scholarly journals P fimbriae and other adhesins enhance intestinal persistence of Escherichia coli in early infancy

1998 ◽  
Vol 121 (3) ◽  
pp. 599-608 ◽  
Author(s):  
I. ADLERBERTH ◽  
C. SVANBORG ◽  
B. CARLSSON ◽  
L. MELLANDER ◽  
L.-Å. HANSON ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Line ◽  
Intestinal Epithelial Cells ◽  
Antigen Expression ◽  
Intestinal Epithelial ◽  
E Coli ◽  
O Antigen ◽  
Ht 29 ◽  
Intestinal Persistence

Resident and transient Escherichia coli strains were identified in the rectal flora of 22 Pakistani infants followed from birth to 6 months of age. All strains were tested for O-antigen expression, adhesin specificity (P fimbriae, other mannose-resistant adhesins or type 1 fimbriae) and adherence to the colonic cell line HT-29. Resident strains displayed higher mannose- resistant adherence to HT-29 cells, and expressed P fimbriae (P=0·0036) as well as other mannose-resistant adhesins (P=0·012) more often than transient strains. In strains acquired during the first month of life, P fimbriae were 12 times more frequent in resident than in transient strains (P=0·0006). The O-antigen distribution did not differ between resident and transient strains, and none of the resident P-fimbriated strains belonged to previously recognized uropathogenic clones. The results suggest that adhesins mediating adherence to intestinal epithelial cells, especially P fimbriae, enhance the persistence of E. coli in the large intestine of infants.

Immunogenicity Evaluation of Chimeric Subunit Vaccine Comprising Adhesion Coli Surface Antigens from Enterotoxigenic Escherichia coli

2019 ◽  
Vol 29 (1-6) ◽  
pp. 91-100
Author(s):  
Dorna Khoobbakht ◽  
Shohreh Zare Karizi ◽  
Mohammad Javad  Motamedi ◽  
Rouhollah Kazemi ◽  
Pooneh Roghanian ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Subunit Vaccine ◽  
Fusion Gene ◽  
Intestinal Epithelial Cells ◽  
High Titer ◽  
Chimeric Protein ◽  
Amino Acid Sequences ◽  
Intestinal Epithelial ◽  
E Coli

Enterotoxigenic <i>Escherichia coli</i> (ETEC) is the most common agent of diarrhea morbidity in developing countries. ETEC adheres to host intestinal epithelial cells via various colonization factors. The CooD and CotD proteins play a significant role in bacteria binding to the intestinal epithelial cells as adhesin tip subunits of CS1 and CS2 pili. The purpose here was to design a new construction containing <i>cooD</i> and <i>cotD</i> genes and use several types of bioinformatics software to predict the structural and immunological properties of the designed antigen. The fusion gene was synthesized with codon bias of <i>E. coli</i> in order to increase the expression level of the protein. The amino acid sequences, protein structure, and immunogenicity properties of potential antigens were analyzed in silico. The chimeric protein was expressed in <i>E. coli</i>BL21 (DE3). The antigenicity of the recombinant proteins was verified by Western blotting and ELISA. In order to assess the induced immunity, the immunized mice were challenged with wild-type ETEC by an intraperitoneal route. Immunological analyses showed the production of a high titer of IgG serum with no sign of serum-mucosal IgA antibody response. The result of the challenge assay showed that 30% of immunized mice survived. The results of this study showed that CooD-CotD recombinant protein can stimulate immunity against ETEC. The designed chimera could be a prototype for the subunit vaccine, which is worthy of further consideration.

scholarly journals Adherent-Invasive E. coli: Update on the Lifestyle of a Troublemaker in Crohn’s Disease

2020 ◽  
Vol 21 (10) ◽  
pp. 3734 ◽  
Author(s):  
Mélissa Chervy ◽  
Nicolas Barnich ◽  
Jérémy Denizot
Keyword(s):  
Escherichia Coli ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Genetic Factors ◽  
Intestinal Epithelial Cells ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
E Coli ◽  
The Subject ◽  
The Impact

Besides genetic polymorphisms and environmental factors, the intestinal microbiota is an important factor in the etiology of Crohn’s disease (CD). Among microbiota alterations, a particular pathotype of Escherichia coli involved in the pathogenesis of CD abnormally colonizes the intestinal mucosa of patients: the adherent-invasive Escherichia coli (AIEC) pathobiont bacteria, which have the abilities to adhere to and to invade intestinal epithelial cells (IECs), as well as to survive and replicate within macrophages. AIEC have been the subject of many studies in recent years to unveil some genes linked to AIEC virulence and to understand the impact of AIEC infection on the gut and consequently their involvement in CD. In this review, we describe the lifestyle of AIEC bacteria within the intestine, from the interaction with intestinal epithelial and immune cells with an emphasis on environmental and genetic factors favoring their implantation, to their lifestyle in the intestinal lumen. Finally, we discuss AIEC-targeting strategies such as the use of FimH antagonists, bacteriophages, or antibiotics, which could constitute therapeutic options to prevent and limit AIEC colonization in CD patients.

scholarly journals Probiotic Escherichia coli Nissle 1917 and Commensal E. coli K12 Differentially Affect the Inflammasome in Intestinal Epithelial Cells

Digestion ◽  
2014 ◽  
Vol 89 (2) ◽  
pp. 110-118 ◽  
Author(s):  
Helen M. Becker ◽  
Aretussa Apladas ◽  
Michael Scharl ◽  
Michael Fried ◽  
Gerhard Rogler
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
E Coli

scholarly journals Inflammation-Induced Acid Tolerance GenesgadABin Luminal Commensal Escherichia coli Attenuate Experimental Colitis

2013 ◽  
Vol 81 (10) ◽  
pp. 3662-3671 ◽  
Author(s):  
Sandrine Tchaptchet ◽  
Ting-Jia Fan ◽  
Laura Goeser ◽  
Alexi Schoenborn ◽  
Ajay S. Gulati ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Immune Responses ◽  
Intestinal Inflammation ◽  
Intestinal Epithelial Cells ◽  
Acid Tolerance ◽  
Experimental Colitis ◽  
Intestinal Epithelial ◽  
Content Type ◽  
E Coli ◽  
Chronic Intestinal Inflammation

ABSTRACTDysregulated immune responses to commensal intestinal bacteria, includingEscherichia coli, contribute to the development of inflammatory bowel diseases (IBDs) and experimental colitis. Reciprocally,E. coliresponds to chronic intestinal inflammation by upregulating expression of stress response genes, includinggadAandgadB. GadAB encode glutamate decarboxylase and protectE. colifrom the toxic effects of low pH and fermentation acids, factors present in the intestinal lumen in patients with active IBDs. We hypothesized thatE. coliupregulatesgadABduring inflammation to enhance its survival and virulence. Using real-time PCR, we determinedgadABexpression in luminalE. colifrom ex-germfree wild-type (WT) and interleukin-10 (IL-10) knockout (KO) (IL-10−/−) mice selectively colonized with a commensalE. coliisolate (NC101) that causes colitis in KO mice in isolation or in combination with 7 other commensal intestinal bacterial strains.E. colisurvival and host inflammatory responses were measured in WT and KO mice colonized with NC101 or a mutant lacking thegadABgenes (NC101ΔgadAB). The susceptibility of NC101 and NC101ΔgadABto killing by host antimicrobial peptides and their translocation across intestinal epithelial cells were evaluated using bacterial killing assays and transwell experiments, respectively. We show that expression ofgadABin luminalE. coliincreases proportionately with intestinal inflammation in KO mice and enhances the susceptibility of NC101 to killing by the host antimicrobial peptide cryptdin-4 but decreases bacterial transmigration across intestinal epithelial cells, colonic inflammation, and mucosal immune responses. Chronic intestinal inflammation upregulates acid tolerance pathways in commensalE. coliisolates, which, contrary to our original hypothesis, limits their survival and colitogenic potential. Further investigation of microbial adaptation to immune-mediated inflammation may provide novel insights into the pathogenesis and treatment of IBDs.

scholarly journals Escherichia coli O157:H7 Strains That Persist in Feedlot Cattle Are Genetically Related and Demonstrate an Enhanced Ability To Adhere to Intestinal Epithelial Cells

2009 ◽  
Vol 75 (18) ◽  
pp. 5927-5937 ◽  
Author(s):  
Brandon A. Carlson ◽  
Kendra K. Nightingale ◽  
Gary L. Mason ◽  
John R. Ruby ◽  
W. Travis Choat ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Multiplex Pcr ◽  
Intestinal Epithelial Cells ◽  
Feedlot Cattle ◽  
Pfge Type ◽  
Sample Population ◽  
Intestinal Epithelial ◽  
E Coli ◽  
Multiplex Pcr Assay

ABSTRACT A longitudinal study was conducted to investigate the nature of Escherichia coli O157:H7 colonization of feedlot cattle over the final 100 to 110 days of finishing. Rectal fecal grab samples were collected from an initial sample population of 788 steers every 20 to 22 days and microbiologically analyzed to detect E. coli O157:H7. The identities of presumptive colonies were confirmed using a multiplex PCR assay that screened for gene fragments unique to E. coli O157:H7 (rfbE and fliC h7) and other key virulence genes (eae, stx 1, and stx 2). Animals were classified as having persistent shedding (PS), transient shedding (TS), or nonshedding (NS) status if they consecutively shed the same E. coli O157:H7 genotype (based on the multiplex PCR profile), exhibited variable E. coli O157 shedding, or never shed morphologically typical E. coli O157, respectively. Overall, 1.0% and 1.4% of steers were classified as PS and NS animals, respectively. Characterization of 132 E. coli O157:H7 isolates from PS and TS animals by pulsed-field gel electrophoresis (PFGE) typing yielded 32 unique PFGE types. One predominant PFGE type accounted for 53% of all isolates characterized and persisted in cattle throughout the study. Isolates belonging to this predominant and persistent PFGE type demonstrated an enhanced (P < 0.0001) ability to adhere to Caco-2 human intestinal epithelial cells compared to isolates belonging to less common PFGE types but exhibited equal virulence expression. Interestingly, the attachment efficacy decreased as the genetic divergence from the predominant and persistent subtype increased. Our data support the hypothesis that certain E. coli O157:H7 strains persist in feedlot cattle, which may be partially explained by an enhanced ability to colonize the intestinal epithelium.

scholarly journals Enteropathogenic Escherichia coli Activates Ezrin, Which Participates in Disruption of Tight Junction Barrier Function

2001 ◽  
Vol 69 (9) ◽  
pp. 5679-5688 ◽  
Author(s):  
Ivana Simonovic ◽  
Monique Arpin ◽  
Athanasia Koutsouris ◽  
Holly J. Falk-Krzesinski ◽  
Gail Hecht
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Cytoskeletal Proteins ◽  
Dominant Negative ◽  
Intestinal Epithelial ◽  
E Coli ◽  
Membrane Cytoskeleton ◽  
Intestinal Pathogen ◽  
Response Expression

ABSTRACT Enteropathogenic Escherichia coli (EPEC) is an important human intestinal pathogen, especially in infants. EPEC adherence to intestinal epithelial cells induces the accumulation of a number of cytoskeletal proteins beneath the bacteria, including the membrane-cytoskeleton linker ezrin. Evidence suggests that ezrin can participate in signal transduction. The aim of this study was to determine whether ezrin is activated following EPEC infection and if it is involved in the cross talk with host intestinal epithelial cells. We show here that following EPEC attachment to intestinal epithelial cells there was significant phosphorylation of ezrin, first on threonine and later on tyrosine residues. A significant increase in cytoskeleton-associated ezrin occurred following phosphorylation, suggesting activation of this molecule. Nonpathogenic E. coli and EPEC strains harboring mutations in type III secretion failed to elicit this response. Expression of dominant-negative ezrin significantly decreased the EPEC-elicited association of ezrin with the cytoskeleton and attenuated the disruption of intestinal epithelial tight junctions. These results suggest that ezrin is involved in transducing EPEC-initiated signals that ultimately affect host physiological functions.

scholarly journals The Oxidoreductase DsbA Plays a Key Role in the Ability of the Crohn's Disease-Associated Adherent-Invasive Escherichia coli Strain LF82 To Resist Macrophage Killing

2007 ◽  
Vol 189 (13) ◽  
pp. 4860-4871 ◽  
Author(s):  
Marie-Agnès Bringer ◽  
Nathalie Rolhion ◽  
Anne-Lise Glasser ◽  
Arlette Darfeuille-Michaud
Keyword(s):  
Escherichia Coli ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Coli Strain ◽  
Intestinal Epithelial ◽  
Type 1 Pili ◽  
K 12

ABSTRACT Adherent-invasive Escherichia coli (AIEC) isolated from Crohn's disease patients is able to adhere to and invade intestinal epithelial cells and to replicate in mature phagolysosomes within macrophages. Here, we show that the dsbA gene, encoding a periplasmic oxidoreductase, was required for AIEC strain LF82 to adhere to intestinal epithelial cells and to survive within macrophages. The LF82-ΔdsbA mutant did not express flagella and, probably as a consequence of this, did not express type 1 pili. The role of DsbA in adhesion is restricted to the loss of flagella and type 1 pili, as forced contact between bacteria and cells and induced expression of type 1 pili restored the wild-type phenotype. In contrast, the dsbA gene is essential for AIEC LF82 bacteria to survive within macrophages, irrespective of the loss of flagella and type 1 pilus expression, and the survival ability of LF82-ΔdsbA was as low as that of the nonpathogenic E. coli K-12, which was efficiently killed by macrophages. We also provide evidence that the dsbA gene is needed for LF82 bacteria to grow and survive in an acidic and nutrient-poor medium that partly mimics the harsh environment of the phagocytic vacuole. In addition, under such stress conditions dsbA transcription is highly up-regulated. Finally, the CpxRA signaling pathway does not play a role in regulation of dsbA expression in AIEC LF82 bacteria under conditions similar to those of mature phagolysosomes.

scholarly journals Use of Fluorescence Quantitative Polymerase Chain Reaction (PCR) for the Detection of Escherichia coli Adhesion to Pig Intestinal Epithelial Cells

2016 ◽  
Vol 19 (3) ◽  
pp. 619-625 ◽  
Author(s):  
C.H. Dai ◽  
L.N. Gan ◽  
W.U. Qin ◽  
C. Zi ◽  
G.Q. Zhu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Polymerase Chain Reaction ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Relative Number ◽  
Intestinal Epithelial ◽  
Chain Reaction ◽  
E Coli ◽  
Polymerase Chain

AbstractAn efficient and accurate method to testEscherichia coli(E. coli) adhesion to intestinal epithelial cells will contribute to the study of bacterial pathogenesis and the function of genes that encode receptors related to adhesion. This study used the quantitative real-time polymerase chain reaction (qPCR) method. qPCR primers were designed from thePILINgene ofE. coliF18ab, F18ac, and K88ac, and the pig β-ACTINgene. Total deoxyribonucleic acid (DNA) fromE. coliand intestinal epithelial cells (IPEC-J2 cells) were used as templates for qPCR. The 2−ΔΔCtformula was used to calculate the relative number of bacteria in cultures of different areas. We found that the relative numbers of F18ab, F18ac, and K88ac that adhered to IPEC-J2 cells did not differ significantly in 6-, 12-, and 24-well culture plates. This finding indicated that there was no relationship between the relative adhesion number ofE. coliand the area of cells, so the method of qPCR could accurately test the relative number ofE. coli. This study provided a convenient and reliable testing method for experiments involvingE. coliadhesion, and also provided innovative ideas for similar detection methods.

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