<i>Arcobacter butzleri</i>Induces Barrier Dysfunction in Intestinal HT‐29/B6 Cells

Bücker, Roland; Troeger, Hanno; Kleer, J.; Fromm, Michael; Schulzke, Jörg–Dieter

doi:10.1086/600868

Cited by 64 publications

(29 citation statements)

References 45 publications

(37 reference statements)

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“…This is contrary to other enteric pathogens with a stronger impact on TJs, e.g. enteropathogenic Escherichia coli or Arcobacter butzleri [12]. Our results did not display an overall alteration of the TJ.…”

Section: Discussioncontrasting

confidence: 99%

“…This drift of claudins out of the TJ to intracellular compartments could not be confirmed in confocal laser-scanning microscopy of immunostainings (data not shown). However, 24 h postinfection claudin-5 mRNA level was reduced to 49±16% ( P <0.05, n = 4), suggesting expression regulation from the gene, likewise in Arcobacter butzleri infection [12]; a close relative, belonging to the epsilon-proteobacteria.…”

Section: Resultsmentioning

confidence: 91%

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Oral and Fecal Campylobacter concisus Strains Perturb Barrier Function by Apoptosis Induction in HT-29/B6 Intestinal Epithelial Cells

Nielsen

Ejlertsen

et al. 2011

PLoS ONE

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Campylobacter concisus infections of the gastrointestinal tract can be accompanied by diarrhea and inflammation, whereas colonization of the human oral cavity might have a commensal nature. We focus on the pathophysiology of C. concisus and the effects of different clinical oral and fecal C. concisus strains on human HT-29/B6 colon cells. Six oral and eight fecal strains of C. concisus were isolated. Mucus-producing HT-29/B6 epithelial monolayers were infected with the C. concisus strains. Transepithelial electrical resistance (Rt) and tracer fluxes of different molecule size were measured in Ussing chambers. Tight junction (TJ) protein expression was determined by Western blotting, and subcellular TJ distribution was analyzed by confocal laser-scanning microscopy. Apoptosis induction was examined by TUNEL-staining and Western blot of caspase-3 activation. All strains invaded confluent HT-29/B6 cells and impaired epithelial barrier function, characterized by a time- and dose-dependent decrease in Rt either after infection from the apical side but even more from the basolateral compartment. TJ protein expression changes were sparse, only in apoptotic areas of infected monolayers TJ proteins were redistributed. Solely the barrier-forming TJ protein claudin-5 showed a reduced expression level to 66±8% (P<0.05), by expression regulation from the gene. Concomitantly, Lactate dehydrogenase release was elevated to 3.1±0.3% versus 0.7±0.1% in control (P<0.001), suggesting cytotoxic effects. Furthermore, oral and fecal C. concisus strains elevated apoptotic events to 5-fold. C. concisus-infected monolayers revealed an increased permeability for 332 Da fluorescein (1.74±0.13 vs. 0.56±0.17 10−6 cm/s in control, P<0.05) but showed no difference in permeability for 4 kDa FITC-dextran (FD-4). The same was true in camptothecin-exposed monolayers, where camptothecin was used for apoptosis induction.In conclusion, epithelial barrier dysfunction by oral and fecal C. concisus strains could mainly be assigned to apoptotic leaks together with moderate TJ changes, demonstrating a leak-flux mechanism that parallels the clinical manifestation of diarrhea.

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Section: Discussioncontrasting

confidence: 99%

Section: Resultsmentioning

confidence: 91%

Oral and Fecal Campylobacter concisus Strains Perturb Barrier Function by Apoptosis Induction in HT-29/B6 Intestinal Epithelial Cells

Nielsen

Ejlertsen

et al. 2011

PLoS ONE

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“…One possibility is that impaired production of antimicrobial defensins associated with CARD15/NOD2 mutations could facilitate bacterial translocation into the mucosa, leading to inflammation and cytokine-mediated TJ changes. [72][73][74][75][76] In support of this thesis, CARD15/NOD2 knockout mice, which are more susceptible to TNBS colitis, show intestinal changes that include enhanced bacterial translocation, elevated TNFa, IFNg, and IL-4, decreased ZO-1 and -2, and increased permeability. 77 Although potential changes in the expression of claudin proteins were not reported, all 3 cytokines are known to have significant effects on TJ protein expression, including the regulation of claudin-2.…”

Section: Crohn's Diseasementioning

confidence: 72%

Claudin-2 as a mediator of leaky gut barrier during intestinal inflammation

et al. 2015

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“…Arcobacter species were reported to have ability to adhere and invade the intestinal epithelial cells of host and induce inflammatory responses [17]. Arcobacter infection was reported to be associated with leak flux type of watery diarrhea resulting from epithelial barrier dysfunction [18], and adhesion, invasion and toxin production could be the mechanisms of Arcobacter pathogenicity [9,19]. …”

Section: Resultsmentioning

confidence: 99%

Virulence gene profiles of Arcobacter species isolated from animals, foods of animal origin, and humans in Andhra Pradesh, India

et al. 2017

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Aim::This study aimed to detect putative virulence genes in Arcobacter species of animal and human origin.Materials and Methods::A total of 41 Arcobacter isolates (16 Arcobacter butzleri, 13 Arcobacter cryaerophilus, and 12 Arcobacter skirrowii) isolated from diverse sources such as fecal swabs of livestock (21), raw foods of animal origin (13), and human stool samples (7) were subjected to a set of six uniplex polymerase chain reaction assays targeting Arcobacter putative virulence genes (ciaB, pldA, tlyA, mviN, cadF, and cj1349).Results::All the six virulence genes were detected among all the 16 A. butzleri isolates. Among the 13 A. cryaerophilus isolates, cadF, ciaB, cj1349, mviN, pldA, and tlyA genes were detected in 61.5, 84.6, 76.9, 76.9, 61.5, and 61.5% of isolates, respectively. Among the 12 A. skirrowii isolates, cadF, ciaB, cj1349, mviN, pldA, and tlyA genes were detected in 50.0, 91.6, 83.3, 66.6, 50, and 50% of isolates, respectively.Conclusion::Putative virulence genes were detected in majority of the Arcobacter isolates examined. The results signify the potential of Arcobacter species as an emerging foodborne pathogen.

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Arcobacter butzleriInduces Barrier Dysfunction in Intestinal HT‐29/B6 Cells

Abstract: A. butzleri induces epithelial barrier dysfunction by changes in tight junction proteins and induction of epithelial apoptosis, which are mechanisms that are consistent with a leak flux type of diarrhea in A. butzleri infection.

Cited by 64 publications

References 45 publications

Oral and Fecal Campylobacter concisus Strains Perturb Barrier Function by Apoptosis Induction in HT-29/B6 Intestinal Epithelial Cells

Oral and Fecal Campylobacter concisus Strains Perturb Barrier Function by Apoptosis Induction in HT-29/B6 Intestinal Epithelial Cells

Claudin-2 as a mediator of leaky gut barrier during intestinal inflammation

Virulence gene profiles of Arcobacter species isolated from animals, foods of animal origin, and humans in Andhra Pradesh, India

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