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Background Psychological co-morbidities in irritable bowel syndrome (IBS) have been widely recognized, whereas less is known regarding the role of gut microbial and host metabolic changes in clinical and psychological symptoms in IBS. Results A total of 70 diarrhoea-predominant IBS (IBS-D) patients and 46 healthy controls were enrolled in this study. Stool and urine samples were collected from both groups for 16S rRNA gene sequencing and metabolomic analysis. The results showed that fecal microbiota in IBS-D featured depleted Faecalibacterium (adjusted P =  0.034), Eubacterium rectale group (adjusted P =  0.048), Subdoligranulum (adjusted P =  0.041) and increased Prevotella (adjusted P =  0.041). O-ureido-L-serine, 3,4-dihydroxybenzenesulfonic acid and (R)-2-Hydroxyglutarate demonstrated lower urinary concentrations in IBS-D patients. We further built correlation matrices between gut microbe abundance, differentiated metabolite quantities and clinical parameters. Dialister manifested negative association with IBS severity ( r  = − 0.285, P  = 0.017), anxiety ( r  = − 0.347, P  = 0.003) and depression level ( r  = − 0.308, P  = 0.010). Roseburia was negatively associated with IBS severity ( r  = − 0.298, P  = 0.012). Twenty metabolites correlated with anxiety or depression levels, including 3,4-dihydroxymandelaldehyde with SAS ( r  = − 0.383, P  = 0.001), 1-methylxanthine with SDS ( r  = − 0.347, P  = 0.004) and 1D-chiro-inositol with SAS ( r  = − 0.336, P  = 0.005). In analysis of microbe-metabolite relationship, 3,4-dihydroxymandelaldehyde and 1-methylxanthine were negatively correlated with relative abundance of Clostridium sensu stricto . Conclusions Our findings demonstrated altered microbial and metabolomic profiles associated with clinically and psychological symptoms in IBS-D patients, which may provide insights for further investigations.

Autoinducer-2 is a signaling molecule involved in quorum sensing in Escherichia coli . Quorum sensing enables coordinated behavior based on cell density and helps bacteria adapt to their environment. The luxS gene and the lsr locus are involved in the biosynthesis, transport, and intracellular phosphorylation of autoinducer-2. Disruption of autoinducer-2 biosynthesis or transport can reduce biofilm formation, chemotaxis, and the expression of genes relevant for the uropathogenicity of E. coli . Interestingly, most isolates of E. coli phylogroup B2, in which uropathogenic and other extraintestinal pathogenic strains are overrepresented, lack the lsr operon. We show that autoinducer-2-dependent quorum sensing is not fundamentally beneficial for efficient and prolonged urinary bladder colonization. We demonstrate that the lsr -negative asymptomatic bacteriuria isolate 83972 has a higher fitness than its lsr -complemented variant. Using transcriptome analyses, competitive growth assays, and comparisons of selected fitness properties, we show that restoration of the lsr operon in this strain background results in growth retardation, loss of competitiveness, and higher sensitivity to oxidative stress. Our results illustrate that the lack of autoinducer-2-dependent quorum sensing contributes to the well-known fitness and competitiveness of E. coli 83972, on which its effective use for bacterial interference in the urinary bladder relies. It is vital to delve deeper to fully understand the fitness and competitiveness of the ABU strain 83972 if we are to optimize its use in therapeutic colonization. The key is to unravel the underlying molecular mechanisms, thus ensuring the efficacy and safety of this treatment as an alternative to antibiotic therapy.

Chronic bacterial infections on medical devices, including catheter-associated urinary tract infections (CAUTI), are associated with bacterial biofilm communities that are refractory to antibiotic therapy and resistant to host immunity. Previously, we have shown that Pseudomonas aeruginosa can cause CAUTI by forming a device-associated biofilm that is independent of known biofilm exopolysaccharides. Here, we show by RNA-seq that host urine alters the transcriptome of P. aeruginosa by suppressing quorum sensing regulated genes. P. aeruginosa produces acyl homoserine lactones (AHLs) in the presence of urea, but cannot perceive AHLs. Repression of quorum sensing by urine implies that quorum sensing should be dispensable during infection of the urinary tract. Indeed, mutants defective in quorum sensing are able to colonize similarly to wild-type in a murine model of CAUTI. Quorum sensing-regulated processes in clinical isolates are also inhibited by urea. These data show that urea in urine is a natural anti-quorum sensing mechanism in mammals. Pseudomonas aeruginosa can cause chronic infections on medical devices by forming biofilms, a process regulated by quorum sensing (QS). Here, the authors show that P. aeruginosa is unable to perceive QS signals in the presence of either host urine or urea, and clinical isolates are often defective in QS.

Pseudomonas aeruginosa, an opportunistic Gram-negative bacterium, is one of the main sources of infections in healthcare environments, making its detection very important. N-3-oxo-dodecanoyl L-homoserine lactone (3-O-C12-HSL) is a characteristic molecule of quorum sensing—a form of cell-to-cell communication between bacteria—in P. aeruginosa. Its detection can allow the determination of the bacterial population. In this study, the development of the first electrochemical aptasensor for the detection of 3-O-C12-HSL is reported. A carbon-based screen-printed electrode modified with gold nanoparticles proved to be the best platform for the aptasensor. Each step in the fabrication of the aptasensor (i.e., gold nanoparticles’ deposition, aptamer immobilization, incubation with the analyte) was optimized and characterized using cyclic voltammetry, differential pulse voltammetry, and electrochemical impedance spectroscopy. Different redox probes in solution were evaluated, the best results being obtained in the presence of [Fe(CN)6]4−/[Fe(CN)6]3−. The binding affinity of 106.7 nM for the immobilized thiol-terminated aptamer was determined using surface plasmon resonance. The quantification of 3-O-C12-HSL was performed by using the electrochemical signal of the redox probe before and after incubation with the analyte. The aptasensor exhibited a logarithmic range from 0.5 to 30 µM, with a limit of detection of 145 ng mL−1 (0.5 µM). The aptasensor was successfully applied for the analysis of real samples (e.g., spiked urine samples, spiked microbiological growth media, and microbiological cultures).

The fluorescent tag 6-aminoquinolyl- N -hydroxysuccinimidyl carbamate (AQC; AccQ Fluor reagent kit from Waters) is a commercial N-terminal label for proteinogenic amino acids (AAs), designed for reversed-phase separation and quantification of the AA racemates. The applicability of AQC-tagged AAs and AA-type zwitterionic compounds was tested for enantiomer separation on the tert -butyl carbamate modified quinine and quinidine based chiral stationary phases, QN-AX and QD-AX employing polar-organic elution conditions. The investigated test analytes included the enantiomers of the positional isomers of isoleucine (Ile), threonine, homoserine, and 4-hydroxyproline. Furthermore, β-AAs, cyclic, and heterocyclic AAs including trans-2-amino-cyclohexane carboxylic acid and trans-2-aminocyclohexyl sulfonic acid, phenylalanine derivatives substituted with halides with increasing electronegativity and 3,4-dihydroxyphenylalanine, cysteine-related derivatives including homocysteic acid, methionine sulfone, cysteine- S -acetic acid, and cysteine- S -acetamide as well as a small range of aminophosphonic acids were enantioseparated. A mechanistic interaction study of AQC-AAs in comparison with fluoresceine isothiocyanate-labeled AAs was performed. The chiral and chemoselective recognition processes involved in enantiomer separation and retention was systematically discussed. Special emphasis was set on the influential factors exhibited by the chemistry, branching position, and spatial properties of the investigated zwitterionic analytes. The general interest to separate and distinguish between different types of branched-chained AAs and metabolic side products thereof lies in the toxicity of some of these compounds, which makes for instance allo–Ile an attractive candidate in disease-related biomarker research. Figure Separation of the four AQC-tagged isomers of 4-hydroxyproline (trans-D, cis-D, trans-L and cis-L) on the chiral stationary phase QD-AX

Bacterial quorum sensing signal molecules called N-acylhomoserine lactone (AHL) controls the expression of virulence determinants in many Gram-negative bacteria. We determined AHL production in 22 Aeromonas strains isolated from various infected sites from patients (bile, blood, peritoneal fluid, pus, stool and urine). All isolates produced the two principal AHLs, N-butanoylhomoserine lactone (C4-HSL) and N-hexanoyl homoserine lactone (C6-HSL). Ten isolates also produced additional AHLs. This report is the first documentation of Aeromonas sobria producing C6-HSL and two additional AHLs with N-acyl side chain longer than C₆. Our data provides a better understanding of the mechanism(s) of this environmental bacterium emerging as a human pathogen.

Paraoxonase (PON) comprises a trio of mammalian enzymes that have been reported to have a number of roles including the inhibition of bacterial virulence and biofilm formation by microorganisms that quorum sense with acylated homoserine lactones (AHLs). PON have previously been reported to inhibit P. aeruginosa biofilm formation in mammalian airways and skin. An innate immune role for PON in urinary tract infection has not previously been reported. We performed western blots for PON1 in urine from patients with urinary tract infection (UTI), and also tested UTI urine for the presence of AHLs using a cellular reporter system. Urine sample microbiota was assessed through sequencing of the 16S rRNA marker gene. We report here that PON1 was not found in the urine of control subjects, however, in patients with UTI, PON1 was associated with the presence of E. coli in urine. AHLs, but not PON, were found in the bulk urine of those with P. aeruginosa UTI. Microbial consortia of PON positive UTI urine was found to be distinct from PON negative UTI urine; differentially over-represented bacteria in PON positive samples included a number of environmental opportunists. We hypothesize that PON may inhibit the quorum sensing activity of AHLs in UTI, as has previously described in skin and airways. Competing Interest Statement The authors have declared no competing interest.

Paraoxonases are mammalian enzymes that have a number of roles including the inhibition of bacterial virulence and biofilm formation by microorganisms that quorum sense with acylated homoserine lactones. Paraoxonases have previously been reported to inhibit P. aeruginosa biofilm formation in mammalian airways and skin. An innate immune role for paraoxonases in urinary tract infection has not previously been reported. We performed western blots for paraoxonase1 in urine from patients with urinary tract infection; we also tested urinary tract infection urine for the presence of acylated homoserine lactones using a cellular reporter system. We report here that paraoxonase1 was not found with our western blot assay in the urine of normal control patients; in those with urinary tract infection, paraoxonase1 was associated with E. coli UTI. Acylated homoserine lactones, but not paraoxonases, were found in the bulk urine of those with P. aeruginosa urinary tract infection. We hypothesize that paraoxonase may play a similar innate immune role in infected urine as has previously described in skin and airways.