Drosophila immune priming to Enterococcus faecalis relies on immune tolerance rather than resistance
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ABSTRACT:
PROVIDER: PRJNA865019 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20746141_1.fastq.gz | Fastqsanger.gz | |||
| SRR20746141_2.fastq.gz | Fastqsanger.gz | |||
| SRR20746142_1.fastq.gz | Fastqsanger.gz | |||
| SRR20746142_2.fastq.gz | Fastqsanger.gz | |||
| SRR20746143_1.fastq.gz | Fastqsanger.gz |
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Project description:Innate immune priming increases an organism’s survival of a second infection after an initial, non-lethal infection. We used Drosophila melanogaster and an insect-derived strain of Enterococcus faecalis to study transcriptional control of priming. In contrast to other pathogens, the enhanced survival in primed animals does not correlate with decreased E. faecalis load. Further analysis shows that primed organisms tolerate, rather than resist infection. Using RNA-seq of immune tissues, we found many genes were upregulated in only primed flies, suggesting a distinct transcriptional program in response to initial and secondary infections. In contrast, few genes continuously express throughout the experiment or more efficiently re-activate upon reinfection. Priming experiments in immune deficient mutants revealed Imd is largely dispensable for responding to a single infection but needed to fully prime. Together, this indicates the fly’s innate immune response is plastic — differing in immune strategy, transcriptional program, and pathway use depending on infection history.
2022-08-03 | GSE210282 | GEO
Project description:Training and priming of innate immune cells involve preconditioning by PAMPs, DAMPs and/or cytokines that elicits stronger induction of inflammatory genes upon secondary challenge. Previous models distinguish training and priming based upon whether immune activation returns to baseline prior to secondary challenge. Tolerance is a protective mechanism whereby potent stimuli induce refractoriness to secondary challenge. Training and priming are important for innate memory responses that protect against infection, efficacy of vaccines, and maintaining innate immune cells in a state of readiness; tolerance prevents toxicity from excessive immune activation. Dysregulation of these processes can contribute to pathogenesis of autoimmune/inflammatory conditions, post-COVID-19 hyperinflammatory states, or sepsis- associated immunoparalysis. Training, priming and tolerance regulate similar ‘signature’ inflammatory genes such as TNF, IL6 and IL1B and utilize overlapping epigenetic mechanisms. We review how interferons (IFNs), best known for activating Jak-STAT signaling and interferon- stimulated genes, also play a key role regulating training, priming and tolerance via chromatin- mediated mechanisms. We present new data on how monocyte-to-macrophage differentiation modulates IFN-g-mediated priming, changes AP-1 and CEBP activity, and attenuates superinduction of inflammatory genes. We present a ‘training-priming continuum’ model that integrates IFN-mediated priming into current concepts about training and tolerance and proposes a central role for STAT1 and IRF1.
2024-05-22 | GSE262912 | GEO
Project description:Training and priming of innate immune cells involve preconditioning by PAMPs, DAMPs and/or cytokines that elicits stronger induction of inflammatory genes upon secondary challenge. Previous models distinguish training and priming based upon whether immune activation returns to baseline prior to secondary challenge. Tolerance is a protective mechanism whereby potent stimuli induce refractoriness to secondary challenge. Training and priming are important for innate memory responses that protect against infection, efficacy of vaccines, and maintaining innate immune cells in a state of readiness; tolerance prevents toxicity from excessive immune activation. Dysregulation of these processes can contribute to pathogenesis of autoimmune/inflammatory conditions, post-COVID-19 hyperinflammatory states, or sepsis- associated immunoparalysis. Training, priming and tolerance regulate similar ‘signature’ inflammatory genes such as TNF, IL6 and IL1B and utilize overlapping epigenetic mechanisms. We review how interferons (IFNs), best known for activating Jak-STAT signaling and interferon- stimulated genes, also play a key role regulating training, priming and tolerance via chromatin- mediated mechanisms. We present new data on how monocyte-to-macrophage differentiation modulates IFN-g-mediated priming, changes AP-1 and CEBP activity, and attenuates superinduction of inflammatory genes. We present a ‘training-priming continuum’ model that integrates IFN-mediated priming into current concepts about training and tolerance and proposes a central role for STAT1 and IRF1.
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Project description:Effects of heat priming applied to the first generation on tolerance of the successive generation to post-anthesis high temperature stress were investigated. Compared with the progeny of non-heat primed plants (NH), the progeny of heat-primed plants (PH) presented higher grain yield, leaf photosynthesis and activities of antioxidant enzymes and lower cell membrane damage under high temperature stress. In the transcriptome profile, 1430 probes showed obvious difference in expression between PH and NH. These genes were those of signal transduction, transcription, energy, defense, and protein destination and storage, respectively. Pot experiments (25 cm in diameter and 22 cm in depth) were conducted at the Experimental Station of Nanjing Agricultural University, Nanjing, China (32Ë30ʹN and 118Ë42ʹE). During the first generation, wheat plants were divided into two groups: one group were not primed (N) while the other were heat-primed (P) at pre-anthesis (at a day/night temperature of 32/28ËC for two days at the seven-leaf stage and the nine-leaf stage) and post-anthesis (34/30ËC for seven days at the 10th day after anthesis). At maturity, seeds from both groups were harvested. Seedlings (the progeny generation) from each group seed were further divided two sub-groups: one was subjected to high temperature stress at a day/night temperature of 34/30ËC, while the other was set at 26/22ËC for six days from the 10th day after anthesis (DAA). During both priming and high-temperature stress, plants under different treatments were moved into sepatarate growth chambers at preset temperatures. Thereafter, four treatments were established: NC, progeny of non-primed plants without post-anthesis high temperature stress; NH, progeny of non-primed plants with post-anthesis high temperature stress; PC, progeny of primed plants without post-anthesis high temperature stress; and PH, progeny of primed plants with post-anthesis high temperature stress.
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Project description:CroRS is a cell envelope stress response two-component system in the bacterial pathogen Enterococcus faecalis. Antimicrobial tolerance is the ability of an organism to survive, but not proliferate, upon antimicrobial challenge, and is a known precursor to the development of antimicrobial resistance. We have previously shown that CroRS is essential for antimicrobial tolerance in E. faecalis. Therefore, the aim of this experiment was to determine the teixobactin-induced CroRS regulon to identify key pathways of antimicrobial tolerance. To do this, E. faecalis wild-type and a croRS deletion mutant were grown to mid-exponential phase and challenged with and without teixobactin (0.5 ug/ml) for 1 hour. RNA was subsequently extracted, purified and RNA sequenced. RNA libraries were prepped using the Zymo-Seq RiboFree Total RNA-Seq Library Kit. Sequencing was completed using an Illumina MiSeq (v3) system generating 150 bp paired-end reads.
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Project description:Immune tolerance is an active state of unresponsiveness of the immune system to antigens (Ags) that have the potential to induce an immune response1. Such tolerance is beneficial in avoiding autoimmunity and rejection of organ transplants, but detrimental in cancer2. Type 1 conventional dendritic cells (cDC1s) are unique in their efferocytosis3 and cross-presenting abilities4, resulting in T cell-mediated immunity5 or tolerance6-10. However, the mechanisms underlying the tolerogenic function of cDC1s remain largely unknown. Here, we show that the erythropoietin receptor (EpoR) acts as a critical switch that determines the tolerogenic state of cDC1s and the threshold of Ag-specific T cell responses. In total lymphoid irradiation-induced allograft tolerance11,12, EpoR+ cDC1s induce donor-specific CD4+FoxP3+ regulatory T cells (Tregs), and conditional knockout of EpoR in cDC1s abrogates Ag-specific Treg induction, resulting in allograft rejection. In the steady state, EpoR+ migratory cDC1s control Ag-specific Treg induction in peripheral lymph nodes (LNs). In cancer, EpoR is expressed on both tumor Ag-carrying, tumor-infiltrating cDC1s, as well as migratory cDC1s in tumor-draining LNs (tdLNs). Loss of EpoR from cDC1s leads to tumor reduction by enhancing tumor Ag-specific CD8+ T cell priming and generating more precursor exhausted T cells13 in tdLNs, preserving CD8+ T cell precursor-like features and effector function, and reducing Tregs in the tumor. Thus, targeting EpoR on cDC1s to induce or inhibit immune tolerance should enable new ways to treat a variety of diseases.
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