scholarly journals Investigation of Commensal Escherichia coli Populations of Cormorant Hatchlings in the Absence of Anthropogenic Impacts in Remote Areas of West Mongolia

2021 ◽  
Vol 9 (2) ◽  
pp. 372
Author(s):  
Muhammad Moman Khan ◽  
Rafal Kolenda ◽  
Peter Schierack ◽  
Jörg Weinreich ◽  
Stefan Rödiger ◽  
...  
Keyword(s):  
Bacterial Adhesion ◽  
Anthropogenic Impacts ◽  
Intestinal Cell ◽  
Pfge Type ◽  
Intestinal Colonization ◽  
E Coli ◽  
High Adhesion ◽  
Intestinal Cell Line ◽  
Animal Populations ◽  
Adhesion Rate

To increase our understanding of bacterial intestinal colonization in animal populations lacking substantial anthropogenic influence we studied the diversity of E. coli in cormorants from the pristine West-Mongolian steppe. E. coli were isolated from individual birds of two cormorant colonies located on small islands in lakes at least 100 km away from human settlements. Diversity of the isolates was studied using pulsed-field gel electrophoresis (PFGE). 137 isolates of cormorant colony-1 and 75 isolates of cormorant colony-2 resulted in 60 and 33 PFGE types, respectively. Representative strains of each PFGE type were analyzed via PCR in terms of phylogroups and extraintestinal virulence-associated genes (exVAGs). Bacterial adhesion to the chicken intestinal cell line CHIC-8E11 and antimicrobial resistance was also determined. Most isolates belonged to phylogroup B1 (68.3%) followed by B2 and E with B2 harboring the highest total number of exVAGs per isolate. Unexpectedly, a PFGE type with relatively few exVAGs displayed the highest isolation frequency, also showing a high adhesion rate. Comparative analysis of exVAGs to other E. coli populations of wildlife origin revealed that the secreted autotransporter toxin encoding sat gene was only present in cormorants. Overall, E. coli in cormorants maintained a high diversity under minimal anthropogenic influences, which likely enables intestinal colonization.

scholarly journals Mannan rich fraction from yeast modulates inflammatory responses in intestinal cells (HT-29) exposed toEscherichia coli

2019 ◽  
Vol 7 ◽  
Author(s):  
Niall Browne ◽  
Aimee Traynor ◽  
Karina A. Horgan
Keyword(s):  
Inflammatory Responses ◽  
Economic Cost ◽  
Intestinal Cell ◽  
Cell Protein ◽  
Intestinal Cells ◽  
E Coli ◽  
Intestinal Cell Line ◽  
Proinflammatory Responses ◽  
Ht 29

AbstractMannan from yeast has been demonstrated to limit infection in animals susceptible to gastrointestinal infection, including pigs, poultry and cows, by blocking the mechanism by which gram-negative bacteria adhere to and invade the intestines. EnterotoxigenicEscherichia coli(ETEC) cause post weaning diarrhoea (PWD) which results in poor weight gain and potential death at great economic cost to the farmer. A mannan rich fraction (MRF) was assessedin vitrofor its impact on ETEC infection of HT-29 intestinal cell line. Gene expression markers for inflammation (TNFαandIL-1β) and TLR4 (TICAM-1andLY96) associated recognition of bacteria were significantly elevated following exposure toE. colialone, but not in combination with MRF compared to the control. HT-29 cells exposed to MRF alone demonstrated significantly reduced expression of immune signalling genesIRAK1,IRF7andJUNwhen compared to the control. HT-29 cell protein abundance for TNFα and TLR4 associated proteins were significantly increased in response toE. coliexposure alone while no significant change was observed for MRF treatment withE. coliinfection.E. coliadhesion to HT-29 cells was significantly decreased with addition of MRF compared toE. coliinfection alone. The action of MRF demonstrated its potential capacity to limit infection on anin vitrolevel through blocking bacterial interaction with the intestines that leads to infection as marked by a reduction in proinflammatory responses. MRF on its own demonstrated potential anti-inflammatory effects on intestinal cells with the reduction of proinflammatory responses observed.

scholarly journals Afa/Dr Diffusely Adhering Escherichia coli Infection in T84 Cell Monolayers Induces Increased Neutrophil Transepithelial Migration, Which in Turn Promotes Cytokine-Dependent Upregulation of Decay-Accelerating Factor (CD55), the Receptor for Afa/Dr Adhesins

2003 ◽  
Vol 71 (4) ◽  
pp. 1774-1783 ◽  
Author(s):  
Frederic Betis ◽  
Patrick Brest ◽  
Véronique Hofman ◽  
Julie Guignot ◽  
Imad Kansau ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Laboratory Strain ◽  
Intestinal Cell ◽  
Necrosis Factor Alpha ◽  
Decay Accelerating Factor ◽  
E Coli ◽  
Intestinal Cell Line ◽  
Bowel Diseases ◽  
Escherichia Coli Infection ◽  
Human Intestinal Cell Line

ABSTRACT Ulcerative colitis and Crohn's disease are inflammatory bowel diseases thought to involve strains of Escherichia coli. We report here that two wild-type Afa/Dr diffusely adhering E. coli (DAEC) strains, C1845 and IH11128, which harbor the fimbrial F1845 adhesin and the Dr hemagglutinin, respectively, and the E. coli laboratory strain HB101, transformed with the pSSS1 plasmid to produce Afa/Dr F1845 adhesin, all induced interleukin-8 (IL-8) production and transepithelial migration of polymorphonuclear leukocytes (PMNL) in polarized monolayers of the human intestinal cell line T84 grown on semipermeable filters. We observed that after PMNL migration, expression of decay-accelerating factor (DAF, or CD55), the brush border-associated receptor for Afa/Dr adhesins, was strongly enhanced, increasing the adhesion of Afa/Dr DAEC bacteria. When examining the mechanism by which DAF expression was enhanced, we observed that the PMNL transepithelial migration induced epithelial synthesis of tumor necrosis factor alpha and IL-1β, which in turn promoted the upregulation of DAF.

scholarly journals Piracy of Decay-Accelerating Factor (CD55) Signal Transduction by the Diffusely Adhering Strain Escherichia coli C1845 Promotes Cytoskeletal F-Actin Rearrangements in Cultured Human Intestinal INT407 Cells

1998 ◽  
Vol 66 (9) ◽  
pp. 4036-4042 ◽  
Author(s):  
Isabelle Peiffer ◽  
Alain L. Servin ◽  
Marie-Françoise Bernet-Camard
Keyword(s):  
Escherichia Coli ◽  
Signal Transduction ◽  
Protein Tyrosine Kinase ◽  
Cell Entry ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Decay Accelerating Factor ◽  
E Coli ◽  
Intestinal Cell Line ◽  
Fimbrial Adhesin

ABSTRACT Diffusely adhering Escherichia coli (DAEC) C1845 (clinical isolate) harboring the fimbrial adhesin F1845 can infect cultured human differentiated intestinal epithelial cells; this process is followed by the disassembly of the actin network in the apical domain. The aim of this study was to examine the mechanism by which DAEC C1845 promotes F-actin rearrangements. For this purpose, we used a human embryonic intestinal cell line (INT407) expressing the membrane-associated glycosylphosphatidylinositol (GPI) protein-anchored decay-accelerating factor (DAF), the receptor of the F1845 adhesin. We show here that infection of INT407 cells by DAEC C1845 can provoke dramatic F-actin rearrangements without cell entry. Clustering of phosphotyrosines was observed, revealing that the DAEC C1845-DAF interaction involves the recruitment of signal transduction molecules. A pharmacological approach with a subset of inhibitors of signal transduction molecules was used to identify the cascade of signal transduction molecules that are coupled to the DAF, that are activated upon infection, and that promote the F-actin rearrangements. DAEC C1845-induced F-actin rearrangements can be blocked dose dependently by protein tyrosine kinase, phospholipase Cγ, phosphatidylinositol 3-kinase, protein kinase C, and Ca2+inhibitors. F-actin rearrangements and blocking by inhibitors were observed after infection of the cells with two E. colirecombinants carrying the plasmids containing the fimbrial adhesin F1845 or the fimbrial hemagglutinin Dr, belonging to the same family of adhesins. These findings show that the DAEC Dr family of pathogens promotes alterations in the intestinal cell cytoskeleton by piracy of the DAF-GPI signal cascade without bacterial cell entry.

scholarly journals Preliminary Characterization of the Transcriptional Response of the Porcine Intestinal Cell Line IPEC-J2 to EnterotoxigenicEscherichia coli,Escherichia coli, andE. coliLipopolysaccharide

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Marisa M. Geens ◽  
Theo A. Niewold
Keyword(s):  
Escherichia Coli ◽  
Cell Line ◽  
Transcriptional Response ◽  
Intestinal Cell ◽  
Adhesion Assay ◽  
Transcriptional Level ◽  
Suitable Model ◽  
E Coli ◽  
Intestinal Cell Line

IPEC-J2, a promisingin vitromodel system, is not well characterized especially on the transcriptional level, in contrast to human counterparts. The aim of this study was to characterize the gene expression in IPEC-J2 cells when coincubated with enterotoxigenicEscherichia coli(ETEC), nonpathogenicE. coli, andE. coliendotoxin. Apical infection of polarized IPEC-J2 monolayers caused a time-dependent decrease in transepithelial electrical resistance (TEER). Microarray analysis showed up-regulation of interleukins when IPEC-J2 were cocultured withE. colistrains this has so far never been measured in this cell line. Highest IL8 expression was found with the ETEC strain possessing the F4 fimbrium, suggesting IPEC-J2 cells to be F4 receptor positive, confirmed in a brush border membrane adhesion assay. It is concluded that the innate immune responses to pathogens and LPS makes the IPEC-J2 cell line a suitable model for research on intestinal host pathogen interaction.

Kinetics and regulation of a polarized Na(+)-H+ exchanger from Caco-2 cells, a human intestinal cell line

1991 ◽  
Vol 261 (2) ◽  
pp. G229-G238 ◽  
Author(s):  
A. J. Watson ◽  
S. Levine ◽  
M. Donowitz ◽  
M. H. Montrose
Keyword(s):  
Ussing Chamber ◽  
Basolateral Membrane ◽  
Intestinal Cell ◽  
Hypertonic Medium ◽  
Regulatory Pathways ◽  
E Coli ◽  
Phorbol Dibutyrate ◽  
Intestinal Cell Line ◽  
Second Messenger Pathways ◽  
Human Intestinal Cell Line

The kinetics and regulation of Na(+)-H+ exchange were studied using BCECF to measure pHi in Caco-2 cells grown on membrane filters. Na(+)-H+ exchange was defined as a Na(+)-dependent H+ efflux in response to an acid load imposed by an NH4Cl prepulse in the absence of added CO2. Na(+)-H+ exchange was present exclusively on the basolateral membrane, had a Kt (Na+) of 21 +/- 2 mM, and an ID50 for amiloride dependent on medium [Na+] with an apparent Ki for amiloride of 3 microM. Na(+)-H+ exchange rates had a greater than first-order dependence on intracellular [H+], suggesting the presence of an internal proton modifier site. Results also suggest that Na(+)-H+ exchange is kinetically inactivated at resting pHi (7.35 +/- 0.02), since neither removal of Na+ nor addition of amiloride affected resting pHi, although monensin alkalinized cells to pHi 7.6. To evaluate regulation of Na(+)-H+ exchange, cells were exposed to either forskolin, 1,9-dideoxyforskolin (a noncyclase-activating forskolin derivative), 8-BrcAMP, E. coli STa toxin, ionomycin, phorbol dibutyrate, or cellular shrinkage in hypertonic medium. Only forskolin and 1,9-dideoxyforskolin caused a significant change (inhibition) in Na(+)-H+ exchange rate. Experiments performed with the Ussing chamber-voltage clamp technique verified that forskolin, 8-BrcAMP, E. coli STa toxin, ionomycin, and phorbol dibutyrate increased transepithelial Isc, verifying that all the regulatory pathways tested were functional and responsive to agonists. Results suggested that the Isc was due to Cl- secretion, since no net transcellular Na+ or Cl- flux was detected in basal conditions, and the Isc response to forskolin was abolished by omission of serosal Cl-. Because forskolin, but not 1,9-dideoxyforskolin, increased both cellular cAMP and Isc, the inhibition of Na(+)-H+ exchange by forskolin derivatives was mediated by a mechanism not involving activation of adenylyl cyclase. In conclusion, Caco-2 cells use a basolateral Na(+)-H+ exchanger to regulate pHi, but this exchanger is not affected by cell shrinkage or second messenger pathways that regulate Na(+)-H+ exchangers in other cell systems.

Cellulose nanocrystals are effective in inhibiting host cell bacterial adhesion

2017 ◽  
Vol 5 (34) ◽  
pp. 7018-7020 ◽  
Author(s):  
G. D'Orazio ◽  
L. Munizza ◽  
J. Zampolli ◽  
M. Forcella ◽  
L. Zoia ◽  
...  
Keyword(s):  
Host Cell ◽  
Cellulose Nanocrystals ◽  
Bacterial Adhesion ◽  
Cell Monolayer ◽  
Bactericidal Effect ◽  
Intestinal Cell ◽  
E Coli

The use of cellulose nanocrystals (CNCs) as a biomaterial able to inhibit host cell bacterial adhesion is described. Pre-incubation ofE. coliwith a suspension of CNCs affords a significant reduction of bacterial adhesion to intestinal cell monolayer HT29, without exerting a bactericidal effect.

scholarly journals Afa/Dr Diffusely Adhering Escherichia coli C1845 Infection Promotes Selective Injuries in the Junctional Domain of Polarized Human Intestinal Caco-2/TC7 Cells

2000 ◽  
Vol 68 (6) ◽  
pp. 3431-3442 ◽  
Author(s):  
Isabelle Peiffer ◽  
Anne-Béatrice Blanc-Potard ◽  
Marie-Françoise Bernet-Camard ◽  
Julie Guignot ◽  
Alain Barbat ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Brush Border ◽  
Intestinal Cell ◽  
Pathogenic Factor ◽  
Actin Network ◽  
E Coli ◽  
Intestinal Cell Line ◽  
Human Intestinal Cell Line ◽  
Cytoskeleton Rearrangements ◽  
Fimbrial Adhesin

ABSTRACT The Afa/Dr diffusely adhering Escherichia coli (DAEC) C1845 strain harboring the F1845 fimbrial adhesin interacts with the brush border-associated CD55 molecule and promotes elongation of brush border microvilli resulting from rearrangement of the F-actin network. This phenomenon involves the activation of a cascade of signaling coupled to the glycosylphosphatidylinositol-anchored receptor of the F1845 adhesin. We provide evidence that infection of the polarized human intestinal cell line Caco-2/TC7 by strain C1845 is followed by an increase in the paracellular permeability for [3H]mannitol without a decrease of the transepithelial resistance of the monolayers. Alterations in the distribution of tight-junction (TJ)-associated occludin and ZO-1 protein are observed, whereas the distribution of the zonula adherens-associated E-cadherin is not affected. Using the recombinantE. coli strains HB101(pSSS1) and -(pSSS1C) expressing the F1845 fimbrial adhesin, we demonstrate that the adhesin-CD55 interaction is not sufficient for the induction of structural and functional TJ lesions. Moreover, using the actin filament-stabilizing agent Jasplakinolide, we demonstrate that the C1845-induced functional alterations in TJs are independent of the C1845-induced apical cytoskeleton rearrangements. The results indicated that pathogenic factor(s) other than F1845 adhesin may be operant in Afa/Dr DAEC C1845.

scholarly journals Quantitative Approach in the Study of Adhesion of Lactic Acid Bacteria to Intestinal Cells and Their Competition with Enterobacteria

2000 ◽  
Vol 66 (9) ◽  
pp. 3692-3697 ◽  
Author(s):  
Y. K. Lee ◽  
C. Y. Lim ◽  
W. L. Teng ◽  
A. C. Ouwehand ◽  
E. M. Tuomola ◽  
...  
Keyword(s):  
Bacterial Adhesion ◽  
Lactobacillus Rhamnosus ◽  
Intestinal Cell ◽  
Intestinal Cells ◽  
E Coli ◽  
Intestinal Mucus ◽  
Adhesion Sites ◽  
Mixed Suspension ◽  
Mathematical Equations ◽  
Simple Dissociation

ABSTRACT To describe the phenomena of bacterial adhesion to intestinal cells and the competition for adhesion between bacteria, mathematical equations based on a simple dissociation process involving a finite number of bacterial receptors on intestinal cell surface were developed. The equations allow the estimation of the maximum number ofLactobacillus sp. and Escherichia coli cells that can adhere to Caco-2 cells and intestinal mucus; they also characterize the affinity of the bacteria to Caco-2 cells and intestinal and fecal mucus and the theoretical adhesion ratio of two bacteria present in a mixed suspension. The competition for adhesion between Lactobacillus rhamnosus GG and E. coliTG1 appeared to follow the proposed kinetics, whereas the competition between Lactobacillus casei Shirota and E. coliTG1 may involve multiple adhesion sites or a soluble factor in the culture medium of the former. The displacement of the adheredLactobacillus by E. coli TG1 seemed to be a rapid process, whereas the displacement of E. coli TG1 by the Lactobacillus took more than an hour.

scholarly journals Bifidobacterium longum subsp. infantis CECT7210 (B. infantis IM-1®) Displays In Vitro Activity against Some Intestinal Pathogens

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3259
Author(s):  
Lorena Ruiz ◽  
Ana Belén Flórez ◽  
Borja Sánchez ◽  
José Antonio Moreno-Muñoz ◽  
Maria Rodriguez-Palmero ◽  
...  
Keyword(s):  
Infant Health ◽  
Bifidobacterium Longum ◽  
Probiotic Strain ◽  
Intestinal Cell ◽  
Human Gastrointestinal Tract ◽  
E Coli ◽  
Intestinal Cell Line ◽  
Intestinal Pathogens ◽  
Health Promoting

Certain non-digestible oligosaccharides (NDO) are specifically fermented by bifidobacteria along the human gastrointestinal tract, selectively favoring their growth and the production of health-promoting metabolites. In the present study, the ability of the probiotic strain Bifidobacterium longum subsp. infantis CECT7210 (herein referred to as B. infantis IM-1®) to utilize a large range of oligosaccharides, or a mixture of oligosaccharides, was investigated. The strain was able to utilize all prebiotics screened. However, galactooligosaccharides (GOS), and GOS-containing mixtures, effectively increased its growth to a higher extent than the other prebiotics. The best synbiotic combination was used to examine the antimicrobial activity against Escherichia coli, Cronobacter sakazakii, Listeria monocytogenes and Clostridium difficile in co-culture experiments. C. difficile was inhibited by the synbiotic, but it failed to inhibit E. coli. Moreover, Cr. sakazakii growth decreased during co-culture with B. infantis IM-1®. Furthermore, adhesion experiments using the intestinal cell line HT29 showed that the strain IM-1® was able to displace some pathogens from the enterocyte layer, especially Cr. sakazakii and Salmonella enterica, and prevented the adhesion of Cr. sakazakii and Shigella sonnei. In conclusion, a new synbiotic (probiotic strain B. infantis IM-1® and GOS) appears to be a potential effective supplement for maintaining infant health. However, further studies are needed to go more deeply into the mechanisms that allow B.infantis IM-1® to compete with enteropathogens.

scholarly journals Bacterial adhesion to and viability on positively charged polymer surfaces

Microbiology ◽  
2006 ◽  
Vol 152 (12) ◽  
pp. 3575-3583 ◽  
Author(s):  
Akihiko Terada ◽  
Atsushi Yuasa ◽  
Takashi Kushimoto ◽  
Satoshi Tsuneda ◽  
Akio Katakai ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Rate Constant ◽  
Bacterial Adhesion ◽  
Contact Angle Hysteresis ◽  
Polymer Chains ◽  
Wall Structure ◽  
Amino Groups ◽  
E Coli ◽  
High Membrane Potential ◽  
Adhesion Rate

Secondary and tertiary amino groups were introduced into polymer chains grafted onto a polyethylene flat-sheet membrane to evaluate the effects of surface properties on the adhesion and viability of a strain of the Gram-negative bacterium Escherichia coli and a strain of the Gram-positive bacterium Bacillus subtilis. The characterization of the surfaces containing amino groups, i.e. ethylamino (EA) and diethylamino (DEA) groups, revealed that the membrane potentials are proportional to amino-group densities and contact angle hysteresis. A high bacterial adhesion rate constant k was observed at high membrane potential, which indicates that membrane potential could be used as an indicator for estimating bacterial adhesion to the EA and DEA sheets, especially in B. subtilis. The bacterial adhesion rate constant of E. coli markedly increased at a membrane potential higher than −7.8 mV, whereas that of B. subtilis increased at a membrane potential higher than −8.3 mV, at which the dominant effect on bacterial adhesion is expected to change. The viability experiments revealed that approximately 80 % of E. coli cells adhering to the sheets with high membrane potential were inactivated after a contact time of 8 h, whereas 60 % of B. subtilis cells were inactivated. Furthermore, E. coli viability significantly decreased at a membrane potential higher than −8 mV, whereas B. subtilis viability decreased as membrane potential increased, which reflects differences in cell wall structure between E. coli and B. subtilis.

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