Lipopolysaccharide as Shield and Receptor for R-Pyocin-Mediated Killing in
            <i>Pseudomonas aeruginosa</i>

Köhler, Thilo; Donner, Viviane; Delden, Christian van

doi:10.1128/jb.01459-09

Cited by 117 publications

(202 citation statements)

References 27 publications

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“…akhurstii RM1 displayed low sensitivity. These findings show that xenorhabdicin activity is not dictated by bacterial or nematode phylogeny and suggest that sensitivity to xenorhabdicin is determined by structural components of the LPS receptor molecule (18). If this were the case, then the structure of LPS of sensitive strains would be predicted to be similar, while the LPS structure of less sensitive strains would be more divergent.…”

Section: Discussionmentioning

confidence: 86%

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The xnp1 P2-Like Tail Synthesis Gene Cluster Encodes Xenorhabdicin and Is Required for Interspecies Competition

Morales-Soto

Forst

2011

J Bacteriol

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Xenorhabdus nematophila, the mutualistic bacterium of the nematode Steinernema carpocapsae, produces the R-type bacteriocin called xenorhabdicin, which is thought to confer a competitive advantage for growth in the insect host. We have identified a P2-like tail synthesis gene cluster (xnp1) that is required for xenorhabdicin production. The xnp1 genes were expressed constitutively during growth and were induced by mitomycin C. Deletion of either the sheath (xnpS1) or fiber (xnpH1) genes eliminated xenorhabdicin production. Production of R-type bacteriocins in a host organism had not been shown previously. We show that xenorhabdicin is produced in the hemocoel of insects infected with the wild type but not with the ⌬xnpS1 deletion strain. Xenorhabdicin prepared from the wild-type strain killed the potential competitor Photorhabdus luminescens TT01. P. luminescens was eliminated during coculture with wild-type X. nematophila but not with the ⌬xnpS1 strain. Furthermore, P. luminescens inhibited reproduction of S. carpocapsae in insect larvae, while coinjection with wild-type X. nematophila, but not the ⌬xnpS1, strain restored normal reproduction, demonstrating that xenorhabdicin was required for killing P. luminescens and protecting the nematode partner. Xenorhabdicin killed X. nematophila from Steinernema anatoliense, demonstrating for the first time that it possesses intraspecies activity. In addition, activity was variable against diverse strains of Xenorhabdus and Photorhabdus and was not correlated with phylogenetic distance. These findings are discussed in the context of the role of xenorhabdicin in the life cycle of the mutualistic bacterium X. nematophila.

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Section: Discussionmentioning

confidence: 86%

“…They are composed of an outer sheath, an inner tube, and associated tail fibers. R-type pyocins bind via tail fibers to lipopolysaccharide (LPS) receptors on the surface of sensitive bacteria (18,24,27,40). It has been shown that recombination of tail fiber proteins broadens R-type bacteriocin specificity (24).…”

mentioning

confidence: 99%

The xnp1 P2-Like Tail Synthesis Gene Cluster Encodes Xenorhabdicin and Is Required for Interspecies Competition

Morales-Soto

Forst

2011

J Bacteriol

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“…LPS has been linked to antibiotic resistance and immune evasion. Furthermore, LPS is one of the receptors that determines the susceptibility of the bacterium to bacteriophages and pyocins (2)(3)(4). Our ability to control P. aeruginosa infections depends on the availability of accurate typing methods.…”

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confidence: 99%

Application of Whole-Genome Sequencing Data for O-Specific Antigen Analysis and In Silico Serotyping of Pseudomonas aeruginosa Isolates

et al. 2016

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Accurate typing methods are required for efficient infection control. The emergence of whole-genome sequencing (WGS) technologies has enabled the development of genome-based methods applicable for routine typing and surveillance of bacterial pathogens. In this study, we developed the Pseudomonas aeruginosa serotyper (PAst) program, which enabled in silico serotyping of P. aeruginosa isolates using WGS data. PAst has been made publically available as a web service and aptly facilitates highthroughput serotyping analysis. The program overcomes critical issues such as the loss of in vitro typeability often associated with P. aeruginosa isolates from chronic infections and quickly determines the serogroup of an isolate based on the sequence of the O-specific antigen (OSA) gene cluster. Here, PAst analysis of 1,649 genomes resulted in successful serogroup assignments in 99.27% of the cases. This frequency is rarely achievable by conventional serotyping methods. The limited number of nontypeable isolates found using PAst was the result of either a complete absence of OSA genes in the genomes or the artifact of genomic misassembly. With PAst, P. aeruginosa serotype data can be obtained from WGS information alone. PAst is a highly efficient alternative to conventional serotyping methods in relation to outbreak surveillance of serotype O12 and other high-risk clones, while maintaining backward compatibility to historical serotype data. Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen and a major cause of mortality and morbidity among hospitalized and compromised patients, including those with cystic fibrosis (CF). P. aeruginosa is well known for its ability to cause chronic and extensively drug-resistant infections (1). The outer membrane lipopolysaccharide (LPS) layer is a major virulence factor of P. aeruginosa (2). LPS has been linked to antibiotic resistance and immune evasion. Furthermore, LPS is one of the receptors that determines the susceptibility of the bacterium to bacteriophages and pyocins (2-4). Our ability to control P. aeruginosa infections depends on the availability of accurate typing methods. Previously, serotyping was a benchmark typing method for P. aeruginosa. In the 1980s, the International Antigenic Typing Scheme (IATS) was established to classify the species P. aeruginosa into 20 serotypes (O1 to O20) (5-7). Today, serotyping is infrequently used in the clinic for typing purposes, mainly because of the time-consuming protocol, the need for a continuous supply of serotype-specific antisera, and a high prevalence of polyagglutinating or nontypeable isolates.The loss of P. aeruginosa typeability has been known for decades and has often been linked to bacteria isolated from chronic infections, where typeability is lost over time during the course of infection (8, 9). A study performed by Pirnay et al. (10) showed that 65% of all P. aeruginosa isolates examined were either non-or multitypeable and therefore assigning a particular serotype to these strains would be difficult. The occur...

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“…The soluble S-type is similar to colicins of E. coli and is composed of killing and immunity genes. While the R and F type are phage-derived and have different killing and resistance mechanisms, where both consist of only a killing component with no specified immunity that neutralizes the toxin but instead resist via alteration or absence of cell-surface receptors [2,[9][10][11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

“…However, in natural populations of bacteria like P. aeruginosa one strain usually carries and releases multiple types of bacteriocins known as pyocins, which have a diversity of killing and resistance mechanisms in addition to the toxinantitoxin systems [2,7]. For example, three pyocin types exist (S, R and F), with each of these having multiple subtypes with varying toxicity levels [2,[7][8][9][10]. The soluble S-type is similar to colicins of E. coli and is composed of killing and immunity genes.…”

Section: Introductionmentioning

confidence: 99%

Bacteriocin-mediated competition in cystic fibrosis lung infections

et al. 2015

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Bacteriocins are toxins produced by bacteria to kill competitors of the same species. Theory and laboratory experiments suggest that bacteriocin production and immunity play a key role in the competitive dynamics of bacterial strains. The extent to which this is the case in natural populations, especially human pathogens, remains to be tested. We examined the role of bacteriocins in competition using Pseudomonas aeruginosa strains infecting lungs of humans with cystic fibrosis (CF). We assessed the ability of different strains to kill each other using phenotypic assays, and sequenced their genomes to determine what bacteriocins ( pyocins) they carry. We found that (i) isolates from later infection stages inhibited earlier infecting strains less, but were more inhibited by pyocins produced by earlier infecting strains and carried fewer pyocin types; (ii) this difference between early and late infections appears to be caused by a difference in pyocin diversity between competing genotypes and not by loss of pyocin genes within a lineage over time; (iii) pyocin inhibition does not explain why certain strains outcompete others within lung infections; (iv) strains frequently carry the pyocin-killing gene, but not the immunity gene, suggesting resistance occurs via other unknown mechanisms. Our results show that, in contrast to patterns observed in experimental studies, pyocin production does not appear to have a major influence on strain competition during CF lung infections.

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Lipopolysaccharide as Shield and Receptor for R-Pyocin-Mediated Killing in Pseudomonas aeruginosa

Cited by 117 publications

References 27 publications

The xnp1 P2-Like Tail Synthesis Gene Cluster Encodes Xenorhabdicin and Is Required for Interspecies Competition

The xnp1 P2-Like Tail Synthesis Gene Cluster Encodes Xenorhabdicin and Is Required for Interspecies Competition

Application of Whole-Genome Sequencing Data for O-Specific Antigen Analysis and In Silico Serotyping of Pseudomonas aeruginosa Isolates

Bacteriocin-mediated competition in cystic fibrosis lung infections

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