bioRxiv Science⌕ Search

Biology subjects

Nougayrede, J.-P.

Publications and source records attributed to Nougayrede, J.-P..

7 recordsLinked to original sources

Bacterial Hsp90 promotes virulence factor production through maintenance of NRPS megaenzymes

Pathogenic bacteria produce virulence factors critical to host infection. Here, we demonstrate the crucial role of the bacterial Hsp90 chaperone in the production of two major virulence factors, the colibactin genotoxin in Escherichia coli and the pyoverdine siderophore in Pseudomonas aeruginosa. Colibactin, a hybrid polyketide/non-ribosomal peptide (PK-NRP), and pyoverdine, a non-ribosomal peptide (NRP), are metabolites produced by complex biosynthetic pathways involving large cytoplasmic enzymes called megasynthases. Using comparative proteomics, we found that megasynthase abundance was markedly reduced in hsp90 deletion mutants of E. coli and P. aeruginosa compared to wild-type strains. This reduction was independent of transcriptional or translational regulation. We further revealed an interplay between Hsp90 and the HslUV protease in controlling megasynthase levels. Remarkably, we found that Hsp90 stabilizes additional NRP and PK-NRP megasynthases, suggesting a general role for Hsp90 as a chaperone of these enzymes. These findings open new avenues for enhancing the biosynthesis of complex metabolites for biotechnological applications through proteostasis modulation, and may also have implications for combating bacterial infections.

microbiology↗

Development of intimin-enriched outer membrane vesicles (OMVs) as a vaccine to control intestinal carriage of Enterohemorrhagic Escherichia coli

Enterohemorrhagic Escherichia coli (EHEC) are foodborne pathogens causing severe human infections including hemorrhagic colitis and hemolytic uremic syndrome (HUS), particularly in children. Ruminants are the main reservoir of EHEC which colonize their intestinal tract through a mechanism involving the bacterial outer membrane adhesin intimin. Vaccination of cattle has shown efficacy in reducing EHEC O157:H7 shedding in feces. However, most of these vaccines are based on purified proteins and/or require the addition of adjuvants, resulting in expensive vaccines that are not used by breeders. This study introduces the development of a new type of vaccine based on Outer Membrane Vesicles (OMVs) carrying the C-terminal domain of intimin (Int280). A vaccine which combines OMVs carrying luminal Int280 and OMVs displaying surface-exposed Int280 was produced using two addressing systems based on PelB peptide signal and Lpp-OmpA hybrid protein, respectively. This mixed vaccine was tested in a mouse model as a proof of concept using the murine host-specific intestinal pathogen Citrobacter rodentium which shares a similar intimin-based adhesion mechanism with EHEC. Vaccination of mice with OMV-Int280 elicited a strong anti-intimin IgG response. Interestingly, we observed a shortened C. rodentium fecal shedding duration in immunized mice compared to the control group. This OMVs-intimin vaccine therefore represents a promising candidate for the control of EHEC intestinal carriage and fecal shedding in ruminants. IMPORTANCEEnterohemorrhagic Escherichia coli (EHEC) are foodborne pathogenic bacteria causing intestinal infection that may lead to hemorrhagic colitis and hemolytic uremic syndrome (HUS) particularly in young children. There is no effective treatment, and antibiotics are contraindicated because they promote the development of HUS. Vaccination of ruminants, the main reservoir of EHEC, has been proposed as an important strategy to reduce the fecal shedding of EHEC to reduce transmission to humans. Outer Membrane Vesicles (OMVs) derived from E. coli are a highly attractive vaccine platform. Here, we produced OMVs enriched with the C-terminal part of the intimin (Int280). As a proof of concept, we used a mice model of Citrobacter rodentium colonization as a surrogate for EHEC intestinal colonization. Vaccination elicited antibodies against intimin and decreased the duration of fecal shedding of C. rodentium. Therefore, this OMV-Int280 vaccine is a promising candidate to control EHEC intestinal carriage and fecal shedding in ruminants.

microbiology↗

HlyF, an underestimated virulence factor of uropathogenic Escherichia coli

Urinary tract infections (UTIs) are predominantly caused by uropathogenic Escherichia coli (UPEC). By analysing a representative collection of UPEC strains from community-acquired infections, we showed that 20 % of these strains had the ability to produce the protein HlyF. These hlyF+ UPEC strains were the most virulent, mostly responsible for pyelonephritis, often with bloodstream infections. Using a mouse model of UTI, we showed that HlyF was associated with the ability of UPEC to develop a urosepsis, with the presence of bacteria in the spleen and an exacerbated inflammatory response. In contrast to archetypical UPEC strains, hlyF+ UPEC strains are not restricted to phylogroup B2 and harbor a specific repertoire of virulence factors reflecting the fact that HlyF is encoded by conjugative ColV-like plasmids. These plasmids also carry antimicrobial resistance genes, which may facilitate their selection and spreading amongst people receiving antimicrobial therapy. Overall, our data suggest that HlyF is a virulence factor in UPEC and spreading of ColV-like plasmids encoding hlyF warrants further investigation.

microbiology↗

Oxygen inhibits colibactin production by Escherichia coli

Up to 25% of the E. coli strains isolated from the feces of healthy humans harbor the pks genomic island encoding the synthesis of colibactin, a genotoxic metabolite. Evidence is accumulating for an etiologic role of colibactin in colorectal cancer. Little is known about the conditions of expression of colibactin in the gut. The intestine is characterized by a unique oxygenation profile, with a steep gradient between the physiological hypoxic epithelial surface and the anaerobic lumen, which favors the dominance of obligate anaerobes. Here, we report that colibactin production is maximal under anoxic conditions and decreases with increased oxygen concentration. We show that the aerobic respiration control (ArcA) positively regulates colibactin production and genotoxicity of pks+ E. coli in response to oxygen availability. Thus, colibactin synthesis is inhibited by oxygen, indicating that the pks biosynthetic pathway is adapted to the anoxic intestinal lumen and to the hypoxic infected or tumor tissue.

microbiology↗

Insights into the acquisition of the pks island and production of colibactin in the Escherichia coli population

The pks island codes for the enzymes necessary for synthesis of the genotoxin colibactin, which contributes to the virulence of Escherichia coli strains and is suspected of promoting colorectal cancer. From a collection of 785 human and bovine E. coli isolates, we identified 109 strains carrying a highly conserved pks island, mostly from the phylogroup B2, but also from phylogroups A, B1 and D. Different scenarios of pks acquisition were deduced from whole genome sequence and phylogenetic analysis. In the main scenario, pks was introduced and stabilized into certain sequence types (ST) of the B2 phylogroup, such as ST73 and ST95, at the asnW tRNA locus located in the vicinity of the yersiniabactin-encoding High Pathogenicity Island (HPI). In a few B2 strains, pks inserted at the asnU or asnV tRNA loci close to the HPI and occasionally was located next to the remnant of an integrative and conjugative element. In a last scenario specific to B1/A strains, pks was acquired, independently of the HPI, at a non-tRNA locus. All the pks-positive strains except 18 produced colibactin. Sixteen strains contained mutations in clbB or clbD, or a fusion of clbJ and clbK and were no longer genotoxic but most of them still produced low amount of potentially active metabolites associated with the pks island. One strain was fully metabolically inactive without pks alteration, but colibactin production was restored by overexpressing the ClbR regulator. In conclusion, the pks island is not restricted to human pathogenic B2 strains and is more widely distributed in the E. coli population, while preserving its functionality. IMPACT STATEMENTColibactin, a genotoxin associated with the carcinogenicity of certain strains of E. coli, is encoded by a pathogenicity island called pks. We took advantage of a large collection of non-clinical E. coli strains originating from human and bovine hosts to explore the distribution, conservation and functionality of the pks island. We found that the pks island was not only present in the phylogroup B2 (and more specifically to certain B2 sublineages), but also in other genetic phylogroups, highlighting its capacity to disseminate though horizontal gene transfer. We identified various genetic pks configurations indicative of an introduction of the pks island into E. coli on multiple independent occasions. Despite the existence of various acquisition scenarios, we found that the pks sequences were highly conserved and pks-carrying strains were overwhelmingly capable of producing colibactin, suggesting that the pks island is under selective pressure, through the production of colibactin or other secondary metabolites. Future implications include the identification of such metabolites and their biological activities that could be advantageous to E. coli and enable its adaptation to various ecological niches. DATA SUMMARYAll sequence data of the 785 E. coli used in this study are freely available from the NCBI BioProject database (https://www.ncbi.nlm.nih.gov/bioproject/) under the accession number PRJDB5579. This database was updated to include the sequence data obtained using ONT MinION for the E. coli reference strain SP15 and for E. coli strains ECSC054, JML285, KS-NP019, NS-NP030 and SI-NP020. The sequence data of E. coli strain UPEC129 obtained using PacBio instrument were deposited in the NCBI BioProject database and are available at https://www.ncbi.nlm.nih.gov/Traces/study/ under the accession number PRJNA669570. Hybrid MinION-Illumina and PacBio-Illumina assemblies are available at the NCBI nucleotide database. The genome sequences of 36 other E. coli reference strains and 7 non-E. coli strains were retrieved from NCBI.

microbiology↗

A toxic friend: Genotoxic and mutagenic activity of the probiotic strain Escherichia coli Nissle 1917

The probiotic Escherichia coli strain Nissle 1917 (DSM 6601, Mutaflor), generally considered as beneficial and safe, has been used for a century to treat various intestinal diseases. However, Nissle 1917 hosts in its genome the pks pathogenicity island that codes for the biosynthesis of the genotoxin colibactin. Colibactin is a potent DNA alkylator, suspected to play a role in colorectal cancer development. We show in this study that Nissle 1917 is functionally capable of producing colibactin and inducing interstrand crosslinks in the genomic DNA of epithelial cells exposed to the probiotic. This toxicity was even exacerbated with lower doses of the probiotic, when the exposed cells started to divide again but exhibited aberrant anaphases and increased gene mutation frequency. DNA damage was confirmed in vivo in mouse models of intestinal colonization, demonstrating that Nissle 1917 produces the genotoxin in the gut lumen. Although it is possible that daily treatment of adult humans with their microbiota does not produce the same effects, administration of Nissle 1917 as a probiotic or as a chassis to deliver therapeutics might exert long term adverse effects and thus should be considered in a risk versus benefit evaluation. ImportanceNissle 1917 is sold as a probiotic and considered safe even though it is known since 2006 that it encodes the genes for colibactin synthesis. Colibactin is a potent genotoxin that is now linked to causative mutations found in human colorectal cancer. Many papers concerning the use of this strain in clinical applications ignore or elude this fact, or misleadingly suggest that Nissle 1917 does not induce DNA damage. Here, we demonstrate that Nissle 1917 produces colibactin in vitro and in vivo and induces mutagenic DNA damage. This is a serious safety concern that must not be ignored, for the interests of patients, the general public, health care professionals and ethical probiotic manufacturers.

microbiology↗

Uropathogenic E. coli induces DNA damage in the bladder

Urinary tract infections (UTIs) are among the most common outpatient infections, with a lifetime incidence of around 60% in women. We analysed urine samples from 223 patients with community-acquired UTIs and report the presence of a metabolite released during the synthesis of colibactin, a bacterial genotoxin, in 50 of the samples examined. Uropathogenic Escherichia coli strains isolated from these patients, as well as the archetypal E. coli strain UTI89, were found to produce colibactin. In a murine model of UTI, the machinery producing colibactin was expressed during the early hours of the infection, when intracellular bacterial communities form. We observed extensive DNA damage both in umbrella and bladder progenitor cells. To the best of our knowledge this is the first report of colibactin production in UTIs in humans and its genotoxicity in bladder cells. This bacterial genotoxin, which is increasingly suspected to promote colorectal cancer, should also be scrutinised in the context of bladder cancer.

microbiology↗