Epithelial and Mesenchymal Cells in the Bovine Colonic Mucosa Differ in Their Responsiveness to<i>Escherichia coli</i>Shiga Toxin 1

Stamm, Ivonne; Mohr, Melanie; Bridger, P.; Schröpfer, Elmar; König, Matthias; Stoffregen, William C.; Dean-Nystrom, Evelyn A.; Baljer, G.; Menge, Christian

doi:10.1128/iai.00553-08

Cited by 30 publications

(31 citation statements)

References 73 publications

(80 reference statements)

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“…Mucosal antibodies against membrane-associated and secreted STEC proteins, predominantly those implicated in bacterial adhesion to the bovine intestinal mucosa, are readily induced upon experimental STEC infection of calves (40) and may contribute to the reduction in STEC shedding by vaccinated animals (48). Most STEC strains possess adherence traits, but the Stx secreted do not immediately act on bovine epithelial cells (56). Bovine Stx target cells of the adaptive immune system are situated beyond the epithelial (34,37,57).…”

Section: Discussionmentioning

confidence: 99%

“…Strains representative of different PFGE patterns were selected, and the eae subtype was determined by PCR-restriction fragment length polymorphism analysis (51). Adhesion characteristics of the strains to HEp2-cells (ATCC CCL23; LGC-Promochem) and primary bovine colonic crypt cells (56) were detected by a modified Giemsa test (14). The ability to induce reorganization of intracellular actin filaments next to the point of bacterial adhesion was determined in the fluorescent-actin staining test (29), comprising an incubation step (3 h at 37°C) of cell monolayers with washed bacterial suspensions from an overnight culture, an intermediate washing step (cell culture medium) to remove unbound bacteria, and another incubation step (3 h at 37°C) to facilitate formation of a specific adherence pattern.…”

Section: Methodsmentioning

confidence: 99%

“…Cumulating evidence shows that Stx act as immunomodulating agents during bovine STEC infections. Stx1 alters the cytokine expression pattern in mucosal macrophages (56) and intraepithelial lymphocytes (38) and suppresses the activation and proliferation of mucosal and peripheral lymphocytes in vitro (36,37). The development of an adaptive cellular immune response is significantly delayed following experimental infection of calves with Stx2-producing STEC O157:H7 compared to that in animals inoculated with Stx-negative E. coli O157:H7 (22).…”

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confidence: 99%

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Maternally and Naturally Acquired Antibodies to Shiga Toxins in a Cohort of Calves Shedding Shiga-Toxigenic Escherichia coli

Fröhlich

Baljer

Menge

2009

Appl Environ Microbiol

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Calves become infected with Shiga toxin-producing Escherichia coli (STEC) early in life, which frequently results in long-term shedding of the zoonotic pathogen. Little is known about the animals' immunological status at the time of infection. We assessed the quantity and dynamics of maternal and acquired antibodies to Shiga toxins (Stx1 and Stx2), the principal STEC virulence factors, in a cohort of 27 calves. Fecal and serum samples were taken repeatedly from birth until the 24th week of age. Sera, milk, and colostrums of dams were also assessed. STEC shedding was confirmed by detection of stx in fecal cultures. Stx1-and Stx2-specific antibodies were quantified by Vero cell neutralization assay and further analyzed by immunoblotting. By the eighth week of age, 13 and 15 calves had at least one stx 1 -type and at least one stx 2 -type positive culture, respectively. Eleven calves had first positive cultures only past that age. Sera and colostrums of all dams and postcolostral sera of all newborn calves contained Stx1-specific antibodies. Calf serum titers decreased rapidly within the first 6 weeks of age. Only five calves showed Stx1-specific seroconversion. Maternal and acquired Stx1-specific antibodies were mainly directed against the StxA1 subunit. Sparse Stx2-specific titers were detectable in sera and colostrums of three dams and in postcolostral sera of their calves. None of the calves developed Stx2-specific seroconversion. The results indicate that under natural conditions of exposure, first STEC infections frequently coincide with an absence of maternal and acquired Stx-specific antibodies in the animals' sera.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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confidence: 99%

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Maternally and Naturally Acquired Antibodies to Shiga Toxins in a Cohort of Calves Shedding Shiga-Toxigenic Escherichia coli

Fröhlich

Baljer

Menge

2009

Appl Environ Microbiol

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“…Hoey and colleagues 75 reported the finding of Stx receptors in crypt epithelial cells in the intestine, but the toxin does not traffic to the endoplasmic reticulum; it ends up in lysosomes, which probably prevents toxicity. Stamm and colleagues 76 identified novel mesenchymal, nonepithelial Stx target cells in the crypt area of the bovine colonic mucosa. These investigators reported that bovine crypt epithelial cells are resistant to the effects of Stx1, but some intestinal mucosal mesenchymal cells, preliminarily characterized as mucosal macrophages, are Stx1-responsive and may participate in the interaction of STEC with the bovine intestinal mucosa.…”

Section: Proposed Role Of Shiga Toxin In the Bovine Hostmentioning

confidence: 99%

Attaching-effacing Escherichia coli Infections in Cattle

Moxley

Smith

2010

Veterinary Clinics of North America: Food Animal Practice

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Diarrheagenic Escherichia coli are now broadly placed into 6 classes based on virulence mechanisms. One of these classes, enterotoxigenic E coli, is the most common cause of diarrhea in beef and dairy calves in the first 4 days of life. Two other diarrheagenic classes, enterohemorrhagic E coli (EHEC) and enteropathogenic E coli (EPEC), are important causes of disease in human beings, but less well substantiated causes of diarrhea in calves. E coli strains that cause hemorrhagic colitis and hemolytic uremic syndrome in humans, express high levels of Shiga toxin, cause attaching-effacing (A/E) lesions in intestinal epithelial cells, and possess a specific 60-MDa EHEC plasmid are known as EHEC. One feature EHEC and EPEC have in common is the causation of intestinal epithelial lesions known as attaching and effacing (A/E). Attaching-effacing E coli (AEEC) is a designation for those E coli strains known to cause A/E lesions or at least carry the genes for this trait, and therefore include organisms that fall into either the EHEC or EPEC classes. Because cattle are carriers of many different serotypes of EHEC, much emphasis has been placed on the public health and food safety concerns associated with the fecal shedding of these organisms. However, much less emphasis has been given to their roles as diarrheagenic pathogens of cattle. The goal of this article is to address the question of pathogenicity, with a review that focuses on the results of studies of natural and experimental infections with these organisms. The authors conclude that there is overwhelming evidence that many different serogroups of AEEC are diarrheagenic pathogens of calves.

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“…Primary bovine colonic epithelial cells (BCEC prim ) were isolated according to the method of Föllmann et al (2000) with some modifications (Bridger et al 2010;Stamm et al 2008). Briefly, large intestine (colon ascendens) samples were isolated from freshly slaughtered cattle (18-24 months old) from the local abattoir.…”

Section: Isolation and Cultivation Of Bovine Colonic Epithelial Cellsmentioning

confidence: 99%

Suitable in vitro culture of Eimeria bovis meront II stages in bovine colonic epithelial cells and parasite-induced upregulation of CXCL10 and GM-CSF gene transcription

et al. 2015

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We here established a suitable in vitro cell culture system based on bovine colonic epithelial cells (BCEC) for the development of Eimeria bovis merozoites I and the characterization of early parasite-induced innate epithelial host cell reactions as gene transcription of proinflammatory molecules. Both primary and permanent BCEC (BCEC (rim) and BCEC(perm)) were suitable for E. bovis merozoite I invasion and subsequent development of meronts II leading to the release of viable merozoites II. E. bovis merozoite II failed to develop any further neither into gamont nor oocyst stages in BCEC in vitro. E. bovis merozoite I induced innate epithelial host cell reactions at the level of CXC/CCL chemokines (CXCL1, CXCL8, CXCL10, CCL2), IL-6, and GM-CSF gene transcription. Overall, both BCEC types were activated by merozoite I infections since they showed significantly enhanced gene transcript levels of the immunomodulatory molecules CXCL10 and GM-CSF. However, gene transcription profiles of BCEC(prim) and BCEC(perm) revealed different reaction patterns in response to merozoite I infection with regard to quality and kinetics of chemokine/cytokine gene transcription. Although both BCEC types equally showed most prominent responses for CXCL10 and GM-CSF, the induction of CXCL1, CXCL8, CCL2, and IL-6 gene transcripts varied qualitatively and quantitatively. Our results demonstrate that BCEC seem capable to respond to E. bovis merozoite I infection by the upregulation of CXCL10 and GM-CSF gene transcription and therefore probably contribute to host innate effector mechanisms against E. bovis.

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Epithelial and Mesenchymal Cells in the Bovine Colonic Mucosa Differ in Their Responsiveness toEscherichia coliShiga Toxin 1

Cited by 30 publications

References 73 publications

Maternally and Naturally Acquired Antibodies to Shiga Toxins in a Cohort of Calves Shedding Shiga-Toxigenic Escherichia coli

Maternally and Naturally Acquired Antibodies to Shiga Toxins in a Cohort of Calves Shedding Shiga-Toxigenic Escherichia coli

Attaching-effacing Escherichia coli Infections in Cattle

Suitable in vitro culture of Eimeria bovis meront II stages in bovine colonic epithelial cells and parasite-induced upregulation of CXCL10 and GM-CSF gene transcription

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