Molecules Autoinducer 2 and cjA and Their Impact on Gene Expression in Campylobacter jejuni

2018 ◽  
Vol 28 (5) ◽  
pp. 207-215 ◽  
Author(s):  
Martin Teren ◽  
Hana Turonova Michova ◽  
Lucie Vondrakova ◽  
Katerina Demnerova

Quorum sensing is a widespread form of cell-to-cell communication, which is based on the production of signaling molecules known as autoinducers (AIs). The first group contains highly species-specific N-acyl homoserine lactones (N-AHLs), generally known as AI-1, which are produced by AHL synthase. The second group, possessing the characteristic structure of a furanone ring, are known as AI-2. The enzyme responsible for their production is S-ribosylhomocysteine lyase (LuxS). In <i>Campylobacter jejuni</i>, AI-2 and LuxS play a role in many important processes, including biofilm formation, stress response, motility, expression of virulence factors, and colonization. However, neither the receptor protein nor the exact structure of the AI-2 molecule have been identified to date. Similarly, little is known about the possible existence of AHL-synthase producing AI-1 and its impact on gene expression. Recently, an analogue of homoserine lactone, called cjA, was isolated from a cell-free supernatant of <i>C. jejuni</i> strain<i></i> 81–176 and from the food isolate c11. The molecule cjA particularly impacted the expression of virulence factors and biofilm formation. This review summarizes the role of AI-2 and cjA in the context of biofilm formation, motility, stress responses, and expression of virulence factors.

2020 ◽  
Vol 26 ◽  
Author(s):  
Madison Tonkin ◽  
Shama Khan ◽  
Mohmmad Younus Wani ◽  
Aijaz Ahmad

: Quorum sensing is defined as cell to cell communication between microorganisms, which enables microorganisms to behave as multicellular organisms. Quorum sensing enables many collaborative benefits such as synchronisation of virulence factors and biofilm formation. Both quorum sensing as well as biofilm formation encourage the development of drug resistance in microorganisms. Biofilm formation and quorum sensing are causally linked to each other and play role in the pathogenesis of microorganisms. With the increasing drug resistance against the available antibiotics and antifungal medications, scientists are combining different options to develop new strategies. Such strategies rely on the inhibition of the communication and virulence factors rather than on killing or inhibiting the growth of the microorganisms. This review encompasses the communication technique used by microorganisms, how microorganism resistance is linked to quorum sensing and various chemical strategies to combat quorum sensing and thereby drug resistance. Several compounds have been identified as quorum sensing inhibitors and are known to be effective in reducing resistance as they do not kill the pathogens but rather disrupt their communication. Natural compounds have been identified as anti-quorum sensing agents. However, natural compounds present several related disadvantages. Therefore, the need for the development of synthetic or semi-synthetic compounds has arisen. This review argues that anti-quorum sensing compounds are effective in disrupting quorum sensing and could therefore be effective in reducing microorganism drug resistance.


2013 ◽  
Vol 825 ◽  
pp. 107-110
Author(s):  
Sören Bellenberg ◽  
Robert Barthen ◽  
Mario Vera ◽  
Nicolas Guiliani ◽  
Wolfgang Sand

A functional luxIR-type Quorum Sensing (QS) system is present in Acidithiobacillus ferrooxidans. However, cell-cell communication among various acidophilic chemolithoautotrophs growing on pyrite has not been studied in detail. These aspects are the scope of this study with emphasis on the effects exerted by the N-acyl-homoserine lactone (AHL) type signaling molecules which are produced by Acidithiobacillus ferrooxidans. Their effects on attachment and leaching efficiency by other leaching bacteria, such as Acidithiobacillus ferrivorans, Acidiferrobacter spp. SPIII/3 and Leptospirillum ferrooxidans in pure and mixed cultures growing on pyrite is shown.


Marine Drugs ◽  
2019 ◽  
Vol 17 (9) ◽  
pp. 499 ◽  
Author(s):  
Bao Zhang ◽  
Xiyi Zhuang ◽  
Liyun Guo ◽  
Robert J. C. McLean ◽  
Weihua Chu

Quorum quenching (QQ) is a promising alternative infection-control strategy to antibiotics that controls quorum-regulated virulence without killing the pathogens. Aeromonas hydrophila is an opportunistic gram-negative pathogen living in freshwater and marine environments. A. hydrophila possesses an N-acyl homoserine lactone (AHL)-based quorum-sensing (QS) system that regulates virulence, so quorum signal-inactivation (i.e., QQ) may represent a new way to combat A. hydrophila infection. In this study, an AHL lactonase gene, aiiA was cloned from Bacillus sp. strain QSI-1 and expressed in Escherichia coli strain BL21(DE3). The A. hydrophila hexanoyl homoserine lactone (C6-HSL) QS signal molecule was degraded by AiiAQSI-1, which resulted in a decrease of bacterial swimming motility, reduction of extracellular protease and hemolysin virulence factors, and inhibited the biofilm formation of A. hydrophila YJ-1 in a microtiter assay. In cell culture studies, AiiAQSI-1 decreased the ability of A. hydrophila adherence to and internalization by Epithelioma papulosum cyprini (EPC) cells. During in vivo studies, oral administration of AiiAQSI-1 via feed supplementation attenuated A. hydrophila infection in Crucian Carp. Results from this work indicate that feed supplementation with AiiAQSI-1 protein has potential to control A. hydrophila aquaculture disease via QQ.


2004 ◽  
Vol 15 (5) ◽  
pp. 2361-2374 ◽  
Author(s):  
John Isaac Murray ◽  
Michael L. Whitfield ◽  
Nathan D. Trinklein ◽  
Richard M. Myers ◽  
Patrick O. Brown ◽  
...  

We used cDNA microarrays in a systematic study of the gene expression responses of HeLa cells and primary human lung fibroblasts to heat shock, endoplasmic reticulum stress, oxidative stress, and crowding. Hierarchical clustering of the data revealed groups of genes with coherent biological themes, including genes that responded to specific stresses and others that responded to multiple types of stress. Fewer genes increased in expression after multiple stresses than in free-living yeasts, which have a large general stress response program. Most of the genes induced by multiple diverse stresses are involved in cell-cell communication and other processes specific to higher organisms. We found substantial differences between the stress responses of HeLa cells and primary fibroblasts. For example, many genes were induced by oxidative stress and dithiothreitol in fibroblasts but not HeLa cells; conversely, a group of transcription factors, including c-fos and c-jun, were induced by heat shock in HeLa cells but not in fibroblasts. The dataset is freely available for search and download at http://microarray-pubs.stanford.edu/human_stress/Home.shtml .


2007 ◽  
Vol 73 (10) ◽  
pp. 3183-3188 ◽  
Author(s):  
Takenori Ishida ◽  
Tsukasa Ikeda ◽  
Noboru Takiguchi ◽  
Akio Kuroda ◽  
Hisao Ohtake ◽  
...  

ABSTRACT N-Octanoyl cyclopentylamide (C8-CPA) was found to moderately inhibit quorum sensing in Pseudomonas aeruginosa PAO1. To obtain more powerful inhibitors, a series of structural analogs of C8-CPA were synthesized and examined for their ability to inhibit quorum sensing in P. aeruginosa PAO1. The lasB-lacZ and rhlA-lacZ reporter assays revealed that the chain length and the ring structure were critical for C8-CPA analogs to inhibit quorum sensing. N-Decanoyl cyclopentylamide (C10-CPA) was found to be the strongest inhibitor, and its concentrations required for half-maximal inhibition for lasB-lacZ and rhlA-lacZ expression were 80 and 90 μM, respectively. C10-CPA also inhibited production of virulence factors, including elastase, pyocyanin, and rhamnolipid, and biofilm formation without affecting growth of P. aeruginosa PAO1. C10-CPA inhibited induction of both lasI-lacZ by N-(3-oxododecanoyl)-l-homoserine lactone (PAI1) and rhlA-lacZ by N-butanoyl-l-homoserine lactone (PAI2) in the lasI rhlI mutant of P. aeruginosa PAO1, indicating that C10-CPA interferes with the las and rhl quorum-sensing systems via inhibiting interaction between their response regulators (LasR and RhlR) and autoinducers.


2007 ◽  
Vol 189 (8) ◽  
pp. 3051-3062 ◽  
Author(s):  
Xue-Song Zhang ◽  
Rodolfo García-Contreras ◽  
Thomas K. Wood

ABSTRACT DNA microarrays revealed that expression of ycfR, which encodes a putative outer membrane protein, is significantly induced in Escherichia coli biofilms and is also induced by several stress conditions. We show that deletion of ycfR increased biofilm formation fivefold in the presence of glucose; the glucose effect was corroborated by showing binding of the cyclic AMP receptor protein to the ycfR promoter. It appears that YcfR is a multiple stress resistance protein, since deleting ycfR also rendered the cell more sensitive to acid, heat treatment, hydrogen peroxide, and cadmium. Increased biofilm formation through YcfR due to stress appears to be the result of decreasing indole synthesis, since a mutation in the tnaA gene encoding tryptophanase prevented enhanced biofilm formation upon stress and adding indole prevented enhanced biofilm formation upon stress. Deleting ycfR also affected outer membrane proteins and converted the cell from hydrophilic to hydrophobic, as well as increased cell aggregation fourfold. YcfR seems to be involved in the regulation of E. coli K-12 biofilm formation by decreasing cell aggregation and cell surface adhesion, by influencing the concentration of signal molecules, and by interfering with stress responses. Based on our findings, we propose that this locus be named bhsA, for influencing biofilm through hydrophobicity and stress response.


mBio ◽  
2018 ◽  
Vol 9 (4) ◽  
Author(s):  
Fengming Ding ◽  
Ken-Ichi Oinuma ◽  
Nicole E. Smalley ◽  
Amy L. Schaefer ◽  
Omar Hamwy ◽  
...  

ABSTRACTPseudomonas aeruginosauses two acyl-homoserine lactone signals and two quorum sensing (QS) transcription factors, LasR and RhlR, to activate dozens of genes. LasR responds toN-3-oxo-dodecanoyl-homoserine lactone (3OC12-HSL) and RhlR toN-butanoyl-homoserine lactone (C4-HSL). There is a thirdP. aeruginosaacyl-homoserine-lactone-responsive transcription factor, QscR, which acts to dampen or delay activation of genes by LasR and RhlR by an unknown mechanism. To better understand the role of QscR inP. aeruginosaQS, we performed a chromatin immunoprecipitation analysis, which showed this transcription factor bound the promoter of only a single operon of three genes linked toqscR, PA1895 to PA1897. Other genes that appear to be regulated by QscR in transcriptome studies were not direct targets of QscR. Deletion of PA1897 recapitulates the early QS activation phenotype of a QscR-null mutant, and the phenotype of a QscR-null mutant was complemented by PA1895-1897 but not by PA1897 alone. We conclude that QscR acts to modulate quorum sensing through regulation of a single operon, apparently raising the QS threshold of the population and providing a “brake” on QS autoinduction.IMPORTANCEQuorum sensing, a cell-cell communication system, is broadly distributed among bacteria and is commonly used to regulate the production of shared products. An important consequence of quorum sensing is a delay in production of certain products until the population density is high. The bacteriumPseudomonas aeruginosahas a particularly complicated quorum sensing system involving multiple signals and receptors. One of these receptors, QscR, downregulates gene expression, unlike the other receptors inP. aeruginosa. QscR does so by inducing the expression of a single operon whose function provides an element of resistance to a population reaching a quorum. This finding has importance for design of quorum sensing inhibitory strategies and can also inform design of synthetic biological circuits that use quorum sensing receptors to regulate gene expression.


2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Greg Tram ◽  
William P. Klare ◽  
Joel A. Cain ◽  
Basem Mourad ◽  
Stuart J. Cordwell ◽  
...  

Campylobacter jejuni is a foodborne pathogen and an important contributor to gastroenteritis in humans. C. jejuni readily forms biofilms which may play a role in the transmission of the pathogen from animals to humans. Herein, we present RNA sequencing data investigating differential gene expression in biofilm and planktonic C. jejuni. These data provide insight into pathways which may be important to biofilm formation in this organism.


2006 ◽  
Vol 188 (12) ◽  
pp. 4312-4320 ◽  
Author(s):  
Martin Kalmokoff ◽  
Patricia Lanthier ◽  
Tammy-Lynn Tremblay ◽  
Mary Foss ◽  
Peter C. Lau ◽  
...  

ABSTRACT Campylobacter jejuni remains the leading cause of bacterial gastroenteritis in developed countries, and yet little is known concerning the mechanisms by which this fastidious organism survives within its environment. We have demonstrated that C. jejuni 11168 can form biofilms on a variety of surfaces. Proteomic analyses of planktonic and biofilm-grown cells demonstrated differences in protein expression profiles between the two growth modes. Proteins involved in the motility complex, including the flagellins (FlaA, FlaB), the filament cap (FliD), the basal body (FlgG, FlgG2), and the chemotactic protein (CheA), all exhibited higher levels of expression in biofilms than found in stationary-phase planktonic cells. Additional proteins with enhanced expression included those involved in the general (GroEL, GroES) and oxidative (Tpx, Ahp) stress responses, two known adhesins (Peb1, FlaC), and proteins involved in biosynthesis, energy generation, and catabolic functions. An aflagellate flhA mutant not only lost the ability to attach to a solid matrix and form a biofilm but could no longer form a pellicle at the air-liquid interface of a liquid culture. Insertional inactivation of genes that affect the flagellar filament (fliA, flaA, flaB, flaG) or the expression of the cell adhesin (flaC) also resulted in a delay in pellicle formation. These findings demonstrate that the flagellar motility complex plays a crucial role in the initial attachment of C. jejuni 11168 to solid surfaces during biofilm formation as well as in the cell-to-cell interactions required for pellicle formation. Continued expression of the motility complex in mature biofilms is unusual and suggests a role for the flagellar apparatus in the biofilm phenotype.


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