Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mycobacterium tuberculosis hijacks host primary transcripts

ABSTRACT: Mycobacterium tuberculosis hijacks host primary transcripts

PROVIDER: PRJNA393396 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5810180_1.fastq.gz	Fastqsanger.gz
	SRR5810180_2.fastq.gz	Fastqsanger.gz
	SRR5810190_1.fastq.gz	Fastqsanger.gz
	SRR5810190_2.fastq.gz	Fastqsanger.gz
	SRR5810181_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 40

Similar Datasets

Mycobacterium tuberculosis hijacks host primary transcripts

Project description:Intracellular pathogens requires efficient mechanism adapting the environment inside of host cells. Here we show that the transcriptomes of the cellular mycobacterium tuberculosis and of those released from the infected macrophage cells contain a large fraction of human transcripts by RNA polymerase II. Uptake of host pre-mRNAs is coincident with the co-localization of M. tuberculosis with nuclear membrane. The infective M. tuberculosis selectively uptakes snoRNAs.The intracellular pathogens has a preferable capability in taking pre-mRNAs. The host transcripts are not generally spliced nor translated.We suggest that the intracellular bacterium has acquired a mechanism to take transcripts from the host cell nuclus as its own nutrient supply and may help them to survive with hosts.

2021-10-23 | GSE100897 | GEO

Abundant polyadenylation of transcripts and precursor tRNAs in Mycobacterium tuberculosis upon depletion of Rv3907c, the mycobacterial CCA-adding enzyme

Project description:RNA-Seq results accompanying submission of a manuscript: "Depletion of CCA-adding enzyme in Mycobacterium tuberculosis leads to polyadenylation of transcripts and precursor tRNAs" describing the function of the Rv3907c gene product as a CCA-adding enzyme in Mycobacterium tuberculosis.

2023-09-30 | GSE220711 | GEO

Malaria parasite hijacks host complement C3 to facilitate its transmission

Project description:Malaria parasite hijacks host complement C3 to facilitate its transmission

| PRJNA1129548 | ENA

Host directed activity of Pyrazinamide in Mycobacterium tuberculosis infection

2013-06-28 | GSE48027 | GEO

Primary macrophages and J774 cells respond differently to infection with Mycobacterium tuberculosis

Project description:Macrophages play an essential role in the early immune response to Mycobacterium tuberculosis and are the cell type preferentially infected in vivo. Primary macrophages and macrophage-like cell lines are commonly used as infection models, although the physiological relevance of cell lines, particularly for host-pathogen interaction studies, is debatable. Here we use high-throughput RNA-sequencing to analyse transcriptome dynamics of two macrophage models in response to M. tuberculosis infection. Specifically, we study the early response of bone marrow-derived mouse macrophages and cell line J774 to infection with live and -irradiated (killed) M. tuberculosis. We show that infection with live bacilli specifically alters the expression of host genes such as RSAD2, IFIT1/2/3 and RIG-I, whose potential roles in resistance to M. tuberculosis infection have not yet been investigated. In addition, the response of primary macrophages is faster and more intense than that of J774 cells in terms of number of differentially expressed genes and magnitude of induction/repression. Our results point to potentially novel processes leading to immune containment early during M. tuberculosis infection, and support the idea that important differences exist between primary macrophages and cell lines, which should be taken into account when choosing a macrophage model to study host-pathogen interactions.

2016-10-18 | GSE88801 | GEO

Gene expression data from THP-1 cells infected with different Mycobacterium tuberculosis strains

Project description:Host-pathogen interactions in Mycobacterium tuberculosis infection still remain poorly understood. We investigated the host immune response to different reference Mycobacterium tuberculosis strains in THP-1 cells. Major differences in the gene expression profiles were identified in response to infection with these strains. These findings shed new insights into the dynamic variation in tuberculosis immune response and pathogenesis. We used Affymetrix GeneChip Human Exon 1.0 ST microarrays to investigate host differential gene expression in response to different Mycobacterium tuberculosis strains.

2024-10-24 | GSE246736 | GEO

Analyzing the impact of Mycobacterium tuberculosis infection on primary human macrophages

Project description:The success of Mycobacterium tuberculosis (Mtb) as pathogen is tightly linked to its ability to recalibrate host metabolic processes in infected host macrophages. Correspondingly, analysis of RNA-sequencing datasets showed altered gene expression of key metabolic enzymes involved in NAD+, creatine, glucose and glutamine metabolism (e.g NAMPT, IDO1, SLC6A8, CKB, HK2) in Mtb-infected M2 macrophages.

2020-04-16 | GSE148731 | GEO

Host directed activity of Pyrazinamide in Mycobacterium tuberculosis infection

Project description:Pyrazinamide (PZA) is one of the first line antibiotics used for the treatment of tuberculosis (TB). we have used human monocyte and a mouse model of pulmonary TB to investigate whether treatment with PZA, in addition to its known anti-mycobacterial properties, modulate the host immune response during Mycobacterium tuberculosis (Mtb) infection. Mice were infected with Mtb and treatment with PZA was started at 28 days post-infection. At 42 days and 63 days post-infection, group of animals were euthanized and lung tissue was collected to isolate total RNA and used in microarray experiments. Mtb-infected, untreated animals served as controls.

2013-06-28 | E-GEOD-48027 | biostudies-arrayexpress

Metformin alters human host responses to Mycobacterium tuberculosis in-vitro and in healthy human subjects [PBMC RNA-Seq]

Project description:Metformin, the most widely administered diabetes drug, has been proposed as a candidate for host directed therapy for tuberculosis although very little is known about its effects on human host responses to Mycobacterium tuberculosis. When added in vitro to PBMCs isolated from healthy non-diabetic volunteers, metformin increased glycolysis, inhibited the mTOR targets, strongly reduced M. tuberculosis induced production of TNF-alpha (-58%), IFN-gamma (-47%) and IL-beta (-20%), while increasing phagocytosis. In healthy subjects, in vivo metformin intake induced significant transcriptional changes in whole blood and isolated PBMCs, with substantial down-regulation of genes related to inflammation and the type 1 interferon response. Metformin intake also increased monocyte phagocytosis (by 1.5 to 2 fold) and ROS production (+20%). These results show that metformin in humans has a range of potentially beneficial effects on cellular metabolism, immune function and gene-transcriptional level, that affect innate host responses to M. tuberculosis. This underlines the importance of cellular metabolism for host immunity and supports a role for metformin as host-directed therapy for tuberculosis.

2019-06-16 | GSE102677 | GEO

Metformin alters human host responses to Mycobacterium tuberculosis in-vitro and in healthy human subjects [Ex vivo Blood RNA-Seq]

Project description:Metformin, the most widely administered diabetes drug, has been proposed as a candidate for host directed therapy for tuberculosis although very little is known about its effects on human host responses to Mycobacterium tuberculosis. When added in vitro to PBMCs isolated from healthy non-diabetic volunteers, metformin increased glycolysis, inhibited the mTOR targets, strongly reduced M. tuberculosis induced production of TNF-α (-58%), IFN-gamma (-47%) and IL-1β (-20%), while increasing phagocytosis. In healthy subjects, in vivo metformin intake induced significant transcriptional changes in whole blood and isolated PBMCs, with substantial down-regulation of genes related to inflammation and the type 1 interferon response. Metformin intake also increased monocyte phagocytosis (by 1.5 to 2 fold) and ROS production (+20%). These results show that metformin in humans has a range of potentially beneficial effects on cellular metabolism, immune function and gene-transcriptional level, that affect innate host responses to M. tuberculosis. This underlines the importance of cellular metabolism for host immunity and supports a role for metformin as host-directed therapy for tuberculosis.

2019-06-16 | GSE102633 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data