Macrophage-Endothelial Cell Crosstalk Orchestrates Neutrophil Recruitment in Inflamed Mucosa RNA-Seq
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ABSTRACT:
PROVIDER: PRJNA916196 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22895083.fastq.gz | Fastqsanger.gz | |||
| SRR22895084.fastq.gz | Fastqsanger.gz | |||
| SRR22895085.fastq.gz | Fastqsanger.gz | |||
| SRR22895086.fastq.gz | Fastqsanger.gz | |||
| SRR22895087.fastq.gz | Fastqsanger.gz |
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Project description:Macrophage-Endothelial Cell Crosstalk Orchestrates Neutrophil Recruitment in Inflamed Mucosa scRNA-Seq
| PRJNA917196 | ENA
Project description:Rapid neutrophil (PMN) mobilization to sites of insult is critical for host defense and requires crossing of the vascular wall. PMN transendothelial migration (TEM) involves several well-studied sequential adhesive interactions with vascular ECs, however what initiates or terminates this process is not well-understood. Our findings identified a new mechanism where mucosal interstitial macrophages are recruited to interact with the vascular wall and locally prime endothelial cell (EC) responses to accommodate PMN TEM. Using real-time intravital microscopy (IVM) on lipopolysaccharides (LPS)-inflamed intestines in CX3CR1-EGFP macrophage-reporter mice, complemented by whole-mount tissue imaging and flow cytometry, we demonstrate that macrophage presence was critical for the initiation of PMN-EC adhesive interactions and subsequent PMN TEM and accumulation in the intestinal mucosa. Anti CSFR-1 antibody-mediated macrophage depletion in the lamina propria and at the vessel wall significantly reduced PMN adhesion and TEM in inflamed intestines. Vessel associated macrophages (VAMs) were found to trigger localized upregulation of EC ICAM-1 expression and their removal resulted in elimination of the ICAM-1 “hot spots”, impeding PMN-EC interactions. Further mechanistic studies using human clinical specimens, TNFa knockout macrophage chimeras, TNFa/TNF receptor (TNFR) neutralization and multi-cellular macrophage-EC-PMN cocultures revealed a new role for macrophage TNFa and EC TNFRII axis in regulating EC adhesion molecule expression and PMN TEM. As such, our findings identify new, clinically relevant mechanism by which macrophage regulate PMN trafficking in inflamed mucosa.
2023-08-08 | GSE221781 | GEO
Project description:Rapid neutrophil (PMN) mobilization to sites of insult is critical for host defense and requires crossing of the vascular wall. PMN transendothelial migration (TEM) involves several well-studied sequential adhesive interactions with vascular ECs, however what initiates or terminates this process is not well-understood. Our findings identified a new mechanism where mucosal interstitial macrophages are recruited to interact with the vascular wall and locally prime endothelial cell (EC) responses to accommodate PMN TEM. Using real-time intravital microscopy (IVM) on lipopolysaccharides (LPS)-inflamed intestines in CX3CR1-EGFP macrophage-reporter mice, complemented by whole-mount tissue imaging and flow cytometry, we demonstrate that macrophage presence was critical for the initiation of PMN-EC adhesive interactions and subsequent PMN TEM and accumulation in the intestinal mucosa. Anti CSFR-1 antibody-mediated macrophage depletion in the lamina propria and at the vessel wall significantly reduced PMN adhesion and TEM in inflamed intestines. Vessel associated macrophages (VAMs) were found to trigger localized upregulation of EC ICAM-1 expression and their removal resulted in elimination of the ICAM-1 “hot spots”, impeding PMN-EC interactions. Further mechanistic studies using human clinical specimens, TNFa knockout macrophage chimeras, TNFa/TNF receptor (TNFR) neutralization and multi-cellular macrophage-EC-PMN cocultures revealed a new role for macrophage TNFa and EC TNFRII axis in regulating EC adhesion molecule expression and PMN TEM. As such, our findings identify new, clinically relevant mechanism by which macrophage regulate PMN trafficking in inflamed mucosa.
2023-08-08 | GSE221987 | GEO
Project description:Neutrophil (PMN) mobilization to sites of insult is critical for host defense and requires transendothelial migration (TEM). TEM involves several well-studied sequential adhesive interactions with vascular endothelial cells (ECs); however, what initiates or terminates this process is not well-understood. Here, we describe what we believe to be a new mechanism where vessel-associated macrophages through localized interactions primed EC responses to form ICAM-1 "hot spots" to support PMN TEM. Using real-time intravital microscopy of LPS-inflamed intestines in CX3CR1-EGFP macrophage-reporter mice, complemented by whole-mount tissue imaging and flow cytometry, we found that macrophage vessel association is critical for the initiation of PMN-EC adhesive interactions, PMN TEM, and subsequent accumulation in the intestinal mucosa. Anti-colony stimulating factor 1 receptor Ab-mediated macrophage depletion in the lamina propria and at the vessel wall resulted in elimination of ICAM-1 hot spots impeding PMN-EC interactions and TEM. Mechanistically, the use of human clinical specimens, TNF-α-KO macrophage chimeras, TNF-α/TNF receptor (TNF-α/TNFR) neutralization, and multicellular macrophage-EC-PMN cocultures revealed that macrophage-derived TNF-α and EC TNFR2 axis mediated this regulatory mechanism and was required for PMN TEM. As such, our findings identified clinically relevant mechanisms by which macrophages regulate PMN trafficking in inflamed mucosa.
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Project description:Neutrophil recruitment is pivotal to host defense against microbial infection, but also contributes to the immunopathology of disease. We investigated the mechanism of neutrophil recruitment in human infectious disease by bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy (L-lep), and is characterized by neutrophil infiltration in lesions, the most overrepresented biologic functional group was “cell movement” including E-selectin, which was coordinately regulated with IL-1. In vitro activation of TLR2, upregulated in ENL lesions, triggered induction of IL-1, which together with IFN-, induced E-selectin expression on, and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2/FcR activation, neutrophil migration and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease. 6 ENL skin lesions and 7 Lepromatous leprosy skin lesions
2009-06-30 | E-GEOD-16844 | biostudies-arrayexpress
Project description:Analysis of neutrophil proteomic alterations induced by migration towards inflamed joints in juvenile idiopathic arthritis (JIA). In this experiment neutrophil proteomes were investigated after migration towards JIA synovial fluid in an in vitro model of a synovial membrane, compared to neutrophils incubated in synovial fluid without migration. The migration model consisted of transwell inserts with human knee synoviocytes on the undersides and HMEC endothelial cells on the insides, placed in wells containing medium with 10 % JIA synovial fluid.
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Project description:H3K4me3-marked histone orchestrates neutrophil plasticity from immunity to tissue regeneration
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Project description:RNA-seq for inflamed and non-inflamed mucosa in patients with Crohn's disease
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Project description:Neutrophil recruitment is pivotal to host defense against microbial infection, but also contributes to the immunopathology of disease. We investigated the mechanism of neutrophil recruitment in human infectious disease by bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy (L-lep), and is characterized by neutrophil infiltration in lesions, the most overrepresented biologic functional group was 'cell movement' including E-selectin, which was coordinately regulated with IL-1beta. In vitro activation of TLR2, upregulated in ENL lesions, triggered induction of IL-1beta, which together with IFN-gamma, induced E-selectin expression on, and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2/FcR activation, neutrophil migration and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease.
2009-06-30 | GSE16844 | GEO