scholarly journals Adhesion of enteropathogenic, enterotoxigenic and commensal Escherichia coli to the Major Zymogen Granule Membrane Glycoprotein 2

2022 ◽  
Author(s):  
Christin Bartlitz ◽  
Rafał Kolenda ◽  
Jarosław Chilimoniuk ◽  
Krzysztof Grzymajło ◽  
Stefan Rödiger ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Host Specificity ◽  
Pathogenic Bacteria ◽  
Cell Receptor ◽  
Membrane Glycoprotein ◽  
Zymogen Granule ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Granule Membrane

Pathogenic bacteria, such as enteropathogenic (EPEC) and enterotoxigenic Escherichia coli (ETEC), cause diarrhea in mammals. In particular, E. coli colonize and infect the gastrointestinal tract via type 1 fimbriae (T1F). Here the major zymogen granule membrane glycoprotein 2 (GP2) acts as host cell receptor. GP2 is also secreted by the pancreas and various mucous glands, interacting with luminal type 1 fimbriae-positive E. coli . It is unknown whether GP2 isoforms demonstrate specific E. coli pathotype binding. In this study, we investigated interactions of human, porcine and bovine EPEC, ETEC as well as commensal E. coli isolates with human, porcine and bovine GP2. We first defined pathotype- and host-associated FimH variants. Secondly, we could prove that GP2 isoforms bound to FimH variants to varying degrees. However, the GP2-FimH interactions did not seem to be influenced by the host specificity of E. coli . In contrast, soluble GP2 affected ETEC infection and phagocytosis rates of macrophages. Pre-incubation of ETEC pathotype with GP2 reduced infection of cell lines. Furthermore, pre-incubation of E. coli with GP2 improved the phagocytosis rate of macrophages. Our findings suggest that GP2 plays a role in the defense against E. coli infection and in the corresponding host immune response. IMPORTANCE Infection by pathogenic bacteria such as certain Escherichia coli pathotypes results in diarrhea in mammals. Pathogens, including zoonotic agents, can infect different hosts or show host-specificity. There are Escherichia coli strains which are frequently transmitted between humans and animals, whereas other Escherichia coli strains tend to colonize only one host. This host-specificity is still not fully understood. We show that glycoprotein 2 is a selective receptor for particular Escherichia coli strains or variants of the adhesin FimH but not a selector for a species-specific Escherichia coli group. We demonstrate that GP2 is involved in the regulation of colonization and infection and thus represents a molecule of interest for the prevention or treatment of disease.

scholarly journals Role of the ceramide-signaling pathway in cytokine responses to P-fimbriated Escherichia coli.

1996 ◽  
Vol 183 (3) ◽  
pp. 1037-1044 ◽  
Author(s):  
M Hedlund ◽  
M Svensson ◽  
A Nilsson ◽  
R D Duan ◽  
C Svanborg
Keyword(s):  
Escherichia Coli ◽  
Signaling Pathway ◽  
Kinase Inhibitors ◽  
Human Kidney ◽  
Cytokine Response ◽  
Protein Kinase Inhibitors ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Outer Leaflet

Escherichia coli express fimbriae-associated adhesins through which they attach to mucosal cells and activate a cytokine response. The receptors for E. coli P fimbriae are the globoseries of glycosphingolipids; Gal alpha 1-->4Gal beta-containing oligosaccharides bound to ceramide in the outer leaflet of the lipid bilayer. The receptors for type 1 fimbriae are mannosylated glycoproteins rather than glycolipids. This study tested the hypothesis that P-fimbriated E. coli elicit a cytokine response through the release of ceramide in the receptor-bearing cell. We used the A498 human kidney cell line, which expressed functional receptors for P and type 1 fimbriae and secreted higher levels of interleukin (IL)-6 when exposed to the fimbriated strains than to isogenic nonfimbriated controls. P-fimbriated E. coli caused the release of ceramide and increased the phosphorylation of ceramide to ceramide 1-phosphate. The IL-6 response to P-fimbriated E. coli was reduced by inhibitors of serine/threonine kinases but not by other protein kinase inhibitors. In contrast, ceramide levels were not influenced by type 1-fimbriated E. coli, and the IL-6 response was insensitive to the serine/threonine kinase inhibitors. These results demonstrate that the ceramide-signaling pathway is activated by P-fimbriated E. coli, and that the receptor specificity of the P fimbriae influences this process. We propose that this activation pathway contributes to the cytokine induction by P-fimbriated E. coli in epithelial cells.

scholarly journals Uropathogenic Escherichia coli Triggers Oxygen-Dependent Apoptosis in Human Neutrophils through the Cooperative Effect of Type 1 Fimbriae and Lipopolysaccharide

2004 ◽  
Vol 72 (8) ◽  
pp. 4570-4578 ◽  
Author(s):  
Robert Blomgran ◽  
Limin Zheng ◽  
Olle Stendahl
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Human Neutrophils ◽  
Dependent Manner ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
The Difference ◽  
Tract Infections ◽  
Neutrophil Survival

ABSTRACT Type 1 fimbriae are the most commonly expressed virulence factor on uropathogenic Escherichia coli. In addition to promoting avid bacterial adherence to the uroepithelium and enabling colonization, type 1 fimbriae recruit neutrophils to the urinary tract as an early inflammatory response. Using clinical isolates of type 1 fimbriated E. coli and an isogenic type 1 fimbria-negative mutant (CN1016) lacking the FimH adhesin, we investigated if these strains could modulate apoptosis in human neutrophils. We found that E. coli expressing type 1 fimbriae interacted with neutrophils in a mannose- and lipopolysaccharide (LPS)-dependent manner, leading to apoptosis which was triggered by the intracellular generation of reactive oxygen species. This induced neutrophil apoptosis was abolished by blocking FimH-mediated attachment, by inhibiting NADPH oxidase activation, or by neutralizing LPS. In contrast, CN1016, which did not adhere to or activate the respiratory burst of neutrophils, delayed the spontaneous apoptosis in an LPS-dependent manner. This delayed apoptosis could be mimicked by adding purified LPS and was also observed by using fimbriated bacteria in the presence of d-mannose. These results suggest that LPS is required for E. coli to exert both pro- and antiapoptotic effects on neutrophils and that the difference in LPS presentation (i.e., with or without fimbriae) determines the outcome. The present study showed that there is a fine-tuned balance between type 1 fimbria-induced and LPS-mediated delay of apoptosis in human neutrophils, in which altered fimbrial expression on uropathogenic E. coli determines the neutrophil survival and the subsequent inflammation during urinary tract infections.

scholarly journals Isolation and Identification of Escherichia coli O157:H7 Lytic Bacteriophage from Environment Sewage

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Tessa Sjahriani ◽  
Eddy Bagus Wasito ◽  
Wiwiek Tyasningsih
Keyword(s):  
Escherichia Coli ◽  
Host Specificity ◽  
Pathogenic Bacteria ◽  
Statistical Tests ◽  
Plaque Morphology ◽  
Escherichia Coli O157 ◽  
Lytic Bacteriophage ◽  
Foodborne Disease ◽  
Isolation And Identification ◽  
E Coli

Escherichia coli O157:H7 is one of the pathogenic bacteria causing foodborne disease. The use of lytic bacteriophages can be a good solution to overcome the disease. This study is aimed at isolating lytic bacteriophages from environmental sewage with E. coli O157:H7 bacterial cells. The sample used in this study was eight bacteriophages, and the technique used in identifying E. coli O157:H7 carriers of the stx1 and stx2 genes was PCR. The double layer plaque technique was used to classify bacteriophages. Plaque morphology, host specificity, and electron micrograph were used to identify the bacteriophages. The result obtained plaque morphology as a clear zone with the largest diameter size of 3.5 mm. Lytic bacteriophage could infect E. coli O157:H7 at the highest titer of 10 × 10 8   PFU / mL . Bacteriophages have been identified as Siphoviridae and Myoviridae. Phage 3, phage 4, and phage 8 could infect Atypical Diarrheagenic E. coli 1 (aDEC1) due to their host specificity. The Friedman statistical tests indicate that lytic bacteriophage can significantly lyse E. coli O157:H7 ( p = 0.012 ). The lysis of E. coli O157:H7 by phage 1, phage 2, phage 3, and phage 5 bacteriophages was statistically significant, according to Conover’s posthoc test ( p < 0.05 ). The conclusion obtained from this study is that lytic bacteriophages from environmental sewage could lyse E. coli O157:H7. Therefore, it could be an alternative biocontrol agent against E. coli O157:H7 that contaminates food causing foodborne disease.

scholarly journals Selection for non-specific adhesion is a driver of FimH evolution increasing Escherichia coli biofilm capacity

2021 ◽  
Author(s):  
Mari YOSHIDA ◽  
Stanislas THIRIET-RUPERT ◽  
Leonie MAYER ◽  
Christophe BELOIN ◽  
Jean-Marc GHIGO
Keyword(s):  
Escherichia Coli ◽  
Selective Advantage ◽  
Coli Strain ◽  
Adhesion Properties ◽  
Lectin Domain ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Abiotic Surfaces ◽  
Selection For

Bacterial interactions with surfaces rely on the coordinated expression and interplay of surface exposed adhesion factors. However, how bacteria dynamically modulate their vast repertoire of adhesins to achieve surface colonization is not yet well-understood. We used experimental evolution and positive selection for improved adhesion to investigate how an initially poorly adherent Escherichia coli strain increased its adhesion capacities to abiotic surfaces. We showed that all identified evolved clones acquired mutations located almost exclusively in the lectin domain of fimH, the gene coding for the alpha-D-mannose-specific tip adhesin of type 1 fimbriae. While most of these fimH mutants showed reduced mannose-binding ability, they all displayed enhanced binding to abiotic surfaces, indicating a trade-off between FimH-mediated specific and non-specific adhesion properties. Several of the identified mutations were already reported in FimH lectin domain of pathogenic and environmental E. coli, suggesting that, beyond patho-adaptation, FimH microevolution favoring non-specific surface adhesion could constitute a selective advantage for natural E. coli isolates. Consistently, although E. coli deleted for the fim operon still evolves an increased adhesion capacity, mutants selected in the ∆fim background are outcompeted by fimH mutants revealing clonal interference for adhesion. Our study therefore provides insights into the plasticity of E. coli adhesion potential and shows that evolution of type 1 fimbriae is a major driver of the adaptation of natural E. coli to colonization.

scholarly journals Type 1 Fimbriation and Its Phase Switching in Diarrheagenic Escherichia coli Strains

2001 ◽  
Vol 8 (3) ◽  
pp. 489-495 ◽  
Author(s):  
Ken-Ichiro Iida ◽  
Yoshimitsu Mizunoe ◽  
Sun Nyunt Wai ◽  
Shin-Ichi Yoshida
Keyword(s):  
Escherichia Coli ◽  
Invertible Element ◽  
Nucleotide Sequence Analysis ◽  
Phase Variable ◽  
Phase Switching ◽  
E Coli ◽  
Static Culture ◽  
Type 1 Fimbriae ◽  
K 12

ABSTRACT Type 1 fimbriae can be expressed by most Escherichia coli strains and mediate mannose-sensitive (MS) adherence to mammalian epithelial cells. However, the role of type 1 fimbriae in enteric pathogenesis has been unclear. Expression of type 1 fimbriae inE. coli is phase variable and is associated with the inversion of a short DNA element (fim switch). Forty-six strains of diarrheagenic E. coli were examined for the expression of type 1 fimbriae. Only four of these strains were originally type 1 fimbriated. Seventeen strains, originally nonfimbriated, expressed type 1 fimbriae in association with off-to-on inversion of the fim switch, after serial passages in static culture. The switching frequencies of these strains, from fimbriate to nonfimbriate, were greater than that of the laboratory strain E. coli K-12. None of the 16 strains of serovar O157:H7 or O157:H− expressed type 1 fimbriae after serial passages in static culture. The nucleotide sequence analysis of thefim switch region revealed that all of the O157:H7 and O157:H− strains had a 16-bp deletion in the invertible element, and the fim switch was locked in the “off” orientation. The results suggest that expression of type 1 fimbriae may be regulated differently in different E. coli pathogens causing enteric infections.

scholarly journals Increased Type 1 Fimbrial Expression among Commensal Escherichia coli Isolates in the Murine Cecum following Catabolic Stress

1999 ◽  
Vol 67 (2) ◽  
pp. 745-753 ◽  
Author(s):  
Barbara A. Hendrickson ◽  
Jun Guo ◽  
Robert Laughlin ◽  
Yimei Chen ◽  
John C. Alverdy
Keyword(s):  
Escherichia Coli ◽  
Intestinal Epithelium ◽  
Tissue Injury ◽  
Fold Increase ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Colon Cell ◽  
Colon Cell Line

ABSTRACT Although indigenous bacteria intimately colonize the intestinal mucosa, under normal conditions the intestinal epithelial cell is free of adherent bacteria. Nonetheless, commensal bacteria such asEscherichia coli adhere to and translocate across the intestinal epithelium in association with a number of pathologic states including hemorrhagic shock, immunosuppression, traumatic tissue injury, and lack of enteral feedings. The adhesins involved in the adherence of indigenous E. coli to the intestinal epithelium in vivo following catabolic stress are unknown. We have developed a mouse model to study the bacterial adhesins which mediate the increased intestinal adherence of E. coliafter partial hepatectomy and short-term starvation. Our studies demonstrated that hepatectomy and starvation in the mouse were associated with a 7,500-fold increase in the numbers of E. coli bacteria adhering to the cecum. In addition, erythrocyte agglutination studies, as well as immunostaining of fimbrial preparations and electron micrographs of the bacteria, revealed that surface type 1 fimbriae were more abundant in the commensal E. coli harvested from the ceca of the stressed mice. These E. coli isolates adhered to a mouse colon cell line and injected cecal loops in a mannose-inhibitable manner, which suggests a role for type 1 fimbriae in the adherence of the E. coli isolates to the cecum in vivo following host catabolic stress.

scholarly journals Plasmids shape the diverse accessory resistomes of Escherichia coli ST131

2020 ◽  
Author(s):  
Arun Gonzales Decano ◽  
Nghia Tran ◽  
Hawriya Al-Foori ◽  
Buthaina Al-Awadi ◽  
Leigh Campbell ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Type Species ◽  
Pathogenic Bacteria ◽  
Gastrointestinal Microbiome ◽  
Content Type ◽  
E Coli ◽  
Link Type ◽  
Type Iv ◽  
Clade C

The human gut microbiome includes beneficial, commensal and pathogenic bacteria that possess antimicrobial resistance (AMR) genes and exchange these predominantly through conjugative plasmids. Escherichia coli is a significant component of the gastrointestinal microbiome and is typically non-pathogenic in this niche. In contrast, extra-intestinal pathogenic E. coli (ExPEC) including ST131 may occupy other environments like the urinary tract or bloodstream where they express genes enabling AMR and host cell adhesion like type 1 fimbriae. The extent to which commensal E. coli and uropathogenic ExPEC ST131 share AMR genes remains understudied at a genomic level, and we examined this here using a preterm infant resistome. We found that individual ST131 had small differences in AMR gene content relative to a larger shared resistome. Comparisons with a range of plasmids common in ST131 showed that AMR gene composition was driven by conjugation, recombination and mobile genetic elements. Plasmid pEK499 had extended regions in most ST131 Clade C isolates, and it had evidence of a co-evolutionary signal based on protein-level interactions with chromosomal gene products, as did pEK204 that had a type IV fimbrial pil operon. ST131 possessed extensive diversity of selective type 1, type IV, P and F17-like fimbriae genes that was highest in subclade C2. The structure and composition of AMR genes, plasmids and fimbriae vary widely in ST131 Clade C and this may mediate pathogenicity and infection outcomes.

scholarly journals Effects of ompA Deletion on Expression of Type 1 Fimbriae in Escherichia coli K1 Strain RS218 and on the Association of E. coli with Human Brain Microvascular Endothelial Cells

2006 ◽  
Vol 74 (10) ◽  
pp. 5609-5616 ◽  
Author(s):  
Ching-Hao Teng ◽  
Yi Xie ◽  
Sooan Shin ◽  
Francescopaolo Di Cello ◽  
Maneesh Paul-Satyaseela ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Endothelial Cells ◽  
Human Brain ◽  
Microvascular Endothelial Cells ◽  
Mrna Levels ◽  
Brain Microvascular Endothelial Cells ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Microvascular Endothelial

ABSTRACT We have previously shown that outer membrane protein A (OmpA) and type 1 fimbriae are the bacterial determinants involved in Escherichia coli K1 binding to human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier. In investigating the role of OmpA in E. coli K1 binding to HBMEC, we showed for the first time that ompA deletion decreased the expression of type 1 fimbriae in E. coli K1. Decreased expression of type 1 fimbriae in the ompA deletion mutant was largely the result of driving the fim promoter toward the type 1 fimbrial phase-OFF orientation. mRNA levels of fimB and fimE were found to be decreased with the OmpA mutant compared to the parent strain. Of interest, the ompA deletion further decreased the abilities of E. coli K1 to bind to and invade HBMEC under the conditions of fixing type 1 fimbria expression in the phase-ON or phase-OFF status. These findings suggest that the decreased ability of the OmpA mutant to interact with HBMEC is not entirely due to its decreased type 1 fimbrial expression and that OmpA and type 1 fimbriae facilitate the interaction of E. coli K1 with HBMEC at least in an additive manner.

scholarly journals Adhesion of Escherichia Coli to Nanostructured Surfaces and the Role of Type 1 Fimbriae

Nanomaterials ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 2247
Author(s):  
Pawel Kallas ◽  
Håvard J Haugen ◽  
Nikolaj Gadegaard ◽  
John Stormonth-Darling ◽  
Mats Hulander ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Urinary Tract Infections ◽  
Virulence Factor ◽  
Wild Type ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Tract Infections

Bacterial fimbriae are an important virulence factor mediating adhesion to both biotic and abiotic surfaces and facilitating biofilm formation. The expression of type 1 fimbriae of Escherichia coli is a key virulence factor for urinary tract infections and catheter-associated urinary tract infections, which represent the most common nosocomial infections. New strategies to reduce adhesion of bacteria to surfaces is therefore warranted. The aim of the present study was to investigate how surfaces with different nanotopography-influenced fimbriae-mediated adhesion. Surfaces with three different nanopattern surface coverages made in polycarbonate were fabricated by injection molding from electron beam lithography nanopatterned templates. The surfaces were constructed with features of approximately 40 nm width and 25 nm height with 100 nm, 250 nm, and 500 nm interspace distance, respectively. The role of fimbriae type 1-mediated adhesion was investigated using the E. coli wild type BW25113 and ΔfimA (with a knockout of major pilus protein FimA) and ΔfimH (with a knockout of minor protein FimH) mutants. For the surfaces with nanotopography, all strains adhered least to areas with the largest interpillar distance (500 nm). For the E. coli wild type, no difference in adhesion between surfaces without pillars and the largest interpillar distance was observed. For the deletion mutants, increased adhesion was observed for surfaces without pillars compared to surfaces with the largest interpillar distance. The presence of a fully functional type 1 fimbria decreased the bacterial adhesion to the nanopatterned surfaces in comparison to the mutants.

scholarly journals The importance of P and type 1 fimbriae for the persistence ofEscherichia coliin the human gut

1992 ◽  
Vol 108 (3) ◽  
pp. 415-421 ◽  
Author(s):  
K. Tullus ◽  
I. Kühn ◽  
I. Ørskov ◽  
F. Ørskov ◽  
R. Möllby
Keyword(s):  
Escherichia Coli ◽  
Hela Cell ◽  
Hela Cells ◽  
Human Intestine ◽  
Cell Adherence ◽  
Human Gut ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Faecal Samples

SUMMARYThe faecalEscherichia coliflora was studied in 89 infants. Each infant was followed with a mean of 12 faecal samples (range 5–21) between 0 and 18 months of age. All isolates were assayed for P fimbriae and biochemically phenotyped and the persistence of each strain (phenotype) in the infant's gut was determined. In a subset of strains the occurrence of type 1 fimbriae and adherence to HeLa cells was studied. Thirty-one per cent of isolates belonging to strains colonizing for longer than 6 months expressed P fimbriae compared to 19% of the isolates from strains colonizing 1–6 months or transient strains colonizing less than 1 month. Type 1 fimbriae and adherence to HeLa cells occurred similarly often in all groups of strains. We conclude that P fimbriae, but not type 1 fimbriae or HeLa cell adherence seemed to contribute to the ability of theE. colistrain to colonize the human intestine.

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