Myeloid and epithelial-derived RELM contribute to tissue repair following lung helminth infection
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA988833 | ENA |
REPOSITORIES: ENA
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Project description:This SuperSeries is composed of the SubSeries listed below.
2023-09-25 | GSE236093 | GEO
Project description:Purpose: To investigaet whether an inflammatory immune response at the Ileum can contribute to development and severity of diarrhoea in Merino sheep that are prone and not prone to develop diarrhoea. Methods:Transcriptomes in the Ileum (third part of small intestine) of Merino sheep were analyzed using RNASeq. Functional enrichment of DEGs using GO terms in biological processes and KEGG pathways were studied. PPI (protein-protein interaction) network and sub-network were studied using clusterONE plugin in Cytoscape. Result and conclusion: Although Ileum in not a primary site of helminth (species under study in our experiment), the results indicated that an inflammatory immune response can contribute to development and severity of diarrhoea. The low-diarrhoea animals did not show any signs of immune/inflammatory response. The genes with important roles in the responses to helminth infection could be targeted in breeding programs to prevent diarrhoea.
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Project description:Excessive renal fibrosis is a common pathology in progressive chronic kidney diseases. Inflammatory injury and aberrant repair processes contribute to the development of kidney fibrosis. Myeloid cells, particularly monocytes/macrophages, play a crucial role in kidney fibrosis by releasing their proinflammatory cytokines and extracellular matrix components such as collagen and fibronectin into the microenvironment of the injured kidney. Numerous signaling pathways have been identified in relation to these activities. However, the involvement of metabolic pathways in myeloid cell functions during the development of renal fibrosis remains understudied. In our study, we initially reanalyzed single-cell RNA sequencing data of renal myeloid cells from Dr. Denby’s group and observed an increased glycolytic pathway in myeloid cells that are critical for renal inflammation and fibrosis. To investigate the role of myeloid glycolysis in renal fibrosis, we utilized a model of unilateral ureteral obstruction in mice deficient of Pfkfb3, an activator of glycolysis, in myeloid cells (Pfkfb3ΔMϕ) and their wild type littermates (Pfkfb3WT). We observed a significant reduction in fibrosis in the obstructive kidneys of Pfkfb3ΔMϕ mice compared to Pfkfb3WT mice. This was accompanied by a substantial decrease in myeloid cell infiltration, as well as a decrease in the numbers of M1 and M2 macrophages and suppression of macrophage to obtain myofibroblast phenotype in the obstructive kidneys of Pfkfb3ΔMϕ mice. Mechanistic studies indicate that glycolytic metabolites stabilize HIF1α, leading to alterations in macrophage phenotypes that contribute to renal fibrosis. In conclusion, our study implicates that targeting myeloid glycolysis represents a novel approach to inhibit renal fibrosis.
2024-03-12 | MTBLS8278 | MetaboLights
Project description:Peripheral innervation plays an important role in regulating tissue repair and regeneration. Here, we provide evidence that injured peripheral nerves provide a reservoir of mesenchymal precursor cells that can directly contribute to murine digit tip regeneration and skin repair. In particular, using single-cell RNA sequencing and lineage tracing we identify transcriptionally-distinct mesenchymal cell populations within the control and injured adult nerve, including neural crest-derived cells in the endoneurium with characteristics of mesenchymal precursor cells. Culture and transplantation studies show that these nerve-derived mesenchymal cells have the potential to differentiate into non-nerve lineages. Moreover, following digit tip amputation, the neural crest-derived nerve mesenchymal cells contribute to the regenerative blastema and ultimately to the regenerated bone. Similarly, neural crest derived nerve mesenchymal cells contribute to the dermis during skin wound healing. These findings support a model where peripheral nerves directly contribute mesenchymal precursor cells to promote repair and regeneration of injured mammalian tissues.
2018-11-29 | GSE120678 | GEO
Project description:Goal: To examine the effects of human resistin during helminth infection. Methodology: To examine the function of human resistin (hResistin), we utilized transgenic mice expressing the human resistin gene along with its entire regulatory region (hRetnTg+). Following infection with the helminth Nippostrongylus brasiliensis, whole lung RNA was sequenced in hRetnTg+ mice, control hRetnTg- and naïve mice. Conclusion: In hRetnTg+ mice, many genes involved in inflammation and the immune system, specifically toll-like receptor signaling and chemokines, are significantly upregulated, suggesting that human resistin promotes TLR signaling and inflammation during helminth infection. Examination of whole lung mRNA from Nippostrongylus brasiliensis-infected lungs at day 7 in mice expressing human resistin
2014-11-14 | E-GEOD-60537 | biostudies-arrayexpress
Project description:Following myocardial infarction, tissue ischemia leads to activation of hypoxia inducible factors. DeBerge et al. demonstrate that HIF-1a and HIF-2a activation in myeloid cells antagonizes cardiac repair pathways through cleavage of cardioprotective MerTK and suppression of anti-inflammatory mitochondrial metabolism, respectively.
2021-07-24 | GSE180678 | GEO
Project description:Goal: To examine the effects of human resistin during helminth infection. Methodology: To examine the function of human resistin (hResistin), we utilized transgenic mice expressing the human resistin gene along with its entire regulatory region (hRetnTg+). Following infection with the helminth Nippostrongylus brasiliensis, whole lung RNA was sequenced in hRetnTg+ mice, control hRetnTg- and naïve mice. Conclusion: In hRetnTg+ mice, many genes involved in inflammation and the immune system, specifically toll-like receptor signaling and chemokines, are significantly upregulated, suggesting that human resistin promotes TLR signaling and inflammation during helminth infection.
2014-11-14 | GSE60537 | GEO
Project description:Helminth infection leads to lung remodelling. We used single cell ATAC sequencing (scRNA-seq) to analyze the changes in lung cells following exposure to N. brasiliensis at day 28 and day 45 post helminth infection
2023-05-31 | GSE228504 | GEO
Project description:Tissue repair is a subset of a broad repertoire of IL-4/IL-13-dependent host responses during helminth infections. Here, we show that IL-4/IL-13 alone were not sufficient, but IL-4/IL-13 together with apoptotic cells induced the tissue repair program in macrophages. Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-resident macrophages and induction of anti-inflammatory/tissue repair genes in the lung following helminth infection or the damage caused by induction of colitis in the gut. In contrast, recognition of apoptotic cells was dispensable for cytokine-dependent induction of pattern recognition receptor, cell adhesion or chemotaxis genes in macrophages. Detection of apoptotic cells can therefore spatially compartmentalize or prevent premature or ectopic activity of pleiotropic, soluble cytokines, such as IL-4/IL-13.
2017-05-11 | GSE98168 | GEO
Project description:Tissue repair is a subset of a broad repertoire of IL-4/IL-13-dependent host responses during helminth infections. Here, we show that IL-4/IL-13 alone were not sufficient, but IL-4/IL-13 together with apoptotic cells induced the tissue repair program in macrophages. Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-resident macrophages and induction of anti-inflammatory/tissue repair genes in the lung following helminth infection or the damage caused by induction of colitis in the gut. In contrast, recognition of apoptotic cells was dispensable for cytokine-dependent induction of pattern recognition receptor, cell adhesion or chemotaxis genes in macrophages. Detection of apoptotic cells can therefore spatially compartmentalize or prevent premature or ectopic activity of pleiotropic, soluble cytokines, such as IL-4/IL-13.
2017-05-11 | GSE98167 | GEO