Database : MEDLINE
Search on : Yersinia and Infections [Words]
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[PMID]: 29263104
[Au] Autor:Zhang Y; Khairallah C; Sheridan BS; van der Velden AWM; Bliska JB
[Ad] Address:Center for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA yue.zhang@stonybrook.edu james.bliska@stonybrook.edu.
[Ti] Title:CCR2 Inflammatory Monocytes Are Recruited to Yersinia pseudotuberculosis Pyogranulomas and Dictate Adaptive Responses at the Expense of Innate Immunity during Oral Infection.
[So] Source:Infect Immun;86(3), 2018 Mar.
[Is] ISSN:1098-5522
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Murine Ly6C inflammatory monocytes (IMs) require CCR2 to leave the bone marrow and enter mesenteric lymph nodes (MLNs) and other organs in response to infection. We are investigating how IMs, which can differentiate into CD11c dendritic cells (DCs), contribute to innate and adaptive immunity to Previously, we obtained evidence that IMs are important for a dominant CD8 T cell response to the epitope YopE and host survival using intravenous infections with attenuated Here we challenged CCR2 or CCR2 mice orally with wild-type to investigate how IMs contribute to immune responses during intestinal infection. Unexpectedly, CCR2 mice did not have reduced survival but retained body weight better and their MLNs cleared faster and with reduced lymphadenopathy compared to controls. Enhanced bacterial clearance in CCR2 mice correlated with reduced numbers of IMs in spleens and increased numbers of neutrophils in livers. imaging of MLNs and spleens from CCR2-GFP mice showed that green fluorescent protein-positive (GFP ) IMs accumulated at the periphery of neutrophil-rich containing pyogranulomas. GFP IMs colocalized with CD11c cells and YopE -specific CD8 T cells in MLNs, suggesting that IM-derived DCs prime adaptive responses in pyogranulomas. Consistently, CCR2 mice had reduced numbers of splenic DCs, YopE -specific CD8 T cells, CD4 T cells, and B cells in organs and lower levels of serum antibodies to antigens. Our data suggest that IMs differentiate into DCs in MLN pyogranulomas and direct adaptive responses in T cells at the expense of innate immunity during oral infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  2 / 9120 MEDLINE  
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[PMID]: 28465342
[Au] Autor:Stefanova D; Raychev A; Arezes J; Ruchala P; Gabayan V; Skurnik M; Dillon BJ; Horwitz MA; Ganz T; Bulut Y; Nemeth E
[Ad] Address:Molecular, Cellular, and Integrative Physiology Graduate Program and.
[Ti] Title:Endogenous hepcidin and its agonist mediate resistance to selected infections by clearing non-transferrin-bound iron.
[So] Source:Blood;130(3):245-257, 2017 07 20.
[Is] ISSN:1528-0020
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The iron-regulatory hormone hepcidin is induced early in infection, causing iron sequestration in macrophages and decreased plasma iron; this is proposed to limit the replication of extracellular microbes, but could also promote infection with macrophage-tropic pathogens. The mechanisms by which hepcidin and hypoferremia modulate host defense, and the spectrum of microbes affected, are poorly understood. Using mouse models, we show that hepcidin was selectively protective against siderophilic extracellular pathogens ( O9) by controlling non-transferrin-bound iron (NTBI) rather than iron-transferrin concentration. NTBI promoted the rapid growth of siderophilic but not nonsiderophilic bacteria in mice with either genetic or iatrogenic iron overload and in human plasma. Hepcidin or iron loading did not affect other key components of innate immunity, did not indiscriminately promote intracellular infections ( ), and had no effect on extracellular nonsiderophilic O8 or Hepcidin analogs may be useful for treatment of siderophilic infections.
[Mh] MeSH terms primary: Catheter-Related Infections/immunology
Hemochromatosis/immunology
Hepcidins/immunology
Iron Overload/immunology
Iron/metabolism
Staphylococcal Infections/immunology
[Mh] MeSH terms secundary: Animals
Binding, Competitive
Catheter-Related Infections/metabolism
Catheter-Related Infections/microbiology
Catheter-Related Infections/mortality
Disease Models, Animal
Disease Resistance
Gene Expression
Hemochromatosis/metabolism
Hemochromatosis/microbiology
Hemochromatosis/mortality
Hepcidins/agonists
Hepcidins/deficiency
Hepcidins/genetics
Humans
Iron/immunology
Iron Overload/metabolism
Iron Overload/microbiology
Iron Overload/mortality
Mice
Mice, Inbred C57BL
Mice, Knockout
Mycobacterium tuberculosis/drug effects
Mycobacterium tuberculosis/growth & development
Mycobacterium tuberculosis/metabolism
Oligopeptides/pharmacology
Protein Binding
Staphylococcal Infections/metabolism
Staphylococcal Infections/microbiology
Staphylococcal Infections/mortality
Staphylococcus aureus
Survival Analysis
Transferrin/genetics
Transferrin/metabolism
Yersinia enterocolitica/drug effects
Yersinia enterocolitica/growth & development
Yersinia enterocolitica/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Hamp1 protein, mouse); 0 (Hepcidins); 0 (Oligopeptides); 0 (Transferrin); E1UOL152H7 (Iron)
[Em] Entry month:1708
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170504
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-03-772715

  3 / 9120 MEDLINE  
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[PMID]: 29497015
[Au] Autor:Kumar S; Hedrick V; Mattoo S
[Ad] Address:Department of Biological Sciences, Purdue University, 915 West State Street, West Lafayette, IN 47907, USA.
[Ti] Title:YopT domain of the PfhB2 toxin from Pasteurella multocida: protein expression, characterization, crystallization and crystallographic analysis.
[So] Source:Acta Crystallogr F Struct Biol Commun;74(Pt 3):128-134, 2018 Mar 01.
[Is] ISSN:2053-230X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pasteurella multocida causes respiratory-tract infections in a broad range of animals, as well as opportunistic infections in humans. P. multocida secretes a multidomain toxin called PfhB2, which contains a YopT-like cysteine protease domain at its C-terminus. The YopT domain of PfhB2 contains a well conserved Cys-His-Asp catalytic triad that defines YopT family members, and shares high sequence similarity with the prototype YopT from Yersinia sp. To date, only one crystal structure of a YopT family member has been reported; however, additional structural information is needed to help characterize the varied substrate specificity and enzymatic action of this large protease family. Here, a catalytically inactive C3733S mutant of PfhB2 YopT that provides enhanced protein stability was used with the aim of gaining structural insight into the diversity within the YopT protein family. To this end, the C3733S mutant of PfhB2 YopT has been successfully cloned, overexpressed, purified and crystallized. Diffraction data sets were collected from native crystals to 3.5 Šresolution and a single-wavelength anomalous data set was collected from an iodide-derivative crystal to 3.2 Šresolution. Data pertaining to crystals belonging to space group P3 , with unit-cell parameters a = 136.9, b = 136.9, c = 74.7 Šfor the native crystals and a = 139.2, b = 139.2, c = 74.7 Šfor the iodide-derivative crystals, are discussed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:In-Data-Review
[do] DOI:10.1107/S2053230X18000857

  4 / 9120 MEDLINE  
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[PMID]: 29390040
[Au] Autor:Heine W; Beckstette M; Heroven AK; Thiemann S; Heise U; Nuss AM; Pisano F; Strowig T; Dersch P
[Ad] Address:Department of Molecular Infection Biology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
[Ti] Title:Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency.
[So] Source:PLoS Pathog;14(2):e1006858, 2018 Feb.
[Is] ISSN:1553-7374
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Gastrointestinal infections caused by enteric yersiniae can become persistent and complicated by relapsing enteritis and severe autoimmune disorders. To establish a persistent infection, the bacteria have to cope with hostile surroundings when they transmigrate through the intestinal epithelium and colonize underlying gut-associated lymphatic tissues. How the bacteria gain a foothold in the face of host immune responses is poorly understood. Here, we show that the CNFY toxin, which enhances translocation of the antiphagocytic Yop effectors, induces inflammatory responses. This results in extensive tissue destruction, alteration of the intestinal microbiota and bacterial clearance. Suppression of CNFY function, however, increases interferon-γ-mediated responses, comprising non-inflammatory antimicrobial activities and tolerogenesis. This process is accompanied by a preterm reprogramming of the pathogen's transcriptional response towards persistence, which gives the bacteria a fitness edge against host responses and facilitates establishment of a commensal-type life style.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.ppat.1006858

  5 / 9120 MEDLINE  
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[PMID]: 29260747
[Au] Autor:Belaia OF; Yudina YV; Volchkova EV; Payevskaya OA; Belaya YA; Gyulazyan NM; Zuyevskaya SN
[Ad] Address:I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
[Ti] Title:Vyiavlenie Shiga-toksina u bol'nykh ostrymi kishechnymi infektsiiami v prisutstvii mono- i mikst-O-antigenov vozbuditelei. [Identification of Shiga toxin in patients with acute intestinal infections in the presence of mono- and mixed-O-antigens of pathogens].
[So] Source:Ter Arkh;89(11):55-59, 2017.
[Is] ISSN:0040-3660
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:AIM: To investigate the time course of changes in the detection rates and levels of Shiga toxin antigen (STA) in their stool and middle-molecule circulating immune complexes (CICs) containing IgG (IgG CIC) in patients with acute intestinal infections (AIIs) in the presence of the body's circulation of mono- and mixed-LPS/O-antigens of intestinal pathogens. SUBJECTS AND METHODS: A total of 147 patients aged 15 to 55 years who had been hospitalized with AIIs were examined. The diagnosis was bacteriologically verified in 19% of the patients; in the others, it was confirmed by the detection of LPS/O-antigens of Shigella, Salmonella, Yersinia, and Campylobacter in their stool by means of the reaction of coagglutination (RCA) on glass slides. Plates for RCA displayed STA in the fecal and IgG CIC samples. RESULTS: Mono- and mixed infections were detected in 32 and 68%, respectively. The RCA plates exhibited STA in 25.2% of the fecal samples and in 90.5% of the IgG CIC ones from patients with AIIs and did not in those from donors. In monoinfection, the detection rates and levels of STA in the feces became lower in the course of the disease and remained unchanged in IgG CIC and the levels of STA also decreased in the feces, but increased in IgG CIC in mixed infection. CONCLUSION: In 25.2% of the patients with early AIIs, their stools show free STA; its detection rate and levels are significantly higher in mixed infections than those in monoinfection. The level of STA in serum IgG CIC was significantly higher in mixed infection, suggesting an active immune response to the pathogen. Given that the Shiga toxin-producing strains are present in patients with AIIs, caution should be exercised in the choice of an antibacterial drug to prevent horizontal gene transfer and to enhance toxin production and the body's intoxication. One of the advantages of RCA is the possibility of rapidly changing the spectrum of test systems, depending on the region of their application and the epidemiological situation.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:In-Process
[do] DOI:10.17116/terarkh2017891155-59

  6 / 9120 MEDLINE  
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[PMID]: 29421357
[Au] Autor:Bancerz-Kisiel A; Szczerba-Turek A; Platt-Samoraj A; Michalczyk M; Szweda W
[Ad] Address:Department of Epizootiology, Faculty of Veterinary Medicine, University of Warmia and Mazury, Oczapowskiego 2, 10-719 Olsztyn, Poland. Electronic address: a.bancerz-kisiel@uwm.edu.pl.
[Ti] Title:Characterisation of ail-positive Yersinia enterocolitica of different biotypes using HRMA.
[So] Source:Int J Food Microbiol;269:46-51, 2018 Mar 23.
[Is] ISSN:1879-3460
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Yersiniosis is one of the four most frequent foodborne zoonotic diseases in Europe, and Yersinia enterocolitica is the primary agent in human infections. The ail gene is an important chromosomal virulence marker of Y. enterocolitica which encodes Ail, a 17-kDa outer membrane protein that promotes attachment and invasion. In the present study, ail-positive Y. enterocolitica strains of different biotypes were examined using high resolution melting analysis (HRMA) and DNA sequencing. Genotype data relating to Y. enterocolitica strains isolated from different sources and belonging to different biotypes were compared. Applied method allowed efficient distinguishing of three genotypes and phylogenetic groups: 1A - included non-pathogenic Y. enterocolitica strains; 1B - consisted of highly pathogenic Y. enterocolitica strains and 2/4 - involved weakly pathogenic Y. enterocolitica strains. Amplicon genotyping based on HRMA supports rapid identification of ail SNPs correlated with biotype of examined Y. enterocolitica strains.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[St] Status:In-Process

  7 / 9120 MEDLINE  
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[PMID]: 29325864
[Au] Autor:Shukla SK; Singh G; Ahmad S; Pant P
[Ad] Address:Multidisciplinary Research Unit, Government Medical College, Haldwani, Nainital, Uttarakhand, India.
[Ti] Title:Infections, genetic and environmental factors in pathogenesis of autoimmune thyroid diseases.
[So] Source:Microb Pathog;116:279-288, 2018 Jan 08.
[Is] ISSN:1096-1208
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:In Autoimmune disease a combination of infection, genetic and environmental factors causes an autoimmune response to the thyroid gland (characterized by lymphocytic infiltrations), thyroid stimulating hormone receptor (TSHR) and different thyroid antigens. Graves' and Hashimoto disease are autoimmune disorders with genetic predisposition. CD40 that stimulates the proliferation and differentiation of lymphocytes is an essential immunomodulatory component for follicular cells in the thyroid and the cell that present the antigen. CD40, PTPN22 and thyroid-specific genes are immunomodulating genes for the TSH receptor and thyroglobulin. CD40 used to be associated with Graves's disease as positional candidate on the basis of Graves' disease linkage study connecting with 20q11 genome chromosomal region. The PTPN22 gene gives rise to a substantial risk of specific autoimmune phenotypes and frequent disease mechanisms. Infections have been implicated in the pathogenesis of AITD including Coxsackie virus, Yersinia enterocolitica, Borrelia burgdorferi, Helicobacter pylori and retroviruses (HTLV-1, HFV, HIV and SV40). Infectious hepatitis C agents are the strongest proof supporting an affiliation with AITD. The essential environmental triggers of AITD are iodine, drugs, infection, smoking and perhaps stress. Autoimmune disease provide important facts on genetic mechanisms that influence the prognosis and treatment of the disease and by recent molecular techniques through gene expression study by quantitative Real Time-PCR and microarray, we can identify novel genes which are responsible for Graves' and Hashimoto disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:Publisher

  8 / 9120 MEDLINE  
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[PMID]: 29221731
[Au] Autor:Han SJ; Glatman Zaretsky A; Andrade-Oliveira V; Collins N; Dzutsev A; Shaik J; Morais da Fonseca D; Harrison OJ; Tamoutounour S; Byrd AL; Smelkinson M; Bouladoux N; Bliska JB; Brenchley JM; Brodsky IE; Belkaid Y
[Ad] Address:Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.
[Ti] Title:White Adipose Tissue Is a Reservoir for Memory T Cells and Promotes Protective Memory Responses to Infection.
[So] Source:Immunity;47(6):1154-1168.e6, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:White adipose tissue bridges body organs and plays a fundamental role in host metabolism. To what extent adipose tissue also contributes to immune surveillance and long-term protective defense remains largely unknown. Here, we have shown that at steady state, white adipose tissue contained abundant memory lymphocyte populations. After infection, white adipose tissue accumulated large numbers of pathogen-specific memory T cells, including tissue-resident cells. Memory T cells in white adipose tissue expressed a distinct metabolic profile, and white adipose tissue from previously infected mice was sufficient to protect uninfected mice from lethal pathogen challenge. Induction of recall responses within white adipose tissue was associated with the collapse of lipid metabolism in favor of antimicrobial responses. Our results suggest that white adipose tissue represents a memory T cell reservoir that provides potent and rapid effector memory responses, positioning this compartment as a potential major contributor to immunological memory.
[Mh] MeSH terms primary: Adipose Tissue, White/transplantation
CD4-Positive T-Lymphocytes/immunology
CD8-Positive T-Lymphocytes/immunology
Immunologic Memory
Toxoplasmosis/immunology
Yersinia pseudotuberculosis Infections/immunology
[Mh] MeSH terms secundary: Adipose Tissue, White/immunology
Animals
Bacterial Proteins/genetics
Bacterial Proteins/metabolism
CD4-Positive T-Lymphocytes/microbiology
CD4-Positive T-Lymphocytes/parasitology
CD8-Positive T-Lymphocytes/microbiology
CD8-Positive T-Lymphocytes/parasitology
Gene Expression
Genes, Reporter
Interferon-gamma/genetics
Interferon-gamma/immunology
Interleukin-17/genetics
Interleukin-17/immunology
Interleukin-5/genetics
Interleukin-5/immunology
Lipid Metabolism
Luminescent Proteins/genetics
Luminescent Proteins/metabolism
Mice
Mice, Inbred C57BL
Mice, Transgenic
Survival Analysis
Tissue Transplantation
Toxoplasma/immunology
Toxoplasmosis/genetics
Toxoplasmosis/mortality
Toxoplasmosis/parasitology
Tumor Necrosis Factor-alpha/genetics
Tumor Necrosis Factor-alpha/immunology
Yersinia pseudotuberculosis/immunology
Yersinia pseudotuberculosis Infections/genetics
Yersinia pseudotuberculosis Infections/microbiology
Yersinia pseudotuberculosis Infections/mortality
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Bacterial Proteins); 0 (Interleukin-17); 0 (Interleukin-5); 0 (Luminescent Proteins); 0 (Tumor Necrosis Factor-alpha); 0 (yellow fluorescent protein, Bacteria); 82115-62-6 (Interferon-gamma)
[Em] Entry month:1712
[Cu] Class update date: 180210
[Lr] Last revision date:180210
[Js] Journal subset:IM
[Da] Date of entry for processing:171210
[St] Status:MEDLINE

  9 / 9120 MEDLINE  
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[PMID]: 29357958
[Au] Autor:Walter F; Ott JJ; Claus H; Krause G
[Ad] Address:Institute of Medical Biostatistics, Epidemiology and Informatics,University Mainz,Mainz,Germany.
[Ti] Title:Sex- and age patterns in incidence of infectious diseases in Germany: analyses of surveillance records over a 13-year period (2001-2013).
[So] Source:Epidemiol Infect;146(3):372-378, 2018 Feb.
[Is] ISSN:1469-4409
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Sex differences in the incidence of infections may indicate different risk factors and behaviour but have not been analysed across pathogens. Based on 3.96 million records of 33 pathogens in Germany, notified from 2001 to 2013, we applied Poisson regression to generate age-standardised incidence rate ratios and assessed their distribution across age and sex. The following trends became apparent: (a) pathogens with male incidence preponderance at infant and child age (meningococcal disease (incidence rate ratio (IRR) = 1.19, 95% CI 1.03-1.38, age = 0-4); influenza (IRR = 1.09, 95% CI 1.06-1.13, age = 0-4)), (b) pathogens with sex-switch in incidence preponderance at puberty (e.g. norovirus (IRR = 1.10, 95% CI 1.02-1.19 in age = 5-14, IRR = 0.96, 95% CI 0.93-0.99, age ⩾ 60), (c) pathogens with general male incidence preponderance (bacterial/parasitic infections with campylobacter, Yersinia and Giardia), (d) pathogens with male incidence preponderance at juvenile and adult age (sexually transmitted or vector-borne infections (combined-IRR = 2.53, 95% CI 2.36-2.71, age = 15-59), (e) pathogens with male preponderance at older age (tick-borne encephalitis - IRR = 2.75, 95% CI 1.21-6.24, listeriosis - IRR = 2.06, 95% CI 1.38-3.06, age ⩾ 60). Risk factor concepts only partly serve to interpret similarities of grouped infections, i.e. transmission-related explanations and sex-specific exposures not consistently explain the pattern of food-borne infections (b). Sex-specific differences in infectious disease incidence are well acknowledged regarding the sexually transmitted diseases. This has led to designing gender-specific prevention strategies. Our data suggest that for infections with other transmission routes, gender-specific approaches can also be of benefit and importance.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180209
[Lr] Last revision date:180209
[St] Status:In-Data-Review
[do] DOI:10.1017/S0950268817002771

  10 / 9120 MEDLINE  
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[PMID]: 29341217
[Au] Autor:Horne SM; Schroeder M; Murphy J; Prüß BM
[Ad] Address:Department of Microbiological Sciences, North Dakota State University, Fargo, ND, USA.
[Ti] Title:Acetoacetate and ethyl acetoacetate as novel inhibitors of bacterial biofilm.
[So] Source:Lett Appl Microbiol;, 2018 Jan 16.
[Is] ISSN:1472-765X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Acetoacetate (AAA) was identified as a biofilm inhibitor in a previous study, where the effect of 190 carbon and nitrogen sources on biofilm amounts by Escherichia coli O157:H7 was determined. With this study, we tested the effect of AAA on growth and biofilm amounts of Cronobacter sakazakii, Serratia marcescens and Yersinia enterocolitica. AAA reduced growth and biofilm amounts of the three pathogens, albeit at rather high concentrations of 10 to 35 mg ml . Acetoacetate at a concentration of 5 mg ml reduced Y. enterocolitica mRNA transcripts of the flagellar master regulator operon flhD, the invasion gene inv, and the adhesion gene yadA. Transcription of the regulator of plasmid-encoded virulence genes virF, the plasmid-encoded virulence gene yopQ, and ymoA were largely unaffected by AAA. Importantly, AAA did not cause an increase in transcription of any of the tested virulence genes. As a more cost efficient homologue of AAA, the effect of ethyl acetoacetate (EAA) was tested. EAA reduced growth, biofilm amounts and live bacterial cell counts up to 3 logs. IC values ranged from 0·31 mg ml to 5·6 mg ml . In summary, both AAA and EAA inhibit biofilm, but EAA appears to be more effective. SIGNIFICANCE AND IMPACT OF THE STUDY: Bacterial biofilms are communities of bacteria that form on surfaces and are extremely difficult to remove by conventional physical or chemical techniques, antibiotics or the human immune system. Despite advanced technologies, biofilm still contributes to 60 to 80% of human bacterial infections (NIH and CDC) and cause problems in many natural, environmental, bioindustrial or food processing settings. The discovery of novel substances that inhibit biofilm without increasing the virulence of the bacteria opens doors for countless applications where a reduction of biofilm is desired.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180209
[Lr] Last revision date:180209
[St] Status:Publisher
[do] DOI:10.1111/lam.12852


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