Dynamics of microbiota beyond host death
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ABSTRACT:
PROVIDER: PRJEB26643 | ENA |
REPOSITORIES: ENA
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Project description:Parasite biology, by its very nature, cannot be understood without integrating it with that of the host, nor can the host response be adequately explained without considering the activity of the parasite. However, due to experimental limitations, molecular studies of parasite-host systems have been predominantly one-sided investigations focusing on either of the partners. Here we conduct a joint dual RNA-seq time course analysis of filarial parasite and host mosquito to better understand the parasite processes underlying development in, and interaction with, the host tissue from the establishment of infection to the emergence of infective-stage larva. Using the Brugia malayi-Aedes aegypti system, we report the parasite gene transcription dynamics, which exhibit a highly ordered developmental program consisting of a series of cyclical and state-transitioning temporal patterns. And, we contextualize these parasite data in relation to the concurrent dynamics of the host transcriptome. Comparative analyses using uninfected tissues and different host strains reveal the influence of parasite development on the host gene transcription as well as the influence of host environment on the parasite gene transcription. Furthermore, we critically evaluate the life-cycle transcriptome of B. malayi by comparing developmental stages in the mosquito relative to those in the mammalian host, providing insight into gene expression changes underpinning the mosquito-borne parasitic lifestyle of this heteroxenous parasite. Time-course mRNA profiles of filarial parasite Brugia malayi and host mosqutio Aedes aegypti were generated by deep sequencing using Illumina GAIIx.
2014-04-15 | E-GEOD-53664 | biostudies-arrayexpress
Project description: Not available
| S-EPMC6052066 | biostudies-literature
Project description:We report the temporal dynamics of differential gene expression between primed and unprimed beetles infected with the entomopathogen Bt
2017-02-28 | GSE95387 | GEO
Project description:Parasite biology, by its very nature, cannot be understood without integrating it with that of the host, nor can the host response be adequately explained without considering the activity of the parasite. However, due to experimental limitations, molecular studies of parasite-host systems have been predominantly one-sided investigations focusing on either of the partners. Here we conduct a joint dual RNA-seq time course analysis of filarial parasite and host mosquito to better understand the parasite processes underlying development in, and interaction with, the host tissue from the establishment of infection to the emergence of infective-stage larva. Using the Brugia malayi-Aedes aegypti system, we report the parasite gene transcription dynamics, which exhibit a highly ordered developmental program consisting of a series of cyclical and state-transitioning temporal patterns. And, we contextualize these parasite data in relation to the concurrent dynamics of the host transcriptome. Comparative analyses using uninfected tissues and different host strains reveal the influence of parasite development on the host gene transcription as well as the influence of host environment on the parasite gene transcription. Furthermore, we critically evaluate the life-cycle transcriptome of B. malayi by comparing developmental stages in the mosquito relative to those in the mammalian host, providing insight into gene expression changes underpinning the mosquito-borne parasitic lifestyle of this heteroxenous parasite.
2014-04-15 | GSE53664 | GEO
Project description:Whole-genome expression dynamics of cyanopodovirus P-SSP7 and its host Prochlorococcus strain MED4 have been reported. To investigate whether cyanopodoviruses infecting Prochlorococcus and Synechococcus have similar transcription strategy and host response to phage infection, genomic and transcriptomic analyses were conducted on cyanopodovirus S-SBP1 that infects Synechococcus strain WH7803. S-SBP1 has a latent period of 8 h and a burst size of 30 progeny phages per cell. S-SBP1 was most similar to cyanopodovirus S-RIP2 that also infects Synechococcus WH7803, in terms of whole genome phylogenetic relationship and average nucleotide identity (ANI). Three hypervariable genomic islands were found when comparing the genomes of S-SBP1 and S-RIP2, and single nucleotide variants (SNV) were observed on three genes of S-SBP1, which are located within the island regions. Based on RNA-seq analysis, genes of S-SBP1 were clustered into three temporal express classes, with gene content within each class similar to that of P-SSP7. Thirty-two host genes were upregulated during phage infection, including those involved in carbon metabolism, ribosome component and stress response. These upregulated genes were also similar to those of Prochlorococcus MED4 in response to infection by P-SSP7. Our study demonstrates a programmed temporal expression pattern of cyanopodoviruses and hosts during infection.
2020-12-07 | GSE150732 | GEO
Project description:Immune cells need to swiftly and effectively respond to invading pathogens. This response relies heavily on rapid protein synthesis and accurate cellular targeting to ensure pathogen destruction. In return, pathogens intercept this response so they can survive and proliferate. To gain insight into this dynamic interface, we combined click-chemistry with pulsed stable isotope labelling of amino acids (pSILAC-AHA) and quantified the newly synthesised host proteome during macrophage infection with the model intracellular bacterial pathogen, Salmonella enterica Typhimurium (STm). We monitored newly synthesized proteins across different compartments and during different infection stages, and used available proteomics data in response to LPS to deconvolute the STm-specific response. Within this rich resource, we detect aberrant trafficking of lysosomal proteases to the extracellular space and the nucleus, the latter of which correlates with signatures of cell death. Pharmacological cathepsin inhibition suppressed caspase-11 dependent macrophage cell death, thus demonstrating an active role for cathepsins during STm induced pyroptosis. Our study illustrates the utility of resolving the host proteome dynamics during infection to drive the discovery of novel biological mechanisms at the host-microbe interface.
2020-01-24 | PXD010179 | Pride
Project description:Ebola virus (EBOV) causes epidemics with high mortality, yet remains understudied due to the challenge of experimentation in high-containment and outbreak settings. Here, we used single-cell transcriptomics and CyTOF-based single-cell protein quantification to characterize peripheral immune cells during EBOV infection in rhesus monkeys. We obtained 100,000 transcriptomes and 15,000,000 protein profiles, providing insight into pathogenesis: e.g., immature, proliferative monocyte-lineage cells with reduced antigen presentation capacity replace conventional monocyte subsets, while lymphocytes upregulate apoptosis genes and decline in abundance. By quantifying intracellular viral RNA, we identify molecular determinants of tropism among circulating immune cells and examine temporal dynamics in viral and host gene expression. Within infected cells, EBOV down-regulates STAT1 mRNA and interferon signaling, and up-regulates putative pro-viral genes (e.g., DYNLL1 and HSPA5), nominating pathways the virus manipulates for its replication. This study sheds light on EBOV tropism, replication dynamics, and elicited immune response, and provides a framework for characterizing host-virus interactions under maximum containment.
2020-09-23 | GSE158390 | GEO
Project description:Abstract: The type three secretion system 1 (T3SS1) of the marine bacterium, Vibrio parahaemolyticus, orchestrates a host cell death comprised of distinct stages defined by the action of specific effectors. To understand how the host responds to the T3SS1, we analyzed gene expression changes over time in infected primary fibroblasts by RNA-seq. The host cell’s transcriptional response was rapid, robust and temporally distinct. Despite the lethal action of the T3SS1 effectors, network analysis indicated that the integrated host transcriptional response to T3SS1 effectors activated cell survival and repressed cell death networks, suggesting that T3SS1 masks its cytotoxicity to the host cell. Pathway analysis revealed that signaling through several pathways, including MAPK pathways, was specifically altered by T3SS1. Overall, this temporal analysis of T3SS1-mediated subversion of host cell signaling revealed cytoprotective pathways that are likely hijacked by many bacterial pathogens to ensure survival. Methods: We employed genome-wide transcriptional profiling methods (RNA-seq) to measure changes in gene expression over time in response to infection with POR4:T3SS1- or POR3:T3SS1+. Time points were collected 45, 60, 75 and 90 minutes post-infection. In total, libraries from 27 samples (triplicates of uninfected, POR3/4 at t=45, 60, 75, and 90 minutes) were sequenced and mapped to the human genome. EdgeR was used for differential expression analysis using statistical cutoffs of of false discovery rate (FDR) ≤0.01, log2counts-per-million (log2CPM) ≥0 and fold change (FC) cutoffs of -1.5≥ FC ≥1.5
2017-04-28 | GSE93783 | GEO
Project description:Host-virus transcriptome dynamics determined from RNA-sequencing
| PRJNA302091 | ENA