacterium tumefaciens, but had little effect on the growth of Escherichia coli and Salmonella Typhimurium. The growth suppression effect was obvious when P. aeruginosa was cultivated in M9 minimal media, and the suppression was not due to pyocyanin, a well-known antimicrobial toxin secreted by P. aeruginosa. By performing transposon mutagenesis, PA5070 encoding TatC was identified, and the culture supernatant of its mutant did not suppress the growth. HPLC analysis of supernatants showed that pyoverdine was a secondary metabolite present in culture supernatants of the wild-type strain, but not in those of the PA5070 mutant. Supplementation of FeCl2 as a source of iron compromised the growth suppression effect of supernatants and also recovered biofilm formation of S. aureus, indicating that pyoverdine-mediated iron acquisition is responsible for the growth suppression. Thus, this study provides the action of TatC-dependent pyoverdine translocation for the growth suppression of other bacteria, and it might aid understanding of the impact of P. aeruginosa in the complex community of bacterial species upon coinfection.
Insights
Pseudomonas aeruginosa coinfections suppress other bacteria by secreting pyoverdine, a molecule that chelates iron. This iron acquisition mechanism, dependent on TatC, impacts bacterial community dynamics during polymicrobial infections.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Infections often involve polymicrobial communities, not single pathogens.
- The impact of Pseudomonas aeruginosa on other bacteria during coinfection is poorly understood.
- Pseudomonas aeruginosa is a common opportunistic pathogen implicated in various infections.
Purpose of the Study:
- To investigate the effect of Pseudomonas aeruginosa on the growth of other bacterial species during coinfection.
- To identify the mechanism by which Pseudomonas aeruginosa suppresses the growth of co-infecting bacteria.
- To elucidate the role of specific molecules and genes in this growth suppression.
Main Methods:
- Preparation and testing of cell-free culture supernatants from Pseudomonas aeruginosa.
- Transposon mutagenesis to identify genes involved in growth suppression.
- High-Performance Liquid Chromatography (HPLC) analysis to detect metabolites.
- Iron supplementation experiments to assess the role of iron acquisition.
Main Results:
- Pseudomonas aeruginosa culture supernatants suppressed the growth of several bacterial strains, including Corynebacterium glutamicum and Staphylococcus aureus, but not Escherichia coli or Salmonella Typhimurium.
- The gene PA5070, encoding TatC, was identified as crucial for this growth suppression.
- Pyoverdine, a siderophore, was identified as the metabolite responsible for growth suppression, mediating iron acquisition.
- Iron supplementation reversed the growth suppression and restored biofilm formation in Staphylococcus aureus.
Conclusions:
- TatC-dependent translocation of pyoverdine by Pseudomonas aeruginosa is responsible for suppressing the growth of other bacteria.
- This mechanism of iron acquisition plays a significant role in shaping bacterial community dynamics during coinfections.
- Understanding this interaction is vital for comprehending the ecological impact of Pseudomonas aeruginosa in polymicrobial environments.
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