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Taenia crassiceps excreted/secreted products alters the microRNA profile and regulates the pro-inflammatory response of M1 macrophages

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE125172 | GEO | 2019/05/15

REPOSITORIES: GEO

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Taenia crassiceps excreted/secreted products alters the microRNA profile and regulates the pro-inflammatory response of M1 macrophages [miRNA]

Project description:We tested the ability of helminth Taenia crassiceps parasite excreted/secreted products (TcES) to induce a regulatory-associated profile in bone-marrow derived macrophages (BMDMs). We also compared gene expression and microRNA profile of BMDMs exposed to TcES with those exposed to LPS which elicits a well-known inflammatory program.

2019-05-15 | GSE125171 | GEO

Taenia crassiceps excreted/secreted products alters the microRNA profile and regulates the pro-inflammatory response of M1 macrophages [mRNA]

2019-05-15 | GSE125170 | GEO

Taenia crassiceps excreted/secreted products alters the microRNA profile and regulates the pro-inflammatory response of M1 macrophages

Project description:Taenia crassiceps excreted/secreted products alters the microRNA profile and regulates the pro-inflammatory response of M1 macrophages

| PRJNA515470 | ENA

Taenia crassiceps excreted/secreted products alters the microRNA profile and regulates the pro-inflammatory response of M1 macrophages [mRNA]

Project description:Taenia crassiceps excreted/secreted products alters the microRNA profile and regulates the pro-inflammatory response of M1 macrophages [mRNA]

| PRJNA515473 | ENA

Taenia crassiceps excreted/secreted products alters the microRNA profile and regulates the pro-inflammatory response of M1 macrophages [miRNA]

Project description:Taenia crassiceps excreted/secreted products alters the microRNA profile and regulates the pro-inflammatory response of M1 macrophages [miRNA]

| PRJNA515477 | ENA

<i>Taenia crassiceps</i>-Excreted/Secreted Products Induce a Defined MicroRNA Profile that Modulates Inflammatory Properties of Macrophages.

Project description:Helminth parasites modulate immune responses in their host to prevent their elimination and to establish chronic infections. Our previous studies indicate that Taenia crassiceps-excreted/secreted antigens (TcES) downregulate inflammatory responses in rodent models of autoimmune diseases, by promoting the generation of alternatively activated-like macrophages (M2) in vivo. However, the molecular mechanisms triggered by TcES that modulate macrophage polarization and inflammatory response remain unclear. Here, we found that, while TcES reduced the production of inflammatory cytokines (IL-6, IL-12, and TNFα), they increased the release of IL-10 in LPS-induced bone marrow-derived macrophages (BMDM). However, TcES alone or in combination with LPS or IL-4 failed to increase the production of the canonical M1 or M2 markers in BMDM. To further define the anti-inflammatory effect of TcES in the response of LPS-stimulated macrophages, we performed transcriptomic array analyses of mRNA and microRNA to evaluate their levels. Although the addition of TcES to LPS-stimulated BMDM induced modest changes in the inflammatory mRNA profile, it induced the production of mRNAs associated with the activation of different receptors, phagocytosis, and M2-like phenotype. Moreover, we found that TcES induced upregulation of specific microRNAs, including miR-125a-5p, miR-762, and miR-484, which are predicted to target canonical inflammatory molecules and pathways in LPS-induced BMDM. These results suggest that TcES can modulate proinflammatory responses in macrophages by inducing regulatory posttranscriptional mechanisms and hence reduce detrimental outcomes in hosts running with inflammatory diseases.

| S-EPMC6536978 | biostudies-literature

MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL.

Project description:Many microRNAs (miRNAs) are selectively expressed in mammalian immune cells and have been linked to immune responses in host defense and autoimmune disease. In macrophages, miRNAs regulate cell metabolism by repressing the expression of genes such as transcription factors, enzymes, and metabolism-related molecules, as well as the expression of genes that impact inflammatory responses and phenotype determination. Previous studies showed that miR-22 plays a role in a variety of biological processes, such as cancer cell growth, cell survival, and cell expansion. In CD4 + T cells of inflammatory bowel disease patients, miR-22 is upregulated and regulates inflammasome-mediated responses. However, it has not yet been determined how miR-22 contributes to the activation of innate immune cells. In this study, we identified a mechanism of toll-like receptors- (TLR-) dependent miR-22 induction that regulates the downstream signaling pathway linking inflammatory responses and macrophage polarization. MiR-22 is induced via TLR-signaling, which regulates the induction of Slc2a1 (glucose transporter 1 and Glut1) and Tnfsf9 (tumor necrosis factor 9, 4-1BB ligand, and 4-1BBL) mRNAs that contribute to sustained inflammatory responses and the polarization of macrophages. Our observations support further efforts to explore a potential therapeutic strategy using miR-22 for the modulation of excessive macrophage activation for the treatment of inflammatory diseases.

| S-EPMC10352528 | biostudies-literature

Modulation of Pro-Oxidant and Pro-Inflammatory Activities of M1 Macrophages by the Natural Dipeptide Carnosine.

Project description:Carnosine is a natural endogenous dipeptide widely distributed in mammalian tissues, existing at particularly high concentrations in the muscles and brain and possesses well-characterized antioxidant and anti-inflammatory activities. In an in vitro model of macrophage activation, induced by lipopolysaccharide + interferon-gamma (LPS + IFN-γ), we here report the ability of carnosine to modulate pro-oxidant and pro-inflammatory activities of macrophages, representing the primary cell type that is activated as a part of the immune response. An ample set of parameters aimed to evaluate cytotoxicity (MTT assay), energy metabolism (HPLC), gene expressions (high-throughput real-time PCR (qRT-PCR)), protein expressions (western blot) and nitric oxide production (qRT-PCR and HPLC), was used to assess the effects of carnosine on activated macrophages challenged with a non cytotoxic LPS (100 ng/mL) + IFN-γ (600 U/mL) concentration. In our experimental model, main carnosine beneficial effects were: (1) the modulation of nitric oxide production and metabolism; (2) the amelioration of the macrophage energy state; (3) the decrease of the expressions of pro-oxidant enzymes (Nox-2, Cox-2) and of the lipid peroxidation product malondialdehyde; (4) the restoration and/or increase of the expressions of antioxidant enzymes (Gpx1, SOD-2 and Cat); (5) the increase of the transforming growth factor-β1 (TGF-β1) and the down-regulation of the expressions of interleukins 1β and 6 (IL-1β and IL-6) and 6) the increase of the expressions of Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase-1 (HO-1). According to these results carnosine is worth being tested in the treatment of diseases characterized by elevated levels of oxidative stress and inflammation (atherosclerosis, cancer, depression, metabolic syndrome, and neurodegenerative diseases).

| S-EPMC7038063 | biostudies-literature

Extracellular Vesicles Secreted by TDO2-Augmented Fibroblasts Regulate Pro-inflammatory Response in Macrophages.

Project description:Extracellular vesicles (EVs) are secreted lipid bilayer vesicles that mediate cell to cell communication and are effectors of cell therapy. Previous work has shown that canonical Wnt signaling is necessary for cell and EV therapeutic potency. Tryptophan 2,3-dioxygenase (TDO2) is a target gene of canonical Wnt signaling. Augmenting TDO2 in therapeutically inert fibroblasts endows their EVs with immunomodulatory capacity including attenuating inflammatory signaling in macrophages. Transcriptomic analysis showed that macrophages treated with EVs from fibroblasts overexpressing TDO2 had blunted inflammatory response compared to control fibroblast EVs. In vivo, EVs from TDO2-overexpressing fibroblasts preserved cardiac function. Taken together, these results describe the role of a major canonical Wnt-target gene (TDO2) in driving the therapeutic potency of cells and their EVs.

| S-EPMC8571098 | biostudies-literature

The macrophage marker translocator protein (TSPO) is down-regulated on pro-inflammatory 'M1' human macrophages.

Project description:The translocator protein (TSPO) is a mitochondrial membrane protein, of as yet uncertain function. Its purported high expression on activated macrophages, has lent utility to TSPO targeted molecular imaging in the form of positron emission tomography (PET), as a means to detect and quantify inflammation in vivo. However, existing literature regarding TSPO expression on human activated macrophages is lacking, mostly deriving from brain tissue studies, including studies of brain malignancy, and inflammatory diseases such as multiple sclerosis. Here, we utilized three human sources of monocyte derived macrophages (MDM), from THP-1 monocytes, healthy peripheral blood monocytes and synovial fluid monocytes from patients with rheumatoid arthritis, to undertake a detailed investigation of TSPO expression in activated macrophages. In this work, we demonstrate a consistent down-regulation of TSPO mRNA and protein in macrophages activated to a pro-inflammatory, or 'M1' phenotype. Conversely, stimulation of macrophages to an M2 phenotype with IL-4, dexamethasone or TGF-β1 did not alter TSPO expression, regardless of MDM source. The reasons for this are uncertain, but our study findings add some supporting evidence for recent investigations concluding that TSPO may be involved in negative regulation of inflammatory responses in macrophages.

| S-EPMC5624624 | biostudies-literature

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