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Discerning the roles of key cytokine signaling pathways in DS HN878 Mtb infection [dataset2]

ABSTRACT: Discerning the roles of key cytokine signaling pathways in DS HN878 Mtb infection [dataset2]

PROVIDER: PRJNA1048967 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27104525_1.fastq.gz	Fastqsanger.gz
	SRR27104525_2.fastq.gz	Fastqsanger.gz
	SRR27104526_1.fastq.gz	Fastqsanger.gz
	SRR27104526_2.fastq.gz	Fastqsanger.gz
	SRR27104527_1.fastq.gz	Fastqsanger.gz

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Discerning the roles of key cytokine signaling pathways in DS HN878 Mtb infection [dataset2]

Project description:We have found that drug-resistant (DR) Mtb infection alters the host pathogen interactions thought to occur during drug-sensitive (DS) Mtb infection. Recent data suggests that lack of IL-1, but not Type I IFN, signaling pathways leads to susceptibility to infection to DR Mtb infection. To understand the pathways involved in maintaining control of DS Mtb infection, we are sequencing the bulk lung cells early in infection.

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Discerning the roles of key cytokine signaling pathways in DR Mtb infection [dataset1]

Project description:We have found that drug-resistant (DR) Mtb infection alters the host pathogen interactions thought to occur during drug-sensitive (DS) Mtb infection. Recent data suggests that lack of both, Type I and IL-1, signaling pathways leads to susceptibility to infection to DR Mtb infection. To understand the pathways involved in maintaining control of DR Mtb infection, we are sequencing the bulk lung cells early in infection.

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Discerning the roles of key cytokine signaling pathways in DR Mtb infection [dataset1]

Project description:Discerning the roles of key cytokine signaling pathways in DR Mtb infection [dataset1]

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Bulk RNA seq of sorted CD11c cells from lungs of uninfected and Mtb infected wild type mice.

Project description:To understand the difference between CD11c population from the uninfected and MTB HN878 infected mice at transcriptome level.

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Early innate immunity determines outcome of Mycobacterium tuberculosis pulmonary infection in rabbits

Project description:In our rabbit model of pulmonary tuberculosis, infection with Mtb HN878, a hyper-virulent W-Beijing strain, results in progressive cavitary disease. However, infection of rabbit lungs with Mtb CDC1551, a hyper-immunogenic strain is effectively controlled overtime, establishing latent Mtb infection. Using these two Mtb strains, we tested the hypothesis that the initial host response in the lungs within hours of infection determines later outcome. The microarray experiments was performed to identify gene expression changes in the Mtb-HN878 or CDC1551- infected rabbit lungs at 3 hours post infection, compared to uninfected naïve rabbit lungs. New Zealand White rabbits were infected with Mtb HN878 or CDC1551 at ~3.5log10. At 3 hours post infection, lung tissue from Mtb-infected and uninfected rabbits were isolated and used for total RNA extraction. Total rabbit lung RNA was used for microarray analysis to determine infection induced changes in host gene expression.

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Mtb-mediated host transcriptional reponse is strain-specific

Project description:CDC1551 induced more vigorous immune response in murine bone marrow derived macrophage (BMM). In contrast, in HN878-infected cells, host transcriptional response was delayed but lasted longer. HN878 induced more genes involved in host lipid metabolism than CDC1551 did. Murine bone marrow derived macrophages were infected with M. tuberculosis CDC1551 or HN878 up to 24 h. Total RNA was processed for microarray and global gene expression was read.

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Mtb-mediated host transcriptional reponse is strain-specific

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Early innate immunity determines outcome of Mycobacterium tuberculosis pulmonary infection in rabbits

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Gene expression profiling of Down Syndrome (DS)-AMKL and non-DS AMKL samples

Project description:The goal of this study is to define a gene expression signature unique to DS-AMKL (acute megakaryoblastic leukemia or FAB M7 leukemia). A similar study was done previously, but using unfractionated patient leukemic samples. In this study, we sorted megakaryocytic leukemia blasts from patients and then compared their gene expression signatures to those from similarly sorted blasts from patients with non-DS AMKL. This allowed us to identify a gene expression signature more unique to DS-AMKL samples.

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