Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384200 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5479993_1.fastq.gz | Fastqsanger.gz | |||
| SRR5479993_2.fastq.gz | Fastqsanger.gz | |||
| SRR5479995_1.fastq.gz | Fastqsanger.gz | |||
| SRR5479995_2.fastq.gz | Fastqsanger.gz | |||
| SRR5479996_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 14 |
Similar Datasets
Project description:Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells
| PRJNA384189 | ENA
Project description:Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells [Run1]
| PRJNA384186 | ENA
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
Project description:Macrophages are a functionally heterogeneous cell population, critical for the clearance of apoptotic cells. Apoptotic cells have so far been regarded as cells with homogeneous characteristics, often neglecting their original cell lineage identity. Contrary to this, we have observed that the identities of apoptotic cells matter, since they diversify the profile of efferocytic macrophages in vitro and in mouse models of tissue damage. Apoptotic neutrophils trigger a tissue remodeling macrophage signature, while T cells and hepatocytes respectively do not change or promote a tolerogenic macrophage response. Accordingly, the in vivo transfer of macrophages fed with apoptotic neutrophils, but not the transfer of macrophages fed with other apoptotic cells, promotes tissue remodeling. Finally, using a mouse model of parasite-induced tissue pathology, we found that the presence of specific apoptotic cells while simultaneously engaging select phagocytic receptors, i.e. AXL and MERTK by apoptotic neutrophils, diversifies macrophage function. These data reveal that the identity of an apoptotic cell should not be neglected since it drives macrophage transcriptomic and functional heterogeneity.
2024-02-16 | E-MTAB-13780 | biostudies-arrayexpress
Project description:Macrophages are a functionally heterogeneous cell population, critical for the clearance of apoptotic cells. Apoptotic cells have so far been regarded as cells with homogeneous characteristics, often neglecting their original cell lineage identity. Contrary to this, we have observed that the identities of apoptotic cells matter, since they diversify the profile of efferocytic macrophages in vitro and in mouse models of tissue damage. Apoptotic neutrophils trigger a tissue remodeling macrophage signature, while T cells and hepatocytes respectively do not change or promote a tolerogenic macrophage response. Accordingly, the in vivo transfer of macrophages fed with apoptotic neutrophils, but not the transfer of macrophages fed with other apoptotic cells, promotes tissue remodeling. Finally, using a mouse model of parasite-induced tissue pathology, we found that the presence of specific apoptotic cells while simultaneously engaging select phagocytic receptors, i.e. AXL and MERTK by apoptotic neutrophils, diversifies macrophage function. These data reveal that the identity of an apoptotic cell should not be neglected since it drives macrophage transcriptomic and functional heterogeneity.
2024-02-16 | E-MTAB-13753 | biostudies-arrayexpress
Project description:IL-13 plays a key role during protective type 2 immune responses at mucosal sites, such as during infection with nematodes. However, dysregulation of IL-13 can also contribute to the pathogenesis of allergic and fibrotic diseases. Matrix remodelling is an important component of repair processes in the lung but is also a hallmark of chronic diseases such as asthma. Since IL-13 shares receptors and signalling pathways with IL-4, disentangling the relative contributions of these two type 2 cytokines has been challenging. Additionally, little is known about the singular role of IL-13 in more acute settings of tissue injury/repair and whether IL-13 regulates remodelling of the extracellular matrix following tissue injury. In this study, we used Nippostrongylus brasiliensis infection as model of acute lung tissue damage and repair by comparing responses between WT and IL-13-deficient mice, in which IL-4 signalling is intact.
2021-06-11 | PXD021853 | Pride
Project description:Immune responses are crucial to maintaining tissue homeostasis upon tissue injury. Upon various types of challenges, macrophages play a central role in regulating inflammation and tissue repair processes. While an immunomodulatory role of Wnt antagonist Dickkopf1 (DKK1) has been implicated, the role of Wnt antagonist DKK1 in regulating macrophage polarization in inflammation and the tissue repair process remains elusive. Here we found that DKK1 induces differential gene expression profiles from type 2-cytokine-activated macrophages to promote inflammation and tissue repair. Importantly, DKK1 induced pro-inflammatory and pro-resolving gene expressions via JNK (c-jun N-terminal kinase) in macrophages. Furthermore, DKK1 potentiated IL-13-mediated macrophage polarization and activation. Co-inhibition of JNK and STAT6 markedly decreased pro-inflammatory and pro-resolving gene expressions by DKK1 and IL-13. Interestingly, thrombocyte-specific deletion of DKK1 in mice reduced monocyte-derived macrophages in the acute sterile bleomycin (BLM)-induced lung injury model, suggesting that thrombocytes communicate with macrophages via DKK1 to orchestrate inflammation-induced injury repair process. Taken together, our study demonstrates DKK1’s role as a key regulatory role in macrophage polarization in the injury-induced inflammation and repair process.
2023-12-06 | GSE247398 | GEO
Project description:The impact of dietary proteins on homeostasis and immune function of the intestine is poorly understood. We here show that physiological uptake of dietary proteins induced an activated, CD4+CD44+Helios+ T cell population, predominantly in Peyer's patches (PP). These cells are distinct from Foxp3+regulatory T cells and microbiota-independent. Dietary protein-reactive T lymphocytes remained innocuous due to an equilibrium between activation and apoptosis. Macrophage mediated uptake of apoptotic T cells from the PP but not from other tissues resulted in strong IL-10 expression. In contrast, replacement of dietary proteins by amino acids resulted in low numbers of activated and apoptotic CD4+CD44+Helios+ T cells together with reduced amounts of IL-10 and downregulation of genes involved in intestinal integrity such as trefoil factors and gastrokines. The impaired intestinal barrier function of these animals was restored after switching to conventional diet, demonstrating the essential role of food proteins for induction of epithelial repair mechanisms and immunological homeostasis. Microarray experiments were performed as dual-color hybridizations on Agilent-014868 Whole Mouse Genome 4x44K catalog arrays. To compensate for dye-specific effects, a dye-reversal color-swap was applied.
2016-07-01 | E-GEOD-66938 | biostudies-arrayexpress
Project description:Effective regeneration after peripheral nerve injury requires macrophage recruitment. We investigated activation of remodeling pathways within the macrophage population when repair is delayed and identified alteration of key upstream regulators of the inflammatory response. We then targeted one of these regulators, using exogenous IL10 to manipulate the response to injury at the repair site. We demonstrate that this approach alters macrophage polarization, promotes macrophage recruitment, axon extension, neuromuscular junction formation and increases the number of regenerating motor units reaching their target. We also demonstrate that this approach can rescue the effects of delayed nerve graft.
2023-06-14 | GSE217172 | GEO