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Early cell death induced by Clostridium difficile TcdB

ABSTRACT: This study primarily shows the transcripts for all genes possibly involved in uptake of C. difficile TcdB. The long term effect of the second receptor binding domain (aa 1101-1873) of TcdB (2 µg/ml) on Hep-2 cells was investigated after 72 hours of incubation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110242 | GEO | 2018/05/31

REPOSITORIES: GEO

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Modeling Clostridium difficile infections

Project description:Clostridium difficile (Cd) is a gram-positive, spore-forming bacterium and the primary cause of nosocomial diarrhea and pseudomembranous colitis. The pathogenicity of Cd has been linked to its production of TcdA and TcdB. While they cause fluid secretion, inflammation, and colonic damage, their respective and synergistic roles have been difficult to ascertain. In infection animal model, TcdB has been demonstrated to be a key virulence factor, and TcdB causes obvious damage in human and porcine colonic explants. Using the colonic epithelia derived from cloned colonic stem cells, we have developed a model to test the response to TcdB. Epithelia generated in air-liquid interface cultures from cloned transverse colon stem cells were challenged with TcdB at different concentrations and durations.

2015-05-29 | GSE63880 | GEO

Effect of tcdR mutation in Clostridium difficile sporulation

Project description:Clostridium difficile is an important nosocomial pathogen and the leading cause of hospital-acquired diarrhea. Antibiotic use is the primary risk factor for the development of C. difficile-associated disease because it disrupts normal protective gut flora and enables C. difficile to colonize the colon. C. difficile damages host tissue by secreting toxins and disseminates by forming spores. The toxin-encoding genes, tcdA and tcdB are part of a pathogenicity locus, which also encodes the gene tcdR that codes for the toxin genes positive regulator. TcdR is an alternate sigma factor that initiates transcription of tcdA and tcdB at their promoters. Alternative sigma factors are known to regulate virulence and virulence associated genes in many pathogenic bacteria. We created a tcdR mutant in the epidemic-type C. difficile R20291 strain in an attempt to identify the global role of tcdR. A site-directed mutation in tcdR affected both toxin production and sporulation in C. difficile R20291. Spores derived from the tcdR mutant were found to be mildly temperature sensitive. Moreover, nearly two fold more taurocholate was needed to germinate spores from the tcdR mutant than the spores prepared from the wild-type parent strain. Comparison of the tcdR mutant transcriptome with the parent strain revealed many differentially expressed late sporulation genes in the tcdR mutant. These data suggests that gene regulatory networks of toxin production and sporulation in Clostridium difficile are linked with each other.

2017-03-07 | GSE85395 | GEO

Human colon epithelial treated with Clostridium difficile Toxins A and B

Project description:Toxin A and B from Clostridium difficile are the primary virulence factors in Clostridium difficile disease. The changes in gene transcription of human colon epithelial cells were investigated in vitro in order to better understand the many effects of both toxins. HCT-8 cells were treated with 100 ng/ml of either Toxin A or B (TcdA or TcdB). RNA was isolated 2, 6, and 24 hours after addition of toxin from untreated and toxin-treated cells.

2012-01-06 | E-GEOD-29008 | biostudies-arrayexpress

Genome-wide expression of the epithelial layer cells of mice injected with Clostridium difficile Toxin A and B

Project description:Toxin A (TcdA) and Toxin B (TcdB), of the pathogen Clostridium difficile, are virulence factors that cause gross pathologic changes (e.g. inflammation, secretion, and diarrhea) in the infected host, yet the molecular and cellular pathways leading to observed host responses are poorly understood. To address this gap, TcdA and/or TcdB were injected into the ceca of mice and the genome-wide transcriptional response of epithelial layer cells was examined. Bioinformatic analysis of gene expression identified sets of cooperatively expressed genes. Further analysis of inflammation associated genes revealed dynamic chemokine responses. In total, 32 samples were analyzed (one microarray per mouse). The sample groups are separated by two factors: Toxin (TcdA, TcdB, TcdA+TcdB, or Sham injection) and endpoint (2, 6, or 16h). TcdA+B at 16h was not included, leaving 11 sample groups. Each sample group included biological triplicates, except TcdA+TcdB at 6h (one array) and Sham injection at 16h (four arrays).

2013-07-30 | E-GEOD-44091 | biostudies-arrayexpress

Early cell death induced by Clostridium difficile TcdB

Project description:Early cell death induced by Clostridium difficile TcdB

| PRJNA433240 | ENA

Genome-wide expression of the epithelial layer cells of mice injected with Clostridium difficile Toxin A and B

2013-07-30 | GSE44091 | GEO

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Clostridioides difficile toxins deregulate tight junction proteins.

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Clostridium difficile response to iron limitation

Project description:C. difficile was grown in BHIS broth or BHIS broth with 75uM dipridyl and gene expression was compared.

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