scholarly journals Apple Flavonoid Phloretin Inhibits Escherichia coli O157:H7 Biofilm Formation and Ameliorates Colon Inflammation in Rats

2011 ◽  
Vol 79 (12) ◽  
pp. 4819-4827 ◽  
Author(s):  
Jin-Hyung Lee ◽  
Sushil Chandra Regmi ◽  
Jung-Ae Kim ◽  
Moo Hwan Cho ◽  
Hyungdon Yun ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Antimicrobial Agents ◽  
Trinitrobenzene Sulfonic Acid ◽  
Content Type ◽  
E Coli ◽  
Colon Inflammation ◽  
K 12

ABSTRACTPathogenic biofilms have been associated with persistent infections due to their high resistance to antimicrobial agents, while commensal biofilms often fortify the host's immune system. Hence, controlling biofilm formation of both pathogenic bacteria and commensal bacteria is important in bacterium-related diseases. We investigated the effect of plant flavonoids on biofilm formation of enterohemorrhagicEscherichia coliO157:H7. The antioxidant phloretin, which is abundant in apples, markedly reducedE. coliO157:H7 biofilm formation without affecting the growth of planktonic cells, while phloretin did not harm commensalE. coliK-12 biofilms. Also, phloretin reducedE. coliO157:H7 attachment to human colon epithelial cells. Global transcriptome analyses revealed that phloretin repressed toxin genes (hlyEandstx2), autoinducer-2 importer genes (lsrACDBF), curli genes (csgAandcsgB), and dozens of prophage genes inE. coliO157:H7 biofilm cells. Electron microscopy confirmed that phloretin reduced fimbria production inE. coliO157:H7. Also, phloretin suppressed the tumor necrosis factor alpha-induced inflammatory responsein vitrousing human colonic epithelial cells. Moreover, in the rat model of colitis induced by trinitrobenzene sulfonic acid (TNBS), phloretin significantly ameliorated colon inflammation and body weight loss. Taken together, our results suggest that the antioxidant phloretin also acts as an inhibitor ofE. coliO157:H7 biofilm formation as well as an anti-inflammatory agent in inflammatory bowel diseases without harming beneficial commensalE. colibiofilms.

scholarly journals Bioinformatic and Molecular Analysis of Inverse Autotransporters from Escherichia coli

mSphere ◽  
2019 ◽  
Vol 4 (4) ◽  
Author(s):  
Kelvin G. K. Goh ◽  
Danilo G. Moriel ◽  
Steven J. Hancock ◽  
Minh-Duy Phan ◽  
Mark A. Schembri
Keyword(s):  
Escherichia Coli ◽  
Cell Surface ◽  
Biofilm Formation ◽  
Secretion System ◽  
Content Type ◽  
E Coli ◽  
Wide Range ◽  
Type V Secretion ◽  
K 12 ◽  
Type V

ABSTRACT Proteins secreted by the type V secretion system possess multiple functions, including the capacity to mediate adhesion, aggregation, and biolfilm formation. The type V secretion system can be divided into five subclasses, one of which is the type Ve system. Proteins of the type Ve secretion system are also referred to as inverse autotransporters (IATs). In this study, we performed an in silico analysis of 126 completely sequenced Escherichia coli genomes available in the NCBI database and identified several distinct IAT-encoding gene families whose distribution varied throughout the E. coli phylogeny. The genes included three characterized IATs (intimin, fdeC, and yeeJ) and four uncharacterized IATs (here named iatA, iatB, iatC, and iatD). The four iat genes were cloned from the completely sequenced environmental E. coli strain SMS-3-5 and characterized. Three of these IAT proteins (IatB, IatC, and IatD) were expressed at the cell surface and possessed the capacity to mediate biofilm formation in a recombinant E. coli K-12 strain. Further analysis of the iatB gene, which showed a unique association with extraintestinal E. coli strains, suggested that its regulation is controlled by the LeuO global regulator. Overall, this study provides new data describing the prevalence, sequence variation, domain structure, function, and regulation of IATs found in E. coli. IMPORTANCE Escherichia coli is one of the most prevalent facultative anaerobes of the human gut. E. coli normally exists as a harmless commensal but can also cause disease following the acquisition of genes that enhance its pathogenicity. Adhesion is an important first step in colonization of the host and is mediated by an array of cell surface components. In E. coli, these include a family of adhesins secreted by the type V secretion system. Here, we identified and characterized new proteins from an emerging subclass of the type V secretion system known as the inverse autotransporters (IATs). We found that IAT-encoding genes are present in a wide range of strains and showed that three novel IATs were localized on the E. coli cell surface and mediated biofilm formation. Overall, this study provides new insight into the prevalence, function, and regulation of IATs in E. coli.

scholarly journals The Gene tia, Harbored by the Subtilase-Encoding Pathogenicity Island, Is Involved in the Ability of Locus of Enterocyte Effacement-Negative Shiga Toxin-Producing Escherichia coli Strains To Invade Monolayers of Epithelial Cells

2017 ◽  
Vol 85 (12) ◽  
Author(s):  
Roslen Bondì ◽  
Paola Chiani ◽  
Valeria Michelacci ◽  
Fabio Minelli ◽  
Alfredo Caprioli ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Shiga Toxin ◽  
Cultured Cells ◽  
Pathogenicity Island ◽  
Content Type ◽  
Cell Monolayers ◽  
E Coli ◽  
Enterocyte Effacement ◽  
K 12

ABSTRACT Locus of enterocyte effacement (LEE)-negative Shiga toxin (Stx)-producing Escherichia coli (STEC) strains are human pathogens that lack the LEE locus, a pathogenicity island (PAI) involved in the intimate adhesion of LEE-positive strains to the host gut epithelium. The mechanism used by LEE-negative STEC strains to colonize the host intestinal mucosa is still not clear. The cell invasion determinant tia, previously described in enterotoxigenic E. coli strains, has been identified in LEE-negative STEC strains that possess the subtilase-encoding pathogenicity island (SE-PAI). We evaluated the role of the gene tia, present in these LEE-negative STEC strains, in the invasion of monolayers of cultured cells. We observed that these strains were able to invade Caco-2 and HEp-2 cell monolayers and compared their invasion ability with that of a mutant strain in which the gene tia had been inactivated. Mutation of the gene tia resulted in a strong reduction of the invasive phenotype, and complementation of the tia mutation with a functional copy of the gene restored the invasion activity. Moreover, we show that the gene tia is overexpressed in bacteria actively invading cell monolayers, demonstrating that tia is involved in the ability to invade cultured monolayers of epithelial cells shown by SE-PAI-positive E. coli, including STEC, strains. However, the expression of the tia gene in the E. coli K-12 strain JM109 was not sufficient, in its own right, to confer to this strain the ability to invade cell monolayers, suggesting that at least another factor must be involved in the invasion ability displayed by the SE-PAI-positive strains.

scholarly journals Type III Secretion-Dependent Sensitivity of Escherichia coli O157 to Specific Ketolides

2015 ◽  
Vol 60 (1) ◽  
pp. 459-470 ◽  
Author(s):  
Romina J. Fernandez-Brando ◽  
Nao Yamaguchi ◽  
Amin Tahoun ◽  
Sean P. McAteer ◽  
Trudi Gillespie ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Type Iii Secretion ◽  
Pathogenic Bacteria ◽  
Bacterial Colonization ◽  
Effector Proteins ◽  
Content Type ◽  
E Coli ◽  
Type Iii ◽  
Bacterial Binding

ABSTRACTA subset of Gram-negative bacterial pathogens uses a type III secretion system (T3SS) to open up a conduit into eukaryotic cells in order to inject effector proteins. These modulate pathways to enhance bacterial colonization. In this study, we screened established bioactive compounds for any that could repress T3SS expression in enterohemorrhagicEscherichia coli(EHEC) O157. The ketolides telithromycin and, subsequently, solithromycin both demonstrated repressive effects on expression of the bacterial T3SS at sub-MICs, leading to significant reductions in bacterial binding and actin-rich pedestal formation on epithelial cells. Preincubation of epithelial cells with solithromycin resulted in significantly less attachment ofE. coliO157. Moreover, bacteria expressing the T3SS were more susceptible to solithromycin, and there was significant preferential killing ofE. coliO157 bacteria when they were added to epithelial cells that had been preexposed to the ketolide. This killing was dependent on expression of the T3SS. Taken together, this research indicates that the ketolide that has accumulated in epithelial cells may traffic back into the bacteria via the T3SS. Considering that neither ketolide induces the SOS response, nontoxic members of this class of antibiotics, such as solithromycin, should be considered for future testing and trials evaluating their use for treatment of EHEC infections. These antibiotics may also have broader significance for treating infections caused by other pathogenic bacteria, including intracellular bacteria, that express a T3SS.

scholarly journals Regulation of Cell Division, Biofilm Formation, and Virulence by FlhC in Escherichia coli O157:H7 Grown on Meat

2011 ◽  
Vol 77 (11) ◽  
pp. 3653-3662 ◽  
Author(s):  
Preeti Sule ◽  
Shelley M. Horne ◽  
Catherine M. Logue ◽  
Birgit M. Prüß
Keyword(s):  
Escherichia Coli ◽  
Cell Division ◽  
Real Time ◽  
Real Time Pcr ◽  
Biofilm Formation ◽  
Parent Strain ◽  
Cellular Functions ◽  
Content Type ◽  
E Coli ◽  
K 12

ABSTRACTTo understand the continuous problems thatEscherichia coliO157:H7 causes as food pathogen, this study assessed global gene regulation in bacteria growing on meat. Since FlhD/FlhC ofE. coliK-12 laboratory strains was previously established as a major control point in transducing signals from the environment to several cellular processes, this study compared the expression pattern of anE. coliO157:H7 parent strain to that of its isogenicflhCmutant. This was done with bacteria that had been grown on meat. Microarray experiments revealed 287 putative targets of FlhC. Real-time PCR was performed as an alternative estimate of transcription and confirmed microarray data for 13 out of 15 genes tested (87%). The confirmed genes are representative of cellular functions, such as central metabolism, cell division, biofilm formation, and pathogenicity. An additional 13 genes from the same cellular functions that had not been hypothesized as being regulated by FlhC by the microarray experiment were tested with real-time PCR and also exhibited higher expression levels in theflhCmutant than in the parent strain. Physiological experiments were performed and confirmed that FlhC reduced the cell division rate, the amount of biofilm biomass, and pathogenicity in a chicken embryo lethality model. Altogether, this study provides valuable insight into the complex regulatory network of the pathogen that enables its survival under various environmental conditions. This information may be used to develop strategies that could be used to reduce the number of cells or pathogenicity ofE. coliO157:H7 on meat by interfering with the signal transduction pathways.

scholarly journals Draft Genome Sequences of Semiconstitutive Red, Dry, and Rough Biofilm-Forming Commensal and Uropathogenic Escherichia coli Isolates

2017 ◽  
Vol 5 (4) ◽  
Author(s):  
Annika Cimdins ◽  
Petra Lüthje ◽  
Fengyang Li ◽  
Irfan Ahmad ◽  
Annelie Brauner ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Molecular Basis ◽  
Draft Genome ◽  
Uropathogenic Escherichia Coli ◽  
Clinical Isolates ◽  
Genome Sequences ◽  
Content Type ◽  
E Coli ◽  
K 12

ABSTRACT Strains of Escherichia coli exhibit diverse biofilm formation capabilities. E. coli K-12 expresses the red, dry, and rough (rdar) morphotype below 30°C, whereas clinical isolates frequently display the rdar morphotype semiconstitutively. We sequenced the genomes of eight E. coli strains to subsequently investigate the molecular basis of semiconstitutive rdar morphotype expression.

scholarly journals Regulation ofwaaHby PhoB during PiStarvation Promotes Biofilm Formation byEscherichia coliO157:H7

2019 ◽  
Vol 201 (18) ◽  
Author(s):  
Philippe Vogeleer ◽  
Antony T. Vincent ◽  
Samuel M. Chekabab ◽  
Steve J. Charette ◽  
Alexey Novikov ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Ecological Niches ◽  
Pho Regulon ◽  
Starvation Stress ◽  
Content Type ◽  
E Coli ◽  
Expression Of Genes ◽  
K 12 ◽  
Pst System

ABSTRACTIn open environments such as water, enterohemorrhagicEscherichia coliO157:H7 responds to inorganic phosphate (Pi) starvation by inducing the Pho regulon controlled by PhoB. This activates the phosphate-specific transport (Pst) system that contains a high-affinity Pitransporter. In the Δpstmutant, PhoB is constitutively activated and regulates the expression of genes in the Pho regulon. Here, we show that Pistarvation and deletion of thepstsystem enhanceE. coliO157:H7 biofilm formation. Among differentially expressed genes of EDL933 grown under Pistarvation conditions and in the Δpstmutant, we have found that a member of the PhoB regulon,waaH, predicted to encode a glycosyltransferase, was highly expressed. Interestingly, WaaH contributed to biofilm formation ofE. coliO157:H7 during both Pistarvation and in the Δpstmutant. In the Δpstmutant, the presence ofwaaHwas associated with lipopolysaccharide (LPS) R3 core type modifications, whereas inE. coliO157:H7,waaHoverexpression had no effect on LPS structure during Pistarvation. Therefore,waaHparticipates inE. coliO157:H7 biofilm formation during Pistarvation, but its biochemical role remains to be clarified. This study highlights the importance of the Pistarvation stress response to biofilm formation, which may contribute to the persistence ofE. coliO157:H7 in the environment.IMPORTANCEEnterohemorrhagicEscherichia coliO157:H7 is a human pathogen that causes bloody diarrhea that can result in renal failure. Outside of mammalian hosts,E. coliO157:H7 survives for extended periods of time in nutrient-poor environments, likely as part of biofilms. InE. coliK-12, the levels of free extracellular Piaffect biofilm formation; however, it was unknown whether Piinfluences biofilm formation byE. coliO157:H7. Our results show that upon Pistarvation, PhoB activateswaaHexpression, which favors biofilm formation byE. coliO157:H7. These findings suggest that WaaH is a target for controlling biofilm formation. Altogether, our work demonstrates how adaptation to Pistarvation allowsE. coliO157:H7 to occupy different ecological niches.

scholarly journals Enzymatically Active and Inactive Phosphodiesterases and Diguanylate Cyclases Are Involved in Regulation of Motility or Sessility in Escherichia coli CFT073

mBio ◽  
2012 ◽  
Vol 3 (5) ◽  
Author(s):  
Rachel R. Spurbeck ◽  
Rebecca J. Tarrien ◽  
Harry L. T. Mobley
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Biofilm Formation ◽  
Second Messenger ◽  
Content Type ◽  
E Coli ◽  
Diguanylate Cyclases ◽  
Genes Encoding ◽  
K 12 ◽  
Messenger Molecule

ABSTRACTIntracellular concentration of cyclic diguanylate monophosphate (c-di-GMP), a second messenger molecule, is regulated in bacteria by diguanylate cyclases (DGCs) (synthesizing c-di-GMP) and phosphodiesterases (PDEs) (degrading c-di-GMP). c-di-GMP concentration ([c-di-GMP]) affects motility and sessility in a reciprocal fashion; high [c-di-GMP] typically inhibits motility and promotes sessility. A c-di-GMP sensor domain, PilZ, also regulates motility and sessility. UropathogenicEscherichia coliregulates these processes during infection; motility is necessary for ascending the urinary tract, while sessility is essential for colonization of anatomical sites. Here, we constructed and screened 32 mutants containing deletions of genes encoding each PDE (n= 11), DGC (n= 13), PilZ (n= 2), and both PDE and DGC (n= 6) domains for defects in motility, biofilm formation, and adherence for the prototypical pyelonephritis isolateE. coliCFT073. Three of 32 mutations affected motility, all of which were in genes encoding enzymatically inactive PDEs. Four PDEs, eight DGCs, four PDE/DGCs, and one PilZ regulated biofilm formation in a medium-specific manner. Adherence to bladder epithelial cells was regulated by [c-di-GMP]. Four PDEs, one DGC, and three PDE/DGCs repress adherence and four DGCs and one PDE/DGC stimulate adherence. Thus, specific effectors of [c-di-GMP] and catalytically inactive DGCs and PDEs regulate adherence and motility in uropathogenicE. coli.IMPORTANCEUropathogenicEscherichia coli(UPEC) contains several genes annotated as encoding enzymes that increase or decrease the abundance of the second messenger molecule, c-di-GMP. While this class of enzymes has been studied in anE. coliK-12 lab strain, these proteins have not been comprehensively examined in UPEC. UPEC utilizes both swimming motility and adherence to colonize and ascend the urinary tract; both of these processes are hypothesized to be regulated by the concentration of c-di-GMP. Here, for the first time, in a uropathogenic strain,E. coliCFT073, we have characterized mutants lacking each protein and demonstrated that the uropathogen has diverged fromE. coliK-12 to utilize these enzymes to regulate adherence and motility by distinct mechanisms.

scholarly journals Effect of Spermidine on Biofilm Formation in Escherichia coli K-12

2021 ◽  
Vol 203 (10) ◽  
Author(s):  
Kullathida Thongbhubate ◽  
Yuko Nakafuji ◽  
Rina Matsuoka ◽  
Sonomi Kakegawa ◽  
Hideyuki Suzuki
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Efflux Pump ◽  
Conclusive Evidence ◽  
Bacterial Biofilm ◽  
Spermidine Synthase ◽  
Periplasmic Binding Protein ◽  
Content Type ◽  
E Coli ◽  
K 12

ABSTRACT Polyamines are essential for biofilm formation in Escherichia coli, but it is still unclear which polyamines are primarily responsible for this phenomenon. To address this issue, we constructed a series of E. coli K-12 strains with mutations in genes required for the synthesis and metabolism of polyamines. Disruption of the spermidine synthase gene (speE) caused a severe defect in biofilm formation. This defect was rescued by the addition of spermidine to the medium but not by putrescine or cadaverine. A multidrug/spermidine efflux pump membrane subunit (MdtJ)-deficient strain was anticipated to accumulate more spermidine and result in enhanced biofilm formation compared to the MdtJ+ strain. However, the mdtJ mutation did not affect intracellular spermidine or biofilm concentrations. E. coli has the spermidine acetyltransferase (SpeG) and glutathionylspermidine synthetase/amidase (Gss) to metabolize intracellular spermidine. Under biofilm-forming conditions, not Gss but SpeG plays a major role in decreasing the too-high intracellular spermidine concentrations. Additionally, PotFGHI can function as a compensatory importer of spermidine when PotABCD is absent under biofilm-forming conditions. Last, we report here that, in addition to intracellular spermidine, the periplasmic binding protein (PotD) of the spermidine preferential ABC transporter is essential for stimulating biofilm formation. IMPORTANCE Previous reports have speculated on the effect of polyamines on bacterial biofilm formation. However, the regulation of biofilm formation by polyamines in Escherichia coli has not yet been assessed. The identification of polyamines that stimulate biofilm formation is important for developing novel therapies for biofilm-forming pathogens. This study sheds light on biofilm regulation in E. coli. Our findings provide conclusive evidence that only spermidine can stimulate biofilm formation in E. coli cells, not putrescine or cadaverine. Last, ΔpotD inhibits biofilm formation even though the spermidine is synthesized inside the cells from putrescine. Since PotD is significant for biofilm formation and there is no ortholog of the PotABCD transporter in humans, PotD could be a target for the development of biofilm inhibitors.

scholarly journals Genotypic and Phenotypic Characteristics Associated with Biofilm Formation by Human Clinical Escherichia coli Isolates of Different Pathotypes

2017 ◽  
Vol 83 (24) ◽  
Author(s):  
Juliane Schiebel ◽  
Alexander Böhm ◽  
Jörg Nitschke ◽  
Michał Burdukiewicz ◽  
Jörg Weinreich ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Polymeric Matrix ◽  
Bacterial Biofilm ◽  
Automated Image Analysis ◽  
Host Immune System ◽  
Content Type ◽  
E Coli ◽  
Initial Adhesion ◽  
K 12

ABSTRACT Bacterial biofilm formation is a widespread phenomenon and a complex process requiring a set of genes facilitating the initial adhesion, maturation, and production of the extracellular polymeric matrix and subsequent dispersal of bacteria. Most studies on Escherichia coli biofilm formation have investigated nonpathogenic E. coli K-12 strains. Due to the extensive focus on laboratory strains in most studies, there is poor information regarding biofilm formation by pathogenic E. coli isolates. In this study, we genotypically and phenotypically characterized 187 human clinical E. coli isolates representing various pathotypes (e.g., uropathogenic, enteropathogenic, and enteroaggregative E. coli). We investigated the presence of biofilm-associated genes (“genotype”) and phenotypically analyzed the isolates for motility and curli and cellulose production (“phenotype”). We developed a new screening method to examine the in vitro biofilm formation ability. In summary, we found a high prevalence of biofilm-associated genes. However, we could not detect a biofilm-associated gene or specific phenotype correlating with the biofilm formation ability. In contrast, we did identify an association of increased biofilm formation with a specific E. coli pathotype. Enteroaggregative E. coli (EAEC) was found to exhibit the highest capacity for biofilm formation. Using our image-based technology for the screening of biofilm formation, we demonstrated the characteristic biofilm formation pattern of EAEC, consisting of thick bacterial aggregates. In summary, our results highlight the fact that biofilm-promoting factors shown to be critical for biofilm formation in nonpathogenic strains do not reflect their impact in clinical isolates and that the ability of biofilm formation is a defined characteristic of EAEC. IMPORTANCE Bacterial biofilms are ubiquitous and consist of sessile bacterial cells surrounded by a self-produced extracellular polymeric matrix. They cause chronic and device-related infections due to their high resistance to antibiotics and the host immune system. In nonpathogenic Escherichia coli, cell surface components playing a pivotal role in biofilm formation are well known. In contrast, there is poor information for their role in biofilm formation of pathogenic isolates. Our study provides insights into the correlation of biofilm-associated genes or specific phenotypes with the biofilm formation ability of commensal and pathogenic E. coli. Additionally, we describe a newly developed method enabling qualitative biofilm analysis by automated image analysis, which is beneficial for high-throughput screenings. Our results help to establish a better understanding of E. coli biofilm formation.

scholarly journals Interleukin-8, CXCL1, and MicroRNA miR-146a Responses to Probiotic Escherichia coli Nissle 1917 and Enteropathogenic E. coli in Human Intestinal Epithelial T84 and Monocytic THP-1 Cells after Apical or Basolateral Infection

2016 ◽  
Vol 84 (9) ◽  
pp. 2482-2492 ◽  
Author(s):  
Harshana Sabharwal ◽  
Christoph Cichon ◽  
Tobias A. Ölschläger ◽  
Ulrich Sonnenborn ◽  
M. Alexander Schmidt
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Pathogenic Bacteria ◽  
Interleukin 8 ◽  
Model Systems ◽  
Probiotic Properties ◽  
Content Type ◽  
E Coli ◽  
Apical Side ◽  
Basolateral Side

Bacterium-host interactions in the gut proceed via directly contacted epithelial cells, the host's immune system, and a plethora of bacterial factors. Here we characterized and compared exemplary cytokine and microRNA (miRNA) responses of human epithelial and THP-1 cells toward the prototype enteropathogenicEscherichia coli(EPEC) strain E2348/69 (O127:H6) and the probiotic strainEscherichia coliNissle 1917 (EcN) (O6:K5:H1). Human T84 and THP-1 cells were used as cell culture-based model systems for epithelial and monocytic cells. Polarized T84 monolayers were infected apically or basolaterally. Bacterial challenges from the basolateral side resulted in more pronounced cytokine and miRNA responses than those observed for apical side infections. Interestingly, the probiotic EcN also caused a pronounced transcriptional increase of proinflammatory CXCL1 and interleukin-8 (IL-8) levels when human T84 epithelial cells were infected from the basolateral side. miR-146a, which is known to regulate adaptor molecules in Toll-like receptor (TLR)/NF-κB signaling, was found to be differentially regulated in THP-1 cells between probiotic and pathogenic bacteria. To assess the roles of flagella and flagellin, we employed several flagellin mutants of EcN. EcN flagellin mutants induced reduced IL-8 as well as CXCL1 responses in T84 cells, suggesting that flagellin is an inducer of this cytokine response. Following infection with an EPEC type 3 secretion system (T3SS) mutant, we observed increased IL-8 and CXCL1 transcription in T84 and THP-1 cells compared to that in wild-type EPEC. This study emphasizes the differential induction of miR-146a by pathogenic and probioticE. colistrains in epithelial and immune cells as well as a loss of probiotic properties in EcN interacting with cells from the basolateral side.

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