Drosophila immune priming to Enterococcus faecalis relies on immune tolerance rather than resistance
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE210282 | GEO | 2022/08/03
REPOSITORIES: GEO
Similar Datasets
Project description:Drosophila immune priming to Enterococcus faecalis relies on immune tolerance rather than resistance
| PRJNA865019 | ENA
Project description:As the brain’s resident immune cells, microglia upregulate inflammatory gene expression to promote immune functions. Following the response to early life infection, microglia can remain in a “primed” state in which a subsequent immune trigger produces a hyper-activation. Paradoxically, multiple repeated immune activating events can lead to tolerance, the suppression of immune gene expression and function. Both priming and tolerance represent a form of cellular memory that may be disrupted in neurodevelopmental disorders and is largely unexplored in microglia. We hypothesize that acute versus repeated immune activation engages expression of distinct sets of genes, leading to either microglial priming or tolerance. Using in vivo peripheral injections of low dose liposaccharide (LPS 500ug/kg intraperitoneal) to mimic bacterial infection in mice, we compared animals recievig 1, 2, 3, or 4 daily doses of LPS compared to Vehicle (PBS) controls. We examined tissue from three brain regions, the hippocampus, striatum and frotal cortex by RNAseq.
2024-09-25 | GSE165287 | GEO
Project description:Baris Hancioglu, David Swigon & Gilles Clermont. A dynamical model of human immune response to influenza A virus infection. Journal of Theoretical Biology 246, 1 (2007).
We present a simplified dynamical model of immune response to uncomplicated influenza A virus (IAV) infection, which focuses on the control of the infection by the innate and adaptive immunity. Innate immunity is represented by interferon-induced resistance to infection of respiratory epithelial cells and by removal of infected cells by effector cells (cytotoxic T-cells and natural killer cells). Adaptive immunity is represented by virus-specific antibodies. Similar in spirit to the recent model of Bocharov and Romanyukha [1994. Mathematical model of antiviral immune response. III. Influenza A virus infection. J. Theor. Biol. 167, 323-360], the model is constructed as a system of 10 ordinary differential equations with 27 parameters characterizing the rates of various processes contributing to the course of disease. The parameters are derived from published experimental data or estimated so as to reproduce available data about the time course of IAV infection in a naïve host. We explore the effect of initial viral load on the severity and duration of the disease, construct a phase diagram that sheds insight into the dynamics of the disease, and perform sensitivity analysis on the model parameters to explore which ones influence the most the onset, duration and severity of infection. To account for the variability and speed of adaptation of the adaptive response to a particular virus strain, we introduce a variable that quantifies the antigenic compatibility between the virus and the antibodies currently produced by the organism. We find that for small initial viral load the disease progresses through an asymptomatic course, for intermediate value it takes a typical course with constant duration and severity of infection but variable onset, and for large initial viral load the disease becomes severe. This behavior is robust to a wide range of parameter values. The absence of antibody response leads to recurrence of disease and appearance of a chronic state with nontrivial constant viral load.
2024-09-02 | BIOMD0000000711 | BioModels
Project description:A. Esteban Hernandez-Vargas & Michael Meyer-Hermann. Innate Immune System Dynamics to Influenza Virus. IFAC Proceedings Volumes 45, 18 (2012).
The understanding of how influenza virus infection activates the immune system is crucial to designing prophylactic and therapeutic strategies against the infection. Nevertheless, the immune response to influenza virus infection is complex and remains largely unknown. In this paper we focus in the innate immune response to influenza virus using a mathematical model, based on interferon-induced resistance to infection of respiratory epithelial cells and the clearance of infected cells by natural killers. Simulation results show the importance of IFN-I to prevent new infections in epithelial cells and to stop the viral explosion during the first two days after infection. Nevertheless, natural killers response might be the most relevant for the first depletion in viral load due to the elimination of infected cells. Based on the reproductive number, the innate immune response is important to control the infection, although it would not be enough to clear completely the virus. The effective coordination between innate and adaptive immune response is essential for the virus eradication.
2024-09-02 | BIOMD0000000710 | BioModels
Project description:Immune protection of the body cavities depends on the swift activation of innate and adaptive immune responses in non-classical secondary lymphoid organs known as fat-associated lymphoid clusters (FALCs). While it is well-established that fibroblastic reticular cells (FRCs) are an integral component of the immune-stimulating infrastructure of lymph nodes and other classical secondary lymphoid organs, it has remained elusive whether and how FRCs in FALCs contribute to peritoneal immunity. Using FRC-specific gene targeting, we found that FALCs are underpinned by an elaborated FRC network and that initiation of peritoneal immunity was governed through FRC activation via MyD88-dependent innate immunological sensing. FRC-specific ablation of Myd88 expression blocked recruitment of inflammatory monocytes into FALCs and subsequent CD4+ T cell-dependent B-cell activation. Moreover, containment of Salmonella infection was compromised in conditionally Myd88-deficient mice indicating that FRCs in FALCs function as initial checkpoint in the orchestration of protective immune responses in the peritoneal cavity.
2018-06-12 | E-MTAB-6886 | biostudies-arrayexpress
Project description:Transcriptomic study of the impact of osmopriming on rape seeds (Brassica napus L.; cv 'Libomir') during priming process and after germination. The assays were replicated twice on two independent priming and germination experiments. Seeds were osmoprimed in PEG solution (-1.2 MPa osmotic potential) during 7 days, dried to initial moisture content and then germinated for 7 hours on water. The analysis during different phases of priming procedure (soaking and drying), after whole osmopriming process and germination were done. 10 samples, four condition experiment; non dried primed seeds (Pnd) vs. dry unprimed seeds (UPd) (PEG soaking), non dried primed seeds (Pnd) vs dry primed seeds (Pd) (drying after soaking), dry primed seeds (Pd) vs. dry unprimed seeds (UPd) (full osmopriming process), primed seeds imbibed on water (P7h) vs unprimed seeds imbibed on water (UP7h) (germination after osmopriming). Biological replicates: 2 replicates for comparison PEG soaking, drying after soaking, full osmopriming process and germination after osmopriming.
2014-11-23 | E-GEOD-61702 | biostudies-arrayexpress
Project description:The innate immune system provides the first response to pathogen infection and orchestrates the activation of the adaptive immune system. Though a large component of the innate immune response is common to all infections, pathogen-specific innate immune responses have been documented as well. The innate immune response is thought to be especially critical for fighting infection with Mycobacterium tuberculosis (MTB), the causative agent of tuberculosis (TB). While TB can be a deadly disease, only 5-10% of individuals infected with MTB develop active disease, and this inter-individual variation is, at least partly, heritable. Studies of inter-individual variation in the innate immune response to MTB infection may therefore shed light on the genetic basis for variation in susceptibility to TB. Yet, to date, we still do not know which properties of the innate immune response are specific to MTB infection and which represent a general response to pathogen infection. To begin addressing this gap, we infected macrophages with eight different bacterial pathogens, including different MTB strains and related mycobacteria, and studied the transcriptional response to infection. We found that although the gene expression changes were largely consistent across the bacterial infection treatments, we were able to identify a novel subset of genes whose regulation was affected specifically by infection with mycobacteria. Genetic variants that are associated with regulatory differences in these genes should be considered candidate loci for explaining inter-individual susceptibility TB. RNA-seq of monocyte-derived macrophages isolated from 6 healthy European males at 4, 18, and 48 hours post-infection with the following 8 bacteria: Mycobacterium tuberculosis (MTB) H37Rv, Mycobacterium tuberculosis GC1237, MTB GC1237, bacillus Calmette-Guérin (BCG), Mycobacterium smegmatis, Yersinia pseudotuberculosis, Salmonella typhimurium, and Staphylococcus epidermidis. table-s1.txt is a tab-delimited text file that contains the batch-corrected log2 counts per million for each of the 156 samples, as well as the Ensembl gene ID and gene name. BCG = bacillus Calmette-Guérin GC = Mycobacterium tuberculosis GC1237 Rv = Mycobacterium tuberculosis (MTB) H37Rv Rv+ = heat-inactivated MTB H37Rv Salm = Salmonella typhimurium Smeg = Mycobacterium smegmatis Staph = Staphylococcus epidermidis Yers = Yersinia pseudotuberculosis
2015-03-31 | E-GEOD-67427 | biostudies-arrayexpress
Project description:The unsurpassed simplicity of the fruitfly’s airway epithelium, that is made of homogenous epithelial cells only, favours its use as a model to study general features and response characteristics of airway epithelia in general. All epithelial cells are able to launch an immune response as characterized by the expression of antimicrobial peptide genes. Infection induces a complex change in the expression profile of these epithelial cells. Outstanding are a priming of the immune system and the launch of a survival program, presumably to counteract infection induced apoptotic signals, which comprises the concurrent expression of known longevity genes such as dFoxo, and dThor. In regions of the airway epithelium with strong immune reactions, a complex remodelling of the airways can be observed, which is characterized by metaplasia and presumably also by hyperplasia of the affected epithelial cells. At the transcriptional level, this reorganization of the airway epithelium is mirrored by a recapitulation of genetic programs that are characteristic for early phases of airway development. Taken together, the response characteristics of the fly’s airway epithelium towards infections discloses features that are known from inflammatory diseases of the human lung, thus opening the opportunity to study fundamental aspects of these diseases in the fly. Keywords: Ectopic activation of IMD, larval airways, third instar larvae, Gal4/UAS-system, two-colour microarrays
2009-05-11 | GSE11442 | GEO
Project description:Enterococcus faecalis (E. faecalis) is a Gram-(+) opportunistic pathogen associated with predominantly nosocomial wound infections. E. faecalis has been shown to suppress or evade immune-mediated clearance by the immune system and promote persistent infection. Here, we sought to interrogate whether E. faecalis infection induces transcriptomic changes in the host at the single-cell resolution using a mouse excisional wound model. Keratinocyte, fibroblast, endothelial and immune cell populations reveal unique clusters in the infected wounds. Cell communication analysis discovered strong ligand-receptor interactions between macrophages and endothelial cells in the infected niche, whilst fibroblast and keratinocytes instruct healing cellular interactions in untreated skin wounds. We also identified differential terminal lineage driving genes, following RNA velocity in each condition. Together, results suggest that E. faecalis infection alters the skin transcriptome, which may help promote the chronicity of bacteria-infected wounds.
2023-12-31 | GSE229257 | GEO
Project description:The innate immune response to a broad class of pathogens is highly conserved across all eukaryotes and has been studied in great detail at the cellular and transcriptomic level in several insect species. However, the commensurate cellular proteomic response, especially of hemocytes, the primary immune cell population in insects, has remained poorly understood. We report on the comprehensive proteogenomic analysis of a phagocyte subpopulation from Anopheles gambiae, the primary malaria mosquito vector in Sub-Saharan Africa. We leveraged the innate phagocytic response of mosquito granulocytes to achieve targeted enrichment for these cells to facilitate the examination of their proteomic response profiles following sugar feeding, as well as non-infectious and infectious blood feeding with Plasmodium falciparum. A comparative integrative-OMICs analysis of existing transcriptomic profiles combined with these proteomic data permitted the delineation of the functional genome of anopheline granulocytes. We observed that phagocytosis, blood feeding, and P. falciparum infection induced dramatic shifts in granulocyte protein expression indicative of broad changes in cellular proliferation and innate immune response priming. Importantly, we identified a large number of hemocyte immune proteins that respond to blood feeding alone, suggesting that granulocytes may play an integral role in an anticipatory immune response prior to immune challenge.
2016-09-26 | PXD001507 | Pride