scholarly journals Comparative Genomics of Atypical Enteropathogenic Escherichia coli from Kittens and Children Identifies Bacterial Factors Associated with Virulence in Kittens

2020 ◽  
Author(s):  
Victoria E. Watson ◽  
Tracy H. Hazen ◽  
David A. Rasko ◽  
Megan E. Jacob ◽  
Johanna R. Elfenbein ◽  
...  

Typical enteropathogenic E. coli (tEPEC) is a leading cause of diarrhea and associated death in children worldwide. Atypical EPEC (aEPEC) lacks the plasmid encoding bundle-forming pili and is considered less virulent, but the molecular mechanisms of virulence is poorly understood. We recently identified kittens as a host for aEPEC where intestinal epithelial colonization was associated with diarrheal disease and death. The purpose of this study was to (1) determine the genomic similarity between kitten aEPEC and human aEPEC isolates and (2) to identify genotypic or phenotypic traits associated with virulence in kitten aEPEC. We observed no differences between kitten and human aEPEC in core genome content or gene cluster sequence identities and no distinguishing genomic content was observed between aEPEC isolates from kittens with nonclinical colonization (NC) versus lethal infection (LI). Variation in adherence pattern and ability to aggregate actin in cultured cells mirrored descriptions of human aEPEC. The aEPEC isolated from kittens with LI were significantly more motile than isolates from kittens with NC. Kittens may serve as a reservoir for aEPEC that are indistinguishable from human aEPEC isolates and may provide a needed comparative animal model for the study of aEPEC pathogenesis. Motility seems to be an important factor in pathogenesis of LI associated with aEPEC in kittens.

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 231 ◽  
Author(s):  
Anand Prakash Singh ◽  
Saima Aijaz

Enteropathogenic E. coli (EPEC) causes acute intestinal infections in infants in the developing world. Infection typically spreads through contaminated food and water and leads to severe, watery diarrhea. EPEC attaches to the intestinal epithelial cells and directly injects virulence factors which modulate multiple signaling pathways leading to host cell dysfunction. However, the molecular mechanisms that regulate the onset of diarrhea are poorly defined. A major target of EPEC is the host cell tight junction complex which acts as a barrier and regulates the passage of water and solutes through the paracellular space. In this review, we focus on the EPEC effectors that target the epithelial barrier, alter its functions and contribute to leakage through the tight junctions.


2011 ◽  
Vol 301 (5) ◽  
pp. C1140-C1149 ◽  
Author(s):  
Valeriy Lukyanenko ◽  
Irina Malyukova ◽  
Ann Hubbard ◽  
Michael Delannoy ◽  
Edgar Boedeker ◽  
...  

Gastrointestinal infection with Shiga toxins producing enterohemorrhagic Escherichia coli causes the spectrum of gastrointestinal and systemic complications, including hemorrhagic colitis and hemolytic uremic syndrome, which is fatal in ∼10% of patients. However, the molecular mechanisms of Stx endocytosis by enterocytes and the toxins cross the intestinal epithelium are largely uncharacterized. We have studied Shiga toxin 1 entry into enterohemorrhagic E. coli-infected intestinal epithelial cells and found that bacteria stimulate Shiga toxin 1 macropinocytosis through actin remodeling. This enterohemorrhagic E. coli-caused macropinocytosis occurs through a nonmuscle myosin II and cell division control 42 (Cdc42)-dependent mechanism. Macropinocytosis of Shiga toxin 1 is followed by its transcytosis to the basolateral environment, a step that is necessary for its systemic spread. Inhibition of Shiga toxin 1 macropinocytosis significantly decreases toxin uptake by intestinal epithelial cells and in this way provides an attractive, antibiotic-independent strategy for prevention of the harmful consequences of enterohemorrhagic E. coli infection.


2003 ◽  
Vol 71 (8) ◽  
pp. 4674-4683 ◽  
Author(s):  
Muna F. Anjum ◽  
Sacha Lucchini ◽  
Arthur Thompson ◽  
Jay C. D. Hinton ◽  
Martin J. Woodward

ABSTRACT The Escherichia coli O26 serogroup includes important food-borne pathogens associated with human and animal diarrheal disease. Current typing methods have revealed great genetic heterogeneity within the O26 group; the data are often inconsistent and focus only on verotoxin (VT)-positive O26 isolates. To improve current understanding of diversity within this serogroup, the genomic relatedness of VT-positive and -negative O26 strains was assessed by comparative genomic indexing. Our results clearly demonstrate that irrespective of virulence characteristics and pathotype designation, the O26 strains show greater genomic similarity to each other than to any other strain included in this study. Our data suggest that enteropathogenic and VT-expressing E. coli O26 strains represent the same clonal lineage and that VT-expressing E. coli O26 strains have gained additional virulence characteristics. Using this approach, we established the core genes which are central to the E. coli species and identified regions of variation from the E. coli K-12 chromosomal backbone.


2010 ◽  
Vol 78 (8) ◽  
pp. 3625-3636 ◽  
Author(s):  
Viktor Merkel ◽  
Barbara Ohder ◽  
Martina Bielaszewska ◽  
Wenlan Zhang ◽  
Angelika Fruth ◽  
...  

ABSTRACT eibG in Shiga toxin-producing Escherichia coli (STEC) O91 encodes a protein (EibG) which binds human immunoglobulins G and A and contributes to bacterial chain-like adherence to human epithelial cells. We investigated the prevalence of eibG among STEC, the phylogeny of eibG, and eibG allelic variations and their impact on the adherence phenotype. eibG was found in 15.0% of 240 eae-negative STEC strains but in none of 157 eae-positive STEC strains. The 36 eibG-positive STEC strains belonged to 14 serotypes and to eight multilocus sequence types (STs), with serotype O91:H14/H− and ST33 being the most common. Sequences of the complete eibG gene (1,527 bp in size) from eibG-positive STEC resulted in 21 different alleles with 88.11% to 100% identity to the previously reported eibG sequence; they clustered into three eibG subtypes (eibG-α, eibG-β, and eibG-γ). Strains expressing EibG-α and EibG-β displayed a mostly typical chain-like adherence pattern (CLAP), with formation of long chains on both human and bovine intestinal epithelial cells, whereas strains with EibG-γ adhered in short chains, a pattern we termed atypical CLAP. The same adherence phenotypes were displayed by E. coli BL21(DE3) clones containing the respective eibG-α, eibG-β, and eibG-γ subtypes. We propose two possible evolutionary scenarios for eibG in STEC: a clonal development of eibG in strains with the same phylogenetic background or horizontal transfer of eibG between phylogenetically unrelated STEC strains.


F1000Research ◽  
2016 ◽  
Vol 4 ◽  
pp. 231 ◽  
Author(s):  
Anand Prakash Singh ◽  
Saima Aijaz

Enteropathogenic E. coli (EPEC) causes acute intestinal infections in infants in the developing world. Infection typically spreads through contaminated food and water and leads to severe, watery diarrhea. EPEC attaches to the intestinal epithelial cells and directly injects virulence factors which modulate multiple signaling pathways leading to host cell dysfunction. However, the molecular mechanisms that regulate the onset of diarrhea are poorly defined. A major target of EPEC is the host cell tight junction complex which acts as a barrier and regulates the passage of water and solutes through the paracellular space. In this review, we focus on the EPEC effectors that target the epithelial barrier, alter its functions and contribute to leakage through the tight junctions.


2021 ◽  
Vol 12 (1) ◽  
pp. 28-40
Author(s):  
Anca Delia Mare ◽  
Cristina Nicoleta Ciurea ◽  
Adrian Man ◽  
Bianca Tudor ◽  
Valeriu Moldovan ◽  
...  

Diarrheal disease is still a major public health concern, as it is still considered an important cause of death in children under five years of age. A few decades ago, the detection of enteropathogenic E. coli was made by detecting the O, H, and K antigens, mostly by agglutination. The recent protocols recommend the molecular methods for diagnosing EPEC, as they can distinguish between typical and atypical EPEC by identifying the presence/absence of specific virulence factors. EPEC are defined as diarrheagenic strains of E. coli that can produce attaching and effacing lesions on the intestinal epithelium while being incapable of producing Shiga toxins and heat-labile or heat-stable enterotoxins. The ability of these strains to produce attaching and effacing lesions enable them to cause localized lesions by attaching tightly to the surface of the intestinal epithelial cells, disrupting the surfaces of the cells, thus leading to the effacement of the microvilli. EPEC are classified on typical and atypical isolates, based on the presence or absence of E. coli adherence factor plasmids. All the EPEC strains are eae positive; typical EPEC strains are eae+, bfpA+, while atypical strains are eae+, bfpA−. No vaccines are currently available to prevent EPEC infections.


2000 ◽  
Vol 68 (12) ◽  
pp. 6790-6797 ◽  
Author(s):  
Craig Altier ◽  
Mitsu Suyemoto ◽  
Sara D. Lawhon

ABSTRACT Penetration of intestinal epithelial cells by Salmonella enterica serovar Typhimurium requires the expression of invasion genes, found in Salmonella pathogenicity island 1 (SPI1), that encode components of a type III secretion apparatus. These genes are controlled in a complex manner by regulators within SPI1, including HilA and InvF, and those outside SPI1, such as the two-component regulators PhoP/PhoQ and BarA/SirA. We report here that epithelial cell invasion requires the serovar Typhimurium homologue ofEscherichia coli csrA, which encodes a regulator that alters the stability of specific mRNA targets. A deletion mutant ofcsrA was unable to efficiently invade cultured epithelial cells and showed reduced expression of four tested SPI1 genes,hilA, invF, sipC, and prgH. Overexpression ofcsrA from an induced araBAD promoter also negatively affected the expression of these genes, indicating that CsrA can act as both a positive and a negative regulator of SPI1 genes and suggesting that the bacterium must tightly control the level or activity of CsrA to achieve maximal invasion. We found that CsrA affected hilA, a regulator of the other three genes we tested, probably by controlling one or more genetic elements that regulate hilA. We also found that both the loss and the overexpression of csrA reduced the expression of two regulators of hilA, hilC and hilD, suggesting that csrA exerts its control of hilAthrough one or both of these regulators. We further found, however, that CsrA could affect the expression of both invF andsipC independent of its effects on hilA. One additional striking phenotype of the csrA mutant, not observed in a comparable E. coli mutant, was its slow growth. Phenotypic revertants that had normal growth rates, while maintaining the csrA mutation, were common. These suppressed strains, however, did not recover the ability to invade cultured cells, indicating that the csrA-mediated loss of invasion cannot be attributed simply to poor growth and that the growth and invasion deficits of the csrA mutant arise from effects of CsrA on different targets.


2018 ◽  
Author(s):  
Stacy A. Malaker ◽  
Kayvon Pedram ◽  
Michael J. Ferracane ◽  
Elliot C. Woods ◽  
Jessica Kramer ◽  
...  

<div> <div> <div> <p>Mucins are a class of highly O-glycosylated proteins that are ubiquitously expressed on cellular surfaces and are important for human health, especially in the context of carcinomas. However, the molecular mechanisms by which aberrant mucin structures lead to tumor progression and immune evasion have been slow to come to light, in part because methods for selective mucin degradation are lacking. Here we employ high resolution mass spectrometry, polymer synthesis, and computational peptide docking to demonstrate that a bacterial protease, called StcE, cleaves mucin domains by recognizing a discrete peptide-, glycan-, and secondary structure- based motif. We exploited StcE’s unique properties to map glycosylation sites and structures of purified and recombinant human mucins by mass spectrometry. As well, we found that StcE will digest cancer-associated mucins from cultured cells and from ovarian cancer patient-derived ascites fluid. Finally, using StcE we discovered that Siglec-7, a glyco-immune checkpoint receptor, specifically binds sialomucins as biological ligands, whereas the related Siglec-9 receptor does not. Mucin-specific proteolysis, as exemplified by StcE, is therefore a powerful tool for the study of glycoprotein structure and function and for deorphanizing mucin-binding receptors. </p> </div> </div> </div>


2019 ◽  
Vol 14 (1) ◽  
pp. 28-31 ◽  
Author(s):  
Rowles H. L.

Probiotics are live microorganisms, which when ingested in sufficient amounts, confer health benefits to the host by improving the gut microflora balance. The purpose of this research was to determine whether commercial probiotic products containing multitude of commensal bacteria would reduce the growth rate of pathogenic bacteria, specifically Escherichia coli and Salmonella typhimurium. Growth curves were established, and the growth rates were compared for samples of E. coli, S. typhimurium, Nature’s Bounty Controlled Delivery probiotic, Sundown Naturals Probiotic Balance probiotic, and cocultures of the pathogenic bacteria mixed with the probiotics. The findings of this research were that the commercial probiotics significantly reduced the growth rate of E. coli and S. typhimurium when combined in cocultures. Probiotics containing multiple strains may be taken prophylactically to reduce the risk of bacterial infections caused by E. coli and S. typhimurium. Probiotics could be used to reduce the high global morbidity and mortality rates of diarrheal disease.


2019 ◽  
Vol 25 (34) ◽  
pp. 3645-3663 ◽  
Author(s):  
Muhammad Ismail ◽  
Kalsoom Akhtar ◽  
M.I. Khan ◽  
Tahseen Kamal ◽  
Murad A. Khan ◽  
...  

: Water pollution due to waste effluents of the textile industry is seriously causing various health problems in humans. Water pollution with pathogenic bacteria, especially Escherichia coli (E. coli) and other microbes is due to the mixing of fecal material with drinking water, industrial and domestic sewage, pasture and agricultural runoff. Among the chemical pollutants, organic dyes due to toxic nature, are one of the major contaminants of industrial wastewater. Adequate sanitation services and drinking quality water would eliminate 200 million cases of diarrhea, which results in 2.1 million less deaths caused by diarrheal disease due to E. coli each year. Nanotechnology is an excellent platform as compared to conventional treatment methods of water treatment and remediation from microorganisms and organic dyes. In the current study, toxicity and carcinogenicity of the organic dyes have been studied as well as the remediation/inactivation of dyes and microorganism has been discussed. Remediation by biological, physical and chemical methods has been reviewed critically. A physical process like adsorption is cost-effective, but can’t degrade dyes. Biological methods were considered to be ecofriendly and cost-effective. Microbiological degradation of dyes is cost-effective, eco-friendly and alternative to the chemical reduction. Besides, certain enzymes especially horseradish peroxidase are used as versatile catalysts in a number of industrial processes. Moreover, this document has been prepared by gathering recent research works related to the dyes and microbial pollution elimination from water sources by using heterogeneous photocatalysts, metal nanoparticles catalysts, metal oxides and enzymes.


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