scholarly journals Chicken Juice Enhances Surface Attachment and Biofilm Formation of Campylobacter jejuni

2014 ◽  
Vol 80 (22) ◽  
pp. 7053-7060 ◽  
Author(s):  
Helen L. Brown ◽  
Mark Reuter ◽  
Louise J. Salt ◽  
Kathryn L. Cross ◽  
Roy P. Betts ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Food Chain ◽  
Biofilm Formation ◽  
Cell Attachment ◽  
Bacterial Attachment ◽  
Poultry Meat ◽  
Abiotic Surface ◽  
Surface Attachment ◽  
Aerobic Conditions ◽  
Content Type

ABSTRACTThe bacterial pathogenCampylobacter jejuniis primarily transmitted via the consumption of contaminated foodstuffs, especially poultry meat. In food processing environments,C. jejuniis required to survive a multitude of stresses and requires the use of specific survival mechanisms, such as biofilms. An initial step in biofilm formation is bacterial attachment to a surface. Here, we investigated the effects of a chicken meat exudate (chicken juice) onC. jejunisurface attachment and biofilm formation. Supplementation of brucella broth with ≥5% chicken juice resulted in increased biofilm formation on glass, polystyrene, and stainless steel surfaces with fourC. jejuniisolates and oneC. coliisolate in both microaerobic and aerobic conditions. When incubated with chicken juice,C. jejuniwas both able to grow and form biofilms in static cultures in aerobic conditions. Electron microscopy showed thatC. jejunicells were associated with chicken juice particulates attached to the abiotic surface rather than the surface itself. This suggests that chicken juice contributes toC. jejunibiofilm formation by covering and conditioning the abiotic surface and is a source of nutrients. Chicken juice was able to complement the reduction in biofilm formation of an aflagellated mutant ofC. jejuni, indicating that chicken juice may support food chain transmission of isolates with lowered motility. We provide here a useful model for studying the interaction ofC. jejunibiofilms in food chain-relevant conditions and also show a possible mechanism forC. jejunicell attachment and biofilm initiation on abiotic surfaces within the food chain.

scholarly journals Biofilm Formation by Campylobacter jejuni Is Increased under Aerobic Conditions

2010 ◽  
Vol 76 (7) ◽  
pp. 2122-2128 ◽  
Author(s):  
Mark Reuter ◽  
Arthur Mallett ◽  
Bruce M. Pearson ◽  
Arnoud H. M. van Vliet
Keyword(s):  
Campylobacter Jejuni ◽  
Food Chain ◽  
Biofilm Formation ◽  
Planktonic Cells ◽  
Aerobic Conditions ◽  
Food Borne ◽  
Passive Release ◽  
Bacterial Gastroenteritis ◽  
Microaerobic Conditions ◽  
Developed World

ABSTRACT The microaerophilic human pathogen Campylobacter jejuni is the leading cause of food-borne bacterial gastroenteritis in the developed world. During transmission through the food chain and the environment, the organism must survive stressful environmental conditions, particularly high oxygen levels. Biofilm formation has been suggested to play a role in the environmental survival of this organism. In this work we show that C. jejuni NCTC 11168 biofilms developed more rapidly under environmental and food-chain-relevant aerobic conditions (20% O2) than under microaerobic conditions (5% O2, 10% CO2), although final levels of biofilms were comparable after 3 days. Staining of biofilms with Congo red gave results similar to those obtained with the commonly used crystal violet staining. The level of biofilm formation by nonmotile aflagellate strains was lower than that observed for the motile flagellated strain but nonetheless increased under aerobic conditions, suggesting the presence of flagellum-dependent and flagellum-independent mechanisms of biofilm formation in C. jejuni. Moreover, preformed biofilms shed high numbers of viable C. jejuni cells into the culture supernatant independently of the oxygen concentration, suggesting a continuous passive release of cells into the medium rather than a condition-specific active mechanism of dispersal. We conclude that under aerobic or stressful conditions, C. jejuni adapts to a biofilm lifestyle, allowing survival under detrimental conditions, and that such a biofilm can function as a reservoir of viable planktonic cells. The increased level of biofilm formation under aerobic conditions is likely to be an adaptation contributing to the zoonotic lifestyle of C. jejuni.

scholarly journals The Host Antimicrobial Protein Calgranulin C Participates in the Control ofCampylobacter jejuniGrowth via Zinc Sequestration

2018 ◽  
Vol 86 (6) ◽  
Author(s):  
Janette M. Shank ◽  
Brittni R. Kelley ◽  
Joseph W. Jackson ◽  
Jessica L. Tweedie ◽  
Dana Franklin ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Poultry Meat ◽  
Antimicrobial Protein ◽  
Dependent Manner ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Full Resolution ◽  
Factor Alpha

ABSTRACTCampylobacter jejuniis a leading cause of bacterially derived gastroenteritis worldwide.Campylobacteris most commonly acquired through the consumption of undercooked poultry meat or through drinking contaminated water. Following ingestion,Campylobacteradheres to the intestinal epithelium and mucus layer, causing toxin-mediated inflammation and inhibition of fluid reabsorption. Currently, the human response to infection is relatively unknown, and animal hosts that model these responses are rare. As such, we examined patient fecal samples for the accumulation of the neutrophil protein calgranulin C during infection withCampylobacter jejuni. In response to infection, calgranulin C was significantly increased in the feces of humans. To determine whether calgranulin C accumulation occurs in an animal model, we examined disease in ferrets. Ferrets were effectively infected byC. jejuni, with peak fecal loads observed at day 3 postinfection and full resolution by day 12. Serum levels of interleukin-10 (IL-10) and tumor necrosis factor alpha (TNF-α) significantly increased in response to infection, which resulted in leukocyte trafficking to the colon. As a result, calgranulin C increased in the feces of ferrets at the time whenC. jejuniloads decreased. Further, the addition of purified calgranulin C toC. jejunicultures was found to inhibit growth in a zinc-dependent manner. These results suggest that upon infection withC. jejuni, leukocytes trafficked to the intestine release calgranulin C as a mechanism for inhibitingC. jejunigrowth.

Application of a Group II Campylobacter Bacteriophage To Reduce Strains of Campylobacter jejuni and Campylobacter coli Colonizing Broiler Chickens

2009 ◽  
Vol 72 (4) ◽  
pp. 733-740 ◽  
Author(s):  
AYMAN EL-SHIBINY ◽  
ANDREW SCOTT ◽  
ANDREW TIMMS ◽  
YASSER METAWEA ◽  
PHILLIPPA CONNERTON ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Food Chain ◽  
Minor Component ◽  
Poultry Meat ◽  
Campylobacter Coli ◽  
Bacteriophage Therapy ◽  
Human Food ◽  
A Genome ◽  
Human Food Chain ◽  
Group Ii

Members of the genus Campylobacter are frequently responsible for human enteric disease worldwide. Persistent Campylobacter contamination of poultry meat is a common problem that represents a significant food safety risk through the consumption of undercooked poultry meat or through cross-contamination of other foods during the preparation of poultry. Bacteriophage therapy is one possible means by which this colonization of poultry could be controlled, thus limiting the entry of Campylobacter into the human food chain. Previously group III phages with genome sizes of approximately 140 kb had been administered to Campylobacter jejuni–colonized poultry. The application of a group II Campylobacter phage, CP220, with a genome size of 197 kb is described here. Phage CP220 was administered to both C. jejuni– and C. coli–colonized birds. A 2-log CFU/g decline in cecal Campylobacter counts was observed after 48 h in birds colonized with C. jejuni HPC5 and administered with a single 7-log PFU dose of CP220. The incidence of phage resistance developing in Campylobacter-colonized chickens upon exposure to virulent phages was determined to be 2%, and the resistant types remained a minor component of the population. To achieve a similar reduction in Campylobacter numbers in C. coli OR12–colonized birds, a 9-log PFU dose of CP220 was required. Using phage to reduce Campylobacter colonization in poultry offers the prospect of a sustainable intervention measure that may limit the entry of these pathogens into the human food chain.

scholarly journals Syndecan-1 Promotes Streptococcus pneumoniae Corneal Infection by Facilitating the Assembly of Adhesive Fibronectin Fibrils

mBio ◽  
2020 ◽  
Vol 11 (6) ◽  
Author(s):  
Akiko Jinno ◽  
Atsuko Hayashida ◽  
Howard F. Jenkinson ◽  
Pyong Woo Park
Keyword(s):  
Streptococcus Pneumoniae ◽  
Basement Membrane ◽  
Cell Surface ◽  
Host Cell ◽  
Cell Biology ◽  
Bacterial Attachment ◽  
Microbial Pathogens ◽  
Surface Attachment ◽  
Content Type ◽  
Corneal Infection

ABSTRACT Subversion of heparan sulfate proteoglycans (HSPGs) is thought to be a common virulence mechanism shared by many microbial pathogens. The prevailing assumption is that pathogens co-opt HSPGs as cell surface attachment receptors or as inhibitors of innate host defense. However, there are few data that clearly support this idea in vivo. We found that deletion of syndecan-1 (Sdc1), a major cell surface HSPG of epithelial cells, causes a gain of function in a mouse model of scarified corneal infection, where Sdc1−/− corneas were significantly less susceptible to Streptococcus pneumoniae infection. Administration of excess Sdc1 ectodomains significantly inhibited S. pneumoniae corneal infection, suggesting that Sdc1 promotes infection as a cell surface attachment receptor. However, S. pneumoniae did not interact with Sdc1 and Sdc1 was shed upon S. pneumoniae infection, indicating that Sdc1 does not directly support S. pneumoniae adhesion. Instead, Sdc1 promoted S. pneumoniae adhesion by driving the assembly of fibronectin (FN) fibrils in the corneal basement membrane to which S. pneumoniae attaches when infecting injured corneas. S. pneumoniae specifically bound to corneal FN via PavA, and PavA deletion significantly attenuated S. pneumoniae virulence in the cornea. Excess Sdc1 ectodomains inhibited S. pneumoniae corneal infection by binding to the Hep II domain and interfering with S. pneumoniae PavA binding to FN. These findings reveal a previously unknown virulence mechanism of S. pneumoniae where key extracellular matrix (ECM) interactions and structures that are essential for host cell homeostasis are exploited for bacterial pathogenesis. IMPORTANCE Bacterial pathogens have evolved several ingenious mechanisms to subvert host cell biology for their pathogenesis. Bacterial attachment to the host ECM establishes a niche to grow and is considered one of the critical steps of infection. This pathogenic mechanism entails coordinated assembly of the ECM by the host to form the ECM structure and organization that are specifically recognized by bacteria for their adhesion. We serendipitously discovered that epithelial Sdc1 facilitates the assembly of FN fibrils in the corneal basement membrane and that this normal biological function of Sdc1 has detrimental consequences for the host in S. pneumoniae corneal infection. Our studies suggest that bacterial subversion of the host ECM is more complex than previously appreciated.

scholarly journals Cellular Response of Campylobacter jejuni to Trisodium Phosphate

2011 ◽  
Vol 78 (5) ◽  
pp. 1411-1415 ◽  
Author(s):  
Charlotte Tandrup Riedel ◽  
Marianne Thorup Cohn ◽  
Richard A. Stabler ◽  
Brendan Wren ◽  
Lone Brøndsted
Keyword(s):  
Campylobacter Jejuni ◽  
Cellular Response ◽  
Efflux Pumps ◽  
Transport Processes ◽  
Trisodium Phosphate ◽  
Poultry Meat ◽  
Heat Sensitivity ◽  
Multidrug Efflux ◽  
Content Type ◽  
Multidrug Efflux Pumps

ABSTRACTThe highly alkaline compound trisodium phosphate (TSP) is used as an intervention to reduce the load ofCampylobacteron poultry meat in U.S. poultry slaughter plants. The aim of the present study was to investigate the cellular responses ofCampylobacter jejuniNCTC11168 when exposed to sublethal concentrations of TSP. Preexposure ofC. jejunito TSP resulted in a significant increase in heat sensitivity, suggesting that a combined heat and TSP treatment may increase reduction ofC. jejuni. A microarray analysis identified a limited number of genes that were differently expressed after sublethal TSP exposure; however, the response was mainly associated with ion transport processes.C. jejuniNCTC11168nhaA1(Cj1655c) andnhaA2(Cj1654c), which encode orthologues to theEscherichia coliNhaA cation/proton antiporter, were able to partially restore TSP, alkaline, and sodium resistance phenotypes to anE. colication/proton antiporter mutant. In addition, inhibition ofresistance-nodulation-celldivision (RND) multidrug efflux pumps by the inhibitor PaβN (Phe-Arg β-naphthylamide dihydrochloride) decreased tolerance to sublethal TSP. Therefore, we propose that NhaA1/NhaA2 cation/proton antiporters and RND multidrug efflux pumps function in tolerance to sublethal TSP exposure inC. jejuni.

scholarly journals A Conserved Regulatory Circuit Controls Large Adhesins in Vibrio cholerae

mBio ◽  
2019 ◽  
Vol 10 (6) ◽  
Author(s):  
Giordan Kitts ◽  
Krista M. Giglio ◽  
David Zamorano-Sánchez ◽  
Jin Hwan Park ◽  
Loni Townsley ◽  
...  
Keyword(s):  
Cell Surface ◽  
Vibrio Cholerae ◽  
Biofilm Formation ◽  
Diarrheal Disease ◽  
Cell Attachment ◽  
Surface Display ◽  
Second Messenger ◽  
Bacterial Biofilm ◽  
Content Type ◽  
Regulatory Circuit

ABSTRACT The dinucleotide second messenger c-di-GMP has emerged as a central regulator of reversible cell attachment during bacterial biofilm formation. A prominent cell adhesion mechanism first identified in pseudomonads combines two c-di-GMP-mediated processes: transcription of a large adhesin and its cell surface display via posttranslational proteolytic control. Here, we characterize an orthologous c-di-GMP effector system and show that it is operational in Vibrio cholerae, where it regulates two distinct classes of adhesins. Through structural analyses, we reveal a conserved autoinhibition mechanism of the c-di-GMP receptor that controls adhesin proteolysis and present a structure of a c-di-GMP-bound receptor module. We further establish functionality of the periplasmic protease controlled by the receptor against the two adhesins. Finally, transcription and functional assays identify physiological roles of both c-di-GMP-regulated adhesins in surface attachment and biofilm formation. Together, our studies highlight the conservation of a highly efficient signaling effector circuit for the control of cell surface adhesin expression and its versatility by revealing strain-specific variations. IMPORTANCE Vibrio cholerae, the causative agent of the diarrheal disease cholera, benefits from a sessile biofilm lifestyle that enhances survival outside the host but also contributes to host colonization and infectivity. The bacterial second messenger c-di-GMP has been identified as a central regulator of biofilm formation, including in V. cholerae; however, our understanding of the pathways that contribute to this process is incomplete. Here, we define a conserved signaling system that controls the stability of large adhesion proteins at the cell surface of V. cholerae, which are important for cell attachment and biofilm formation. Insight into the regulatory circuit underlying biofilm formation may inform targeted strategies to interfere with a process that renders this bacterium remarkably adaptable to changing environments.

scholarly journals Campylobacter jejuni Biofilm Formation Under Aerobic Conditions and Inhibition by ZnO Nanoparticles

2020 ◽  
Vol 11 ◽  
Author(s):  
Xian Zhong ◽  
Qingping Wu ◽  
Jumei Zhang ◽  
Zonghao Ma ◽  
Juan Wang ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Zno Nanoparticles ◽  
Biofilm Formation ◽  
Aerobic Conditions

scholarly journals Multiple Drug-Induced Stress Responses Inhibit Formation of Escherichia coli Biofilms

2020 ◽  
Vol 86 (21) ◽  
Author(s):  
Nataliya A. Teteneva ◽  
Sergey V. Mart’yanov ◽  
María Esteban-López ◽  
Jörg Kahnt ◽  
Timo Glatter ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Stress Responses ◽  
Biofilm Formation ◽  
Molecular Mechanisms ◽  
Drug Repurposing ◽  
Bacterial Attachment ◽  
Bacterial Biofilm ◽  
Multiple Drug ◽  
Content Type ◽  
Approved Drugs

ABSTRACT In most ecosystems, bacteria exist primarily as structured surface-associated biofilms that can be highly tolerant to antibiotics and thus represent an important health issue. Here, we explored drug repurposing as a strategy to identify new antibiofilm compounds, screening over 1,000 compounds from the Prestwick Chemical Library of approved drugs for specific activities that prevent biofilm formation by Escherichia coli. Most growth-inhibiting compounds, which include known antibacterial but also antiviral and other drugs, also reduced biofilm formation. However, we also identified several drugs that were biofilm inhibitory at doses where only a weak effect or no effect on planktonic growth could be observed. The activities of the most specific antibiofilm compounds were further characterized using gene expression analysis, proteomics, and microscopy. We observed that most of these drugs acted by repressing genes responsible for the production of curli, a major component of the E. coli biofilm matrix. This repression apparently occurred through the induction of several different stress responses, including DNA and cell wall damage, and homeostasis of divalent cations, demonstrating that biofilm formation can be inhibited through a variety of molecular mechanisms. One tested drug, tyloxapol, did not affect curli expression or cell growth but instead inhibited biofilm formation by suppressing bacterial attachment to the surface. IMPORTANCE The prevention of bacterial biofilm formation is one of the major current challenges in microbiology. Here, by systematically screening a large number of approved drugs for their ability to suppress biofilm formation by Escherichia coli, we identified a number of prospective antibiofilm compounds. We further demonstrated different mechanisms of action for individual compounds, from induction of replicative stress to disbalance of cation homeostasis to inhibition of bacterial attachment to the surface. Our work demonstrates the potential of drug repurposing for the prevention of bacterial biofilm formation and suggests that also for other bacteria, the activity spectrum of antibiofilm compounds is likely to be broad.

scholarly journals Adhesion, Biofilm Formation, and Genomic Features of Campylobacter jejuni Bf, an Atypical Strain Able to Grow under Aerobic Conditions

2016 ◽  
Vol 7 ◽  
Author(s):  
Vicky Bronnec ◽  
Hana Turoňová ◽  
Agnès Bouju ◽  
Stéphane Cruveiller ◽  
Ramila Rodrigues ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Biofilm Formation ◽  
Aerobic Conditions ◽  
Genomic Features

scholarly journals Self-Regulation and Interplay of Rsm Family Proteins Modulate the Lifestyle of Pseudomonas putida

2016 ◽  
Vol 82 (18) ◽  
pp. 5673-5686 ◽  
Author(s):  
Óscar Huertas-Rosales ◽  
María Isabel Ramos-González ◽  
Manuel Espinosa-Urgel
Keyword(s):  
Pseudomonas Putida ◽  
Biofilm Formation ◽  
Expression Patterns ◽  
Self Regulation ◽  
Bacterial Attachment ◽  
Triple Mutant ◽  
Content Type ◽  
Global Regulators ◽  
Glass Surfaces ◽  
Plastic Surfaces

ABSTRACTIn the plant-beneficial bacteriumPseudomonas putidaKT2440, three genes have been identified that encode posttranscriptional regulators of the CsrA/RsmA family. Their regulatory roles in the motile and sessile lifestyles ofP. putidahave been investigated by generating single-, double-, and triple-null mutants and by overexpressing each protein (RsmA, RsmE, and RsmI) in different genetic backgrounds. Thersmtriple mutant shows reduced swimming and swarming motilities and increased biofilm formation, whereas overexpression of RsmE or RsmI results in reduced bacterial attachment. However, biofilms formed on glass surfaces by the triple mutant are more labile than those of the wild-type strain and are easily detached from the surface, a phenomenon that is not observed on plastic surfaces. Analysis of the expression of adhesins and exopolysaccharides in the different genetic backgrounds suggests that the biofilm phenotypes are due to alterations in the composition of the extracellular matrix and in the timing of synthesis of its elements. We have also studied the expression patterns of Rsm proteins and obtained data that indicate the existence of autoregulation mechanisms.IMPORTANCEProteins of the CsrA/RsmA family function as global regulators in different bacteria. More than one of these proteins is present in certain species. In this study, all of the RsmA homologs inP. putidaare characterized and globally taken into account to investigate their roles in controlling bacterial lifestyles and the regulatory interactions among them. The results offer new perspectives on how biofilm formation is modulated in this environmentally relevant bacterium.

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