Gene expression response to bacterial phagocytosis by S2 cells (control and eater RNAi knock down)
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE31564 | GEO | 2011/08/25
SECONDARY ACCESSION(S): PRJNA145693
REPOSITORIES: GEO
Similar Datasets
Project description:The Drosophila phagocytic receptor Eater is expressed specifically in phagocytic hemocytes. It contributes to host immune defense and is required for survival of bacterial infections. Eater is involved in recognition and phagocytosis of bacteria. We used microarrays to determine whether any gene expression changes after bacterial phagocytosis are dependent on the expression of the phagocytic scavenger receptor Eater. We found transcriptional regulation in response to bacterial internalization, but no significant differences between controls and samples in which eater expression had been diminshed by RNAi eater knock down. Drosophila S2 cells, a hemocyte-derived cell line with phagocytic properties, were exposed to a mixture of Gram-positive and Gram-negative bacteria at conditions of 50% of cell binding. At different time points of synchronized phagocytosis (30, 90 and 180 minutes) total RNA was extracted and subjected to microarray analysis. We compared S2 cells in which Eater expression was decreased by RNA interference with control S2 cells exposed to irrelevant double-stranded (pBR322). Three independent experiments were performed corresponding to three biological replicates. Decreased phagocytosis due to RNAi eater knock down was controlled in all cases.
2011-08-24 | E-GEOD-31564 | biostudies-arrayexpress
Project description:Scavenger receptors on the cell surface of macrophages play an important role in host defence through their ability to bind microbial ligands and induce phagocytosis. Concurrently, signal transduction pathways are initiated that aid in defence mechanisms against the invading microbe. Here we report on the function of scavenger receptor Marco (macrophage receptor with collagenous structure) during infection of zebrafish embryos with Mycobacterium marinum, a close relative of Mycobacterium tuberculosis. Morpholino knockdown demonstrates that Marco is required for the rapid phagocytosis of M. marinum following intravenous infection. Furthermore, gene expression analysis shows that Marco controls the initial transient pro-inflammatory response to M. marinum and remains a determining factor for the immune response signature at later stages of infection. Increased bacterial burden following marco knockdown indicates that this scavenger receptor is important for control of M. marinum growth, likely due to delayed phagocytosis and reduced pro-inflammatory signalling observed under conditions of Marco deficiency
2014-08-06 | GSE58230 | GEO
Project description:Inhalation of the amibient air polution ozone causes lung inflammation and can suppress host defense mechanisms, including impairing macrophage phagocytosis. Ozone reacts with cholesterol in the lung to form oxysterols, like secosterol A and secosterol B, which can form covalent adducts on cellular proteins. How oxysterol-protein adduction modifies the function of lung macrophages is unknown. Herein, we used a preoteomic screen to identify lung macrophage proteins that fomr adducts with ozone-derived oxysterols. Analysis show that the phagocytic receptor CD206 and CD64 formed adducts with secosterol A. Adduction of these receptors with ozone-derived oxysterols impaired ligand binding and corresponded with reduced macrophage phagocytosis. This work suggests a novle mechanism for the suppression of macrophage phagocytosis following ozone exposure through the generation of oxysterols and the formation of oxysterol-protein adducts on phagocytic receptors.
2020-07-18 | PXD019317 | Pride
Project description:Effective innate immunity against many microbial pathogens requires macrophage programs that upregulate phagocytosis and direct antimicrobial pathways, two functions generally assumed to be coordinately regulated. Here the regulation of these key functions was investigated in human blood-derived macrophages. IL-10 induced the phagocytic pathway, including CD209 and scavenger receptors, resulting in phagocytosis of mycobacteria and oxLDL. IL-15 induced the vitamin D-dependent antimicrobial pathway and CD209, yet the cells were less phagocytic. The differential regulation of macrophage functional programs was confirmed by analysis of the spectrum of leprosy lesions: the macrophage phagocytosis pathway was prominent in the clinically progressive, multibacillary form, whereas the vitamin D-dependent antimicrobial pathway predominated in the self-limited form of the disease and in patients undergoing reversal reactions from the multibacillary to the self-limited form. These data indicate that macrophage programs for phagocytosis and antimicrobial responses are distinct and differentially regulated in innate immunity in bacterial infections. Experiment Overall Design: 7 LL lesions, 10 BT lesions, 7 RR lesions
2009-10-30 | E-GEOD-17763 | biostudies-arrayexpress
Project description:Macrophages mediate the elimination of pathogens by phagocytosis resulting in the activation of specific signaling pathways that lead to the production of cytokines, chemokines and other factors. Borrelia burgdorferi, the causative agent of Lyme disease, causes a wide variety of pro-inflammatory symptoms. The proinflammatory capacity of macrophages is intimately related to the internalization of the spirochete. However, most receptors mediating this process are largely unknown. We have applyedapplied a multiomic approach, including the proteomic analysis of B. burgdorferi-containing phagosome-enriched fractions, to identify surface receptors that are involved in the phagocytic capacity of macrophages as well as their inflammatory output. Sucrose gradient protein fractions of human monocyte-derived macrophages exposed to B. burgdorferi contained the phagocytic receptor, CR3/CD14 highlighting the major role played by these proteins in spirochetal phagocytosis. Among others, Other proteins identified proteins include C-type lectins, scavenger receptors or siglecs, and contain uPAR and MARCO. We also identified the Fc gamma receptor pathway as involved both in the phagocytosis of , and TNF induction by B. burgdorferi in the absence of antibodies. The common gamma chain, FcR, mediates the phagocytosis of the spirochete, likely through Fc receptors and C-type lectins, in a process that involves Syk activation. Overall, these findings highlight the complex array of receptors involved in the phagocytic response of macrophages to B. burgdorferi.
2019-12-06 | PXD012854 | Pride
Project description:As is the case in vertebrates, successful mosquito immune responses depend on a complex and carefully orchestrated network of processes in order to defend the host from a foreign invader and to simultaneously maintain a homeostatic environment. Although commonalities exist between immune response mechanisms across phyla, invertebrates (e.g., mosquitoes) lack anticipatory, adaptive immune responses. However, a number of immune response elements, both cellular and humoral, exist to combat infection. Organisms that successfully invade the mosquito body cavity (hemocoel) potentially are subjected to a variety of mosquito defenses including: melanotic encapsulation, the production of antimicrobial peptides (AMPs) or reactive oxygen and nitrogen intermediates, or to engulfment by phagocytic cells. These arrays are used to temporally compare and contrast transcriptome profiles associated with these responses, as manifest in the cells (hemocytes) that circulate in the mosquito body cavity. Hemocytes have documented association with phagocytosis and melanization reactions in mosquitoes, and these responses, to a variety of Gram positive and Gram negative bacteria, have been characterized. Inoculated Escherichia coli elicit a strong phagocytic response, and Micrococcus luteus are rapidly melanized. For transcriptome profiling, inoculated moquitoes are compared to naïve (uninoculated) mosquitoes. Data obtained will begin to clarify the interactive role of hemocyte genes and gene products in orchestrating phagocytic, melanization, and AMP responses against invading bacteria. Keywords: time course
2007-07-01 | GSE4279 | GEO
Project description:Targeting the reprogramming and phagocytic capacities of tumor-associated macrophages (TAMs) has emerged as a therapeutic opportunity for cancer treatment. Here, we demonstrate that leukemic cell phagocytosis triggers the proinflammatory activation of TAMs as demonstrated by the upregulation and dowregulation of, respectively, proinflammatory and anti-inflammatory genes in phagocytic macrophages (Phago+) with respect to non-phagocytic macrophages (Phago-).
2022-10-25 | E-MTAB-12280 | biostudies-arrayexpress
Project description:Effective innate immunity against many microbial pathogens requires macrophage programs that upregulate phagocytosis and direct antimicrobial pathways, two functions generally assumed to be coordinately regulated. Here the regulation of these key functions was investigated in human blood-derived macrophages. IL-10 induced the phagocytic pathway, including CD209 and scavenger receptors, resulting in phagocytosis of mycobacteria and oxLDL. IL-15 induced the vitamin D-dependent antimicrobial pathway and CD209, yet the cells were less phagocytic. The differential regulation of macrophage functional programs was confirmed by analysis of the spectrum of leprosy lesions: the macrophage phagocytosis pathway was prominent in the clinically progressive, multibacillary form, whereas the vitamin D-dependent antimicrobial pathway predominated in the self-limited form of the disease and in patients undergoing reversal reactions from the multibacillary to the self-limited form. These data indicate that macrophage programs for phagocytosis and antimicrobial responses are distinct and differentially regulated in innate immunity in bacterial infections.
2009-10-21 | GSE17763 | GEO
Project description:The phagocytic activity of astrocytes plays an important role in synapse refinement through the elimination of excess synapses during brain development. The adhesion G protein-coupled receptor BAI1/ADGRB1 contributes to phagocytosis in various tissues, including the clearance of apoptotic myoblasts in skeletal muscle and epithelial cells in the intestine. However, the phagocytic function of ADGRB1 in the brain has not been thoroughly investigated. Given that Adgrb1 is highly expressed in astrocytes but not in microglia, we examined changes in astrocyte gene expression resulting from the loss of ADGRB1. RNA-seq analysis revealed that astrocytes lacking ADGRB1 exhibit altered expression of genes associated with cytoskeleton organization and chemotaxis, processes that are required for phagocytosis. Using cultured astrocytes from mice lacking full-length ADGRB1 (Adgrb1exon2-/-) and wildtype (WT) littermates, we found that Adgrb1exon2-/- astrocytes exhibit significantly reduced phagocytic capacity when compared to similarly prepared astrocytes from WT littermates. Immunostaining of astrocytes and pre-synaptic markers showed less engulfed pre-synaptic elements in astrocytes from Adgrb1exon2-/- mutants. Finally, immunostaining of pre-synaptic and post synaptic markers revealed a significantly higher density of excitatory synapses in Adgrb1exon2-/- mutants. These findings highlight the importance of ADGRB1 in synaptic remodeling and raise the possibility that reduced astrocyte-mediated phagocytosis might underlie the behavioral alterations previously observed in Adgrb1exon2-/- mutants, including increased seizure susceptibility and deficits in social memory.
2024-03-19 | GSE255050 | GEO
Project description:During adult hippocampal neurogenesis, the majority of newborn cells undergo apoptosis and are rapidly phagocytosed by resident microglia in order to avoid disturbing the surrounding neurons. Here, we propose that phagocytosis is not merely a passive process of corpse removal but has an active role in maintaining adult hippocampal neurogenesis. First, we found that neurogenesis was disrupted in three defective microglial phagocytosis KO models in vivo (P2Y12, MerTK/Axl , GPR34). We then followed an in vitro approach to perform a transcriptomic analysis of microglial phagocytosis and identified genes involved in metabolism, chromatin remodeling, and neurogenesis-related functions. Finally, we determined that the phagocytic microglia secretome limits the production of new neurons both in vivo and in vitro. Our data suggest that reprogrammed phagocytic microglia acts as a sensor of local cell death, modulating the balance between cell proliferation and cell survival in the neurogenic niche, supporting the long-term maintenance of adult hippocampal neurogenesis.
2020-04-09 | GSE129569 | GEO