Single cell RNA Seq data of BMDM from mouse infected with Salmonella [stat log]
Ontology highlight
ABSTRACT:
ORGANISM(S): Salmonella enterica subsp. enterica serovar Typhimurium str. SL1344
PROVIDER: GSE102162 | GEO | 2017/10/07
SECONDARY ACCESSION(S): PRJNA396894
REPOSITORIES: GEO
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Project description:The interaction between a pathogen and a host is a highly dynamic process in which both agents activate complex programs. Here, we introduce a single-cell RNA-Seq method (scDual-Seq) that simultaneously captures both host and pathogen transcriptomes and use it to study the process of infection of individual mouse macrophages with the intracellular pathogen Salmonella typhimurium. Among the infected macrophages, we found three subpopulations and we show evidence for a linear progression through these subpopulations, supporting a model in which these three states correspond to consecutive stages of infection.
2017-10-07 | GSE102161 | GEO
Project description:The interaction between a pathogen and a host is a highly dynamic process in which both agents activate complex programs. Here, we introduce a single-cell RNA-Seq method (scDual-Seq) that simultaneously captures both host and pathogen transcriptomes and use it to study the process of infection of individual mouse macrophages with the intracellular pathogen Salmonella typhimurium. Among the infected macrophages, we found three subpopulations and we show evidence for a linear progression through these subpopulations, supporting a model in which these three states correspond to consecutive stages of infection.
2017-10-07 | GSE102159 | GEO
Project description:The interaction between a pathogen and a host is a highly dynamic process in which both agents activate complex programs. Here, we introduce a single-cell RNA-Seq method (scDual-Seq) that simultaneously captures both host and pathogen transcriptomes and use it to study the process of infection of individual mouse macrophages with the intracellular pathogen Salmonella typhimurium. Among the infected macrophages, we found three subpopulations and we show evidence for a linear progression through these subpopulations, supporting a model in which these three states correspond to consecutive stages of infection.
2017-10-07 | GSE104678 | GEO
Project description:The interaction between a pathogen and a host is a highly dynamic process in which both agents activate complex programs. Here, we introduce a single-cell RNA-Seq method (scDual-Seq) that simultaneously captures both host and pathogen transcriptomes and use it to study the process of infection of individual mouse macrophages with the intracellular pathogen Salmonella typhimurium. Among the infected macrophages, we found three subpopulations and we show evidence for a linear progression through these subpopulations, supporting a model in which these three states correspond to consecutive stages of infection.
2017-10-07 | GSE102160 | GEO
Project description:Human infection with Cryptococcus neoformans (Cn), a prevalent fungal pathogen, occurs by inhalation and deposition in the lung alveoli of infectious particles. The subsequent host pathogen interaction is multifactorial and can result either in eradication, latency or extra-pulmonary dissemination. Successful control of Cn infection is dependent on host macrophages as shown by numerous studies. However in vitro macrophages display little ability to kill Cn. Recently, we reported that ingestion of Cn by macrophages induces early cell cycle progression that is subsequently followed by mitotic arrest, an event that almost certainly reflects damage to the host cell. The goal of the present work was to understand macrophage pathways affected by Cn toxicity. Infection of J774.16 macrophage-like cell line macrophages by Cn in vitro was associated with changes in gene pattern expression. Concomitantly we observed depolarization of macrophage mitochondria and alterations in protein translation rate. Our results indicate that Cn infection impairs multiple host cellular functions. Therefore we conclude Cn intracellular residence in macrophages undermines the health of these critical phagocytic cells interfering with their ability to clear the fungal pathogen.
2014-12-31 | GSE57720 | GEO
Project description:Purpose: The purpose of this study was to simulataneously examine the host and fungal pathogen transcriptional profiles of four distinct infection fates during macrophage and Candida albicans interactions Methods: Membrane stained (Deep Red),primary, bone marrow derived, murine macrophages and Candida albicans expressing GFP and mCherry were exposed to each other over a four hour time course. Samples were collected at 0, 1, 2 and 4 hours and sorted for four infection subpopulations: 1. Macrophages which phagocytosed live C. albicans (GFP+ /mCherry+ /Deep Red +), 2. Macrophages which phagocytosed dead C. albicans (GFP- /mCherry+ /Deep Red +), 3. Uninfected macrophages(GFP- /mCherry- /Deep Red +) and 4. Unengulfed C. albicans (GFP+ /mCherry + /Deep Red -). Unexposed controls were also collected for some time points (i.e. macrophages never exposed to C. albicans and C. albicans never exposed to macrophages). Single macrophages infected with live or dead C. albicans were also sorted. Smart-seq2 was used to create libraries for both infection subpopulation and single, infected cell samples that were sequenced on Illumina’s Miseqand Nextseq. Basic quality assessment of Illumina reads and sample demultiplexing was done with Picard version 1.107 and Trimmomatic. Samples profiling exclusively the mouse transcriptional response were aligned to the mouse transcriptome generated from the v. Dec. 2011 GRCm38/mm10 and a collection of mouse rRNA sequences from the UCSC genome website. Samples profiling exclusively the yeast transcriptional response were aligned to the C. albicans transcriptome strain SC5314 version A21-s02-m09-r10 downloaded from Candida Genome Database. Samples containing both macrophages and C. albicans were aligned to a “composite transcriptome” made by combining the mouse transcriptome and C. albicans transcriptomes described above and alignment was done via BWA (version 0.7.10-r789.) Multi-reads (reads that aligned to both host and pathogen transcripts) were discarded. Then, each host or pathogen sample file were aligned to its corresponding reference using Bowtie2 and RSEM (v.1.2.21). Transcript abundance was estimated using transcripts per million (TPM). For subpopulation samples, TPM was calculated using edgeR, all as implemented in the Trinity package version 2.1.. Genes were considered differentially expressed only if they had a 4-fold change difference (> 4 FC) in TPM values and a false discovery rate below or equal to 0.001 (FDR < 0.001), unless specified otherwise. For single macrophages infected with C. albicans, samples were aligned to the combined transcriptome as described above and RSEM was used to calculate TPM. Results: We were able to simultaneously measure the host and fungal pathogen transcriptional profiles of four distinct infection fates during macrophage and Candida albicans interactions Conclusions: Our study represents an analysis of both distinct infection populations of macrophages and fungus.
2018-03-12 | GSE111731 | GEO
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
Project description:Background: Mycobacterium avium is an opportunistic pathogen that requires complex multidrug treatment. Macrolides, like clarithromycin, are the cornerstone of treatment, but even macrolide-based treatment regimens have suboptimal outcomes. Combining transcriptomic profiling of macrophages and mycobacteria in an in vitro infection model may increase our understanding of the host-pathogen interaction and the effect of antibiotic treatment. Methods: To investigate the molecular interplay between pathogen and host, we developed an optimized protocol for dual RNA-sequencing of human monocyte-derived macrophages infected with M. avium. Results: Upon phagocytosis, host defense processes including immune activation and pathogen recognition were upregulated, while M. avium upregulated expression of PE/PPE genes, which are important for immune recognition. Clarithromycin did not affect gene regulation of the host; the effect of clarithromycin on M. avium gene expression was very different in RPMI compared to intracellular mycobacteria, likely due to the influence of the host environment on expression of the important regulatory WhiB genes. Conclusions These data identify the distinct stress responses of M. avium upon infection and clarithromycin treatment and underline the importance of taking the intracellular localization and interaction with the host into account when studying antibiotics against intracellular pathogens.
2024-01-01 | GSE213117 | GEO
Project description:Mycobacterium bovis is an intracellular pathogen that causes tuberculosis in cattle. Following infection, the pathogen resides and persists inside host macrophages by subverting host immune responses via a diverse range of mechanisms. Here, a high-density bovine microarray platform was used to examine the bovine monocyte-derived macrophage transcriptome response to M. bovis infection relative to infection with the attenuated vaccine strain, M. bovis Bacille CalmetteM-bM-^@M-^SGuM-CM-)rin. Differentially expressed genes were identified (adjusted P-value M-bM-^IM-$ 0.01) and interaction networks generated across an infection time course of 2, 6 and 24 h. The largest number of biological interactions was observed in the 24 h network, which exhibited small-worldscale-free network properties. The 24 h network featured a small number of key hub and bottleneck gene nodes, including IKBKE, MYC, NFKB1 and EGR1 that differentiated the macrophage response to virulent and attenuated M. bovis strains, possibly via the modulation of host cell death mechanisms. These hub and bottleneck genes represent possible targets for immunomodulation of host macrophages by virulent mycobacterial species that enable their survival within a hostile environment. Affymetrix GeneChipM-BM-. Bovine Genome Arrays were used to examine gene expression from a paired comparison of bovine monocyte-derived macrophages (MDM) after in vitro challenge with Mycobacterium bovis versus M. bovis BCG across a time series of 2 hr, 6 hr and 24 hr post-challenge.
2014-08-01 | E-GEOD-59774 | biostudies-arrayexpress
Project description:The inducible innate immune response to infection requires a concerted process of gene expression that is regulated at multiple levels. Most global analyses of the innate immune response have focused on transcription induced by defined immunostimulatory ligands, such as lipopolysaccharide. However, the response to pathogens involves additional complexity, as pathogens interfere with virtually every step of gene expression. How cells respond to pathogen-mediated disruption of gene expression to nevertheless initiate protective responses remains unclear. We previously discovered that a pathogen-mediated blockade of host protein synthesis provokes the production of specific pro-inflammatory cytokines. It remains unclear how these cytokines are produced despite the global pathogen-induced block of translation. We addressed this question by using parallel RNAseq and ribosome profiling to characterize the response of macrophages to infection with the intracellular bacterial pathogen Legionella pneumophila. Our results reveal that mRNA superinduction is required for the inducible immune response to a bacterial pathogen.
2017-03-28 | GSE89184 | GEO