Transcriptional adaptation to chronic exposure to Cytolethal Distending Toxin in HeLa cells
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ABSTRACT:
PROVIDER: PRJNA637286 | ENA |
REPOSITORIES: ENA
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Project description:The Cytolethal Distending Toxin (CDT) is a bacterial genotoxin that promotes persistent bacterial colonization during infection and is associated with many inflamatory disorders and cancer. At the cellular level, CDT induces DNA damage and inflammatory signatures in host cells. The aim of this study was to better understand the links betwen CDT-mediated genotoxic activity and immunomodulatory effects. HeLa cells were exposed to a chronic (8 weeks) treatment to 0.25 ng/ml of wild-type (WT) or the catalytic mutant H153A (HA) of CDT from Escherichia coli and transcription analysis was performed using Agilent Sureprint G3 Human GE v2 8x60k microarray.
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Project description:Campylobacter jejuni is a major cause of food poisoning worldwide, and remains the main infective agent in gastroenteritis and related intestinal disorders in Europe and the USA. As with all bacterial infections, the stages of adhesion to host tissue, survival in the host and eliciting disease all require the synthesis of proteinaceous virulence factors on the ribosomes of the pathogen. Here, we describe how C. jejuni virulence is attenuated by altering the methylation of its ribosomes to disrupt the composition of its proteome, and how this in turn provides a means of identifying factors that are essential for infection and pathogenesis. Specifically, inactivation of the C. jejuni Cj0588/TlyA methyltransferase prevents methylation of nucleotide C1920 in the 23S rRNA of its ribosomes and reduces the pathogen’s ability to form biofilms, to attach, invade and survive in host cells, and to provoke the innate immune response. Mass spectrometric analyses of C. jejuni TlyA-minus strains revealed an array of subtle changes in the proteome composition. These included reduced amounts of the cytolethal distending toxin (CdtC) and the MlaEFD proteins connected with outer membrane vesicle (OMV) production. Inactivation of the cdtC and mlaEFD genes confirms the importance of the toxin and OMVs in establishing infection. Collectively, the data identify a collection of genes required for the onset of human campylobacteriosis, and serve as a proof of principle for use of this approach in detecting proteins involved in bacterial pathogenesis.
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Project description:Aggregatibacter actinomycetemcomitans is an oral and systemic pathogen associated with aggressive forms of periodontitis, and with endocarditis. Outer membrane vesicles (OMVs) released by this species have been demonstrated to deliver effector proteins such as cytolethal distending toxin (CDT) and leukotoxin (LtxA) into human host cells, and to act as triggers of innate immunity upon carriage of NOD1- and NOD2-active pathogen-associated molecular patterns (PAMPs). To improve our understanding of the pathogenicity-associated functions that A. actinomycetemcomitans exports via OMVs, we have used liquid chromatography-tandem mass spectrometry (LC-MS/MS) to characterize the OMV-associated proteome of a rough-colony type clinical isolate, strain 173 (serotype e). This yielded identification of 151 proteins overlapping in three out of four independent experiments, using density gradient-purified OMVs. Further to confirming the vesicle-associated release of LtxA, and of several proteins earlier demonstrated to act as immunoreactive antigens in the human host, we identified numerous additional putative virulence-related proteins in the A. actinomycetemcomitans OMV proteome, including proteins involved in immune evasion, drug targeting, and iron/nutrient acquisition. In summary our findings are consistent with an OMV-associated proteome that exhibits several offensive and defensive functions, and they provide a comprehensive basis to further disclose roles of A. actinomycetemcomitans OMVs in periodontal and systemic disease.
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Project description:<p>This study contains all authorized whole genome sequence data of the HeLa cell line from datasets currently in dbGaP. These data have been approved for health, medical, and/or biomedical research purposes. Access to these data can be granted for one year. Accessible data will include the studies listed on this page and any additional authorized datasets that become available during this one-year period.</p> <p><a href="http://acd.od.nih.gov/hlgda.htm">The HeLa Genome Data Access Working Group of the Advisory Committee to the Director (ACD)</a> will review requests from the research community for access to these datasets and assess whether the requests align with the terms of use defined in the HeLa Genome Data Use Agreement. The Working Group's findings will be reported to the ACD, and the ACD will make recommendations to the NIH Director about whether a request should be approved or disapproved. The NIH Director will decide whether access to the data will be granted.</p>
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Project description:We examined two variants of the genome-sequenced strain, Campylobacter jejuni NCTC11168, which show marked differences in their virulence properties including colonization of poultry, invasion of Caco-2 cells, and motility. Transcript profiles obtained from whole genome DNA microarrays and proteome analyses demonstrated that these differences are reflected in late flagellar structural components and in virulence factors including those involved in flagellar glycosylation, and cytolethal distending toxin production. We identified putative s28 and s54 promoters for many of the affected genes, and found that greater differences in expression were observed for s28-controlled genes. Inactivation of the gene encoding s28, fliA, resulted in an unexpected increase in transcripts with s54 promoters, as well as decreased transcription of s28-regulated genes. This was unlike the transcription profile observed for the attenuated C. jejuni variant, suggesting that the reduced virulence of this organism was not entirely due to impaired function of s28. However, inactivation of flhA, an important component of the flagellar export apparatus, resulted in expression patterns similar to that of the attenuated variant. These findings indicate that the flagellar regulatory system plays an important role in campylobacter pathogenesis and that flhA is a key element involved in the coordinate regulation of late flagellar genes and of virulence factors in C. jejuni. Furthermore, we provide a model for flagellar regulation, which forms a foundation for the study of the unique regulatory networks in this important human pathogen. Keywords: parallel sample
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