Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16939471_1.fastq.gz | Fastqsanger.gz | |||
| SRR16939471_2.fastq.gz | Fastqsanger.gz | |||
| SRR16939472_1.fastq.gz | Fastqsanger.gz | |||
| SRR16939472_2.fastq.gz | Fastqsanger.gz | |||
| SRR16939473_1.fastq.gz | Fastqsanger.gz |
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Project description:Research on forms of memory in innate immune systems has recently gained momentum with the study of trained immunity in vertebrates and immune priming in invertebrates. Immune priming provides protection against previously encountered pathogens. However, causes and mechanisms of immune priming are still not well understood in most organisms. In this work, we combine RNA sequencing with transmission electron microscopy to investigate the dynamic processes during priming in the gut of a well-established model for oral immune priming, consisting of the host Tribolium castaneum and its entomopathogen Bacillus thuringiensis tenebrionis (Btt). We show that priming with specific, non-infectious pathogen-derived cues causes damage in the gut of T. castaneum larvae, which leads to an early physiological stress response as well as the upregulation of a specific set of immune genes. This response diminishes over time yet enables the gut to upregulate genes known to interfere with Btt virulence when T. castaneum larvae are later exposed to infectious Btt spores. These insights contribute to our understanding of immune priming as a dynamic process where cellular responses in concert with specific gene regulation prepare the gut tissue and thereby enables a more efficient protection against infection. Such work can further help us understand the origin and mechanism of innate immune memory.
2025-06-23 | PXD056451 | JPOST Repository
Project description:The 791spin is the spinosad-selected strain derived from 791a, a laboratory strain derived from a multi-resistant field-collected sample of houseflies. The 791a strain proved highly resistant to pyrethroids and some anticholinesterases and showed some resistance to the chitin synthesis-disrupting larvicides.In order to understand the evolution of insecticide resistance, de novo assembly of a spinosad resistant housefly strain 791spin using 454 technology was initiated Transcriptome analysis of insecticide resistant housefly strain compared to susceptible strain
2015-05-12 | E-GEOD-65891 | biostudies-arrayexpress
Project description:Most organisms are hosts to a wide range of symbionts and commensals, but they might also encounter parasites and pathogens during their lifetime. Therefore, immune strategies to recognize and counteract potential threats have evolved across all kingdoms of life. The most elaborate immune defences are found in vertebrate animals, where responses are classically divided into innate and adaptive. Insects lack the cellular machinery needed to provide adaptive immunity. However, over the past decades, work on immune priming has shown that to a certain degree, insects are indeed capable of specifically recognizing, memorizing, and counteracting certain pathogens. An important piece of the puzzle are the pathogen-associated molecules that induce these immune priming responses. Here, we make use of the model system Tribolium castaneum (T. castaneum) and its pathogen Bacillus thuringiensis (B. thuringiensis), to compare the proteomes of two closely related B. thuringiensis strains that either induce priming via the oral route, or not. We identify proteins that might be immunostimulatory in T. castaneum. The Cry3Aa toxin, an important plasmid-encoded virulence factor of Bacillus thuringiensis bv. tenebrionis (hereafter called Btt) was found to be one of the most promising candidates. We made use of additional B. thuringiensis strains varying in the possession of the Cry-carrying plasmid to experimentally test for its relevance for priming. Our findings will help future studies to focus on specific candidates to perform experiments on the mechanisms and evolution of immune priming.
2023-11-01 | PXD039902 | JPOST Repository
Project description:Hytrosaviridae family members replicate in the salivary glands (SGs) of their adult dipteran hosts and are transmitted to uninfected hosts via saliva during feeding. Despite inducing similar gross symptoms (SG hypertrophy; SGH), hytrosaviruses (SGHVs) have distinct pathobiologies, including sex-ratio distortions in tsetse flies and refusal of infected housefly females to copulate. Via unknown mechanism(s), SGHV replication in other tissues results in reduced fecundity in tsetse flies and total shutdown of vitellogenesis and sterility in housefly females. We hypothesized that vitellogenesis shutdown is caused by virus-induced modulation of hormonal titers. Here, we used RNA-Seq to investigate virus-induced modulation of host genes/pathways in healthy and virus-infected houseflies, and we validated expression of the most significantly modulated genes (n=23) by RT-qPCR. We also evaluated the levels and activities of hemolymph antimicrobial peptides (AMPs), levels of endogenous sesquiterpenoids, and impacts of exogenous hormones on ovarian development in viremic females. Of the 973 housefly unigenes that were significantly modulated (padj ≤ 0.01; log2FC ≤ or ≥ 2.0 ), 446 and 527 genes were downregulated and upregulated, respectively. While the most downregulated genes were related to reproduction (embryogenesis/oogenesis), the repertoire of upregulated genes was overrepresented by genes related to non-self recognition, ubiquitin-protease system, cytoskeletal traffic, cellular proliferation, development and movement, and snRNA processing. Overall, MdSGHV induced upregulation of components of the siRNA, innate antimicrobial immune, and autophagy pathways. MdSGHV reduced hemolymph sesquiterpenoids and completely shut down egg development in viremic females. However, the hormonal rescue of vitellogenesis did not result in egg production. The mechanism underlying MdSGHV-induced sterility has yet to be resolved.
2017-06-13 | GSE88939 | 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:Low neoantigen expression and poor T cell priming underlie early immune escape in cancer
2021-06-17 | MSV000087648 | MassIVE