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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of Mycobacterium tuberculosis grown in vitro and obtained from sputum to investigate the effect of whether they contain lipid bodies

ABSTRACT: Data is also available from http://bugs.sgul.ac.uk/E-BUGS-52

INSTRUMENT(S): Nanodrop N1000 spectrophotometer

ORGANISM(S): Mycobacterium tuberculosis

SUBMITTER:

PROVIDER: E-BUGS-52 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Cytological and transcript analyses reveal fat and lazy persister-like bacilli in tuberculous sputum.

Garton Natalie J NJ Waddell Simon J SJ Sherratt Anna L AL Lee Su-Min SM Smith Rebecca J RJ Senner Claire C Hinds Jason J Rajakumar Kumar K Adegbola Richard A RA Besra Gurdyal S GS Butcher Philip D PD Barer Michael R MR

PLoS medicine 20080401 4

<h4>Background</h4>Tuberculous sputum provides a sample of bacilli that must be eliminated by chemotherapy and that may go on to transmit infection. A preliminary observation that Mycobacterium tuberculosis cells contain triacylglycerol lipid bodies in sputum, but not when growing in vitro, led us to investigate the extent of this phenomenon and its physiological basis.<h4>Methods and findings</h4>Microscopy-positive sputum samples from the UK and The Gambia were investigated for their content o ...[more]

PMID: 18384229

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Microarray analysis of defined Mycobacterium tuberculosis populations using RNA amplification strategies

Project description:Background The amplification of bacterial RNA is required if complex host-pathogen interactions are to be studied where the recovery of bacterial RNA is limited. Here, using a whole genome Mycobacterium tuberculosis microarray to measure cross-genome representation of amplified mRNA populations, we have investigated two approaches to RNA amplification using different priming strategies. The first using oligo-dT primers after polyadenylation of the bacterial RNA, the second using a set of mycobacterial amplification-directed primers. Results The reproducibility, sensitivity, and the representational bias introduced by these amplification systems were examined by contrasting expression profiles of the amplified products from inputs of 500, 50 and 5ng total M.tuberculosis RNA with unamplified RNA from the same source. In addition a model M.tuberculosis system of microaerophilic growth and non-replicating persistence was used to assess the capability of amplified RNA microarray comparisons from an experimental system where RNA yield is restricted. Mycobacterial RNA was reproducibly amplified using both methods from as little as 5ng total RNA (~ equivalent to 2E+05 bacilli). Differential gene expression patterns observed with unamplified RNA in the switch from aerobic to microaerophilic growth were also reflected in the amplified expression profiles. Conclusions Here we describe two reproducible methods of bacterial RNA amplification that will allow previously intractable host-pathogen interactions during bacterial infection to be explored at the whole genome level by RNA profiling. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-42

2008-03-12 | E-BUGS-42 | biostudies-arrayexpress

Examining the basis of isoniazid tolerance in nonreplicating Mycobacterium tuberculosis using transcriptional profiling

Project description:Background: Understanding how growth state influences Mycobacterium tuberculosis responses to antibiotic exposure provides a window into drug action during patient chemotherapy. In this article, we describe the transcriptional programs mediated by isoniazid (INH) during the transition from log-phase to nonreplicating bacilli, from INH-sensitive to INH-tolerant bacilli respectively, using the Wayne model. Results: INH treatment did not elicit a transcriptional response from nonreplicating bacteria under microarophilic conditions (NRP2), unlike the induction of a robust and well-characterized INH signature in log-phase bacilli. Conclusion: The differential regulation (between drug-free NRP2 and log-phase bacilli) of genes directly implicated in INH resistance could not account for the abrogation of INH killing in nongrowing bacilli. Thus, factors affecting the requirement for mycolic acids and the redox status of bacilli are likely responsible for the reduction in INH efficacy. We speculate on additional mechanisms revealed by transcriptome analysis that might account for INH tolerance. Data is also available from <ahref=http://bugs.sgul.ac.uk/E-BUGS-104 target=_blank>BuG@Sbase</a>

2011-01-17 | E-BUGS-104 | biostudies-arrayexpress

Transcription profiling of Mycobacterium tuberculosis treated with benzothiazinones which kill M. tuberculosis by blocking arabinan synthesis

Project description:Data is also available from <ahref=http://bugs.sgul.ac.uk/E-BUGS-80 target=_blank>BuG@Sbase</a>

2009-03-19 | E-BUGS-80 | biostudies-arrayexpress

Transcription profiling of Mycobacterium tuberculosis infected human dendritic cells and macrophages and M. tuberculosis grown aerobically to investigate host-pathogen cross-talk

Project description:Data is also available from http://bugs.sgul.ac.uk/E-BUGS-58

2008-01-04 | E-BUGS-58 | biostudies-arrayexpress

Methionine Sulfoximine Resistance in Mycobacterium tuberculosis Is Due to a Single Nucleotide Deletion Resulting in Increased Expression of the Major Glutamine Synthetase, GlnA1.

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2011-09-06 | E-BUGS-112 | biostudies-arrayexpress

Transcription profiling of Mycobacterium tuberculosis after treatment with ciprofloxacin to investigate the SOS DNA repair response

Project description:Data is also available from http://bugs.sgul.ac.uk/E-BUGS-63

2008-09-26 | E-BUGS-63 | biostudies-arrayexpress

Pain-killer carprofen elicits pleiotropic modes of bactericidal action with potential to reverse antimicrobial resistance in tuberculosis.

Project description:The alarming rise of antimicrobial resistance in Mycobacterium tuberculosis coupled with the shortage of new antibiotics has made tuberculosis (TB) control a global health priority. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the growth of multi-drug resistant isolates of M. tuberculosis. Repurposing NSAIDs, with known clinical properties and safety records, offers a direct route to clinical trials. Therefore we investigated the novel mechanisms of anti-mycobacterial action of the NSAID, carprofen. Integrative molecular and microbiological approaches revealed that carprofen, a bactericidal drug, inhibited bacterial drug efflux mechanisms. In addition, carprofen restricted mycobacterial biofilm-like growth, highlighting the requirement of efflux-mediated communicative systems for the formation of biofilms. Transcriptome profiling revealed that carprofen likely acts by inhibiting respiration through the disruption of membrane potential, which may explain why spontaneous drug-resistant mutants could not be raised due to the pleiotropic nature of carprofen’s anti-tubercular action. This immunomodulatory drug has the potential to reverse TB antimicrobial resistance by inhibiting drug efflux pumps and biofilm formation, and paves a new chemotherapeutic path for tackling tuberculosis.

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Comparative genomic hybridization of the dominant strains of Mycobacterium tuberculosis in a UK South Asian community

Project description:Data is also available from http://bugs.sgul.ac.uk/E-BUGS-44

2007-09-06 | E-BUGS-44 | biostudies-arrayexpress

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2011-04-15 | E-BUGS-111 | biostudies-arrayexpress

Transcription profiling of Mycobacterium bovis and Mycobacterium tuberculosis to identify key gene expression differences

Project description:Data is also available from http://bugs.sgul.ac.uk/E-BUGS-37

2007-10-11 | E-BUGS-37 | biostudies-arrayexpress