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bp(MESH:Phagocytosis)

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Entity

Name
Phagocytosis
Namespace
mesh
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/8ccfed235e418e4c8aa576f9a5ef0f838e794c7f/external/mesh-names.belns

Appears in Networks 2

TFEB enhances astroglial uptake of extracellular tau species and reduces tau spreading v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 12

p(MGI:Tfeb) increases bp(MESH:Phagocytosis) View Subject | View Object

Flow cytometry revealed that Torin1 treatment of TFEB transduced astrocytes increased dye-conjugated pff uptake 63% relative to EGFP transduced controls as shown by median fluorescence in- tensity, while under basal conditions, the TFEB overexpressing astrocytes increased uptake just 18% relative to EGFP expressing controls (Fig. 2 K). Thus, TFEB enhances phagocytic pathways in astrocytes, in particular increasing the uptake of pffs. PubMed:30108137

Appears in Networks:
Annotations
Cell Ontology (CL)
astrocyte

a(CHEBI:heme) negativeCorrelation bp(MESH:Phagocytosis) View Subject | View Object

We focused on macrophage effector functions and found that heme pretreatment (15 min, 3–30 μM unless otherwise indicated) led to a strong, dose-dependent reduction of phagocytosis of E. coli by RAW264.7 macrophages compared with DMSO-treated controls (Fig. 3a,b and Supplementary Fig. 2a). PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Blood
MeSH
Sepsis
Text Location
Results

a(CHEBI:heme) negativeCorrelation bp(MESH:Phagocytosis) View Subject | View Object

Induction of hemolysis with phenylhydrazine or addition of heme to whole blood at concentrations mimicking the physiological range of plasma heme in hemolytic patients (5–50 μM)6 led to a dose-dependent impairment of E. coli phagocytosis by neutrophils and monocytes, as compared with DMSO controls (Fig. 3g and Supplementary Fig. 2n,o), indicating that our mouse model was reflective of human hemolytic conditions. PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

a(CHEBI:quinine) positiveCorrelation bp(MESH:Phagocytosis) View Subject | View Object

The top performing drug identified was the antimalarial compound quinine, which fully restored phagocytosis in the presence of heme, without affecting baseline phagocytosis (Fig. 8a and Supplementary Fig. 8b,c). PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

a(CHEBI:quinine) positiveCorrelation bp(MESH:Phagocytosis) View Subject | View Object

Quinine pretreatment protected RAW264.7 macrophages (Fig. 8b and Supplementary Fig. 8c,d) and human macrophages (Fig. 8c) from heme-induced inhibition of phagocytosis and actin cytoskeleton changes (Supplementary Fig. 8e,f) compared with DMSO-treated cells. PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

a(HM:"Blood Transfusion, Acute") increases bp(MESH:Phagocytosis) View Subject | View Object

The causes for RBC-based toxicant exposures are multifactorial; however, following acute transfusion, the most common occurs during the processes of extravascular hemolysis, which includes macrophage erythrophagocytosis followed by macrophage death [1&&], release of iron, transferrin (Tf) saturation and, finally, accumulation of labile plasma iron (LPI) [2]. PubMed:30281034

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

bp(GO:"actin cytoskeleton reorganization") negativeCorrelation bp(MESH:Phagocytosis) View Subject | View Object

We quantified these changes by automatic image analysis and found that heme-induced cytoskeleton rearrangement led to a significant increase in cell area and perimeter, as well as a decrease in circularity (form factor) (Fig. 4d,e and Supplementary Fig. 3b–d), indicating that the heme-induced defective phagocytic response was likely tied to cytoskeleton rearrangements. PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

bp(GO:"actin cytoskeleton reorganization") negativeCorrelation bp(MESH:Phagocytosis) View Subject | View Object

Together, these data indicate that heme induces extensive actin cytoskeleton alterations, which results in defective phagocytosis and inflammatory cell migration. PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

p(MGI:Dock8) negativeCorrelation bp(MESH:Phagocytosis) View Subject | View Object

Our finding that DOCK8 is necessary for the cytoskeleton changes and disruption of bacterial phagocytosis by heme is consistent with recent studies showing that DOCK8 regulates dendritic cell migration via Cdc42 (refs. 37,44). PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Discussion

p(HGNC:AMBP) decreases bp(MESH:Phagocytosis) View Subject | View Object

The placenta histology revealed an increased erythrophagocytosis in the starved placebo treated animals compared to controls. A1M-treatment appeared to attenuate phagocytosis (Figure 5). PubMed:24489717

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Results

p(MGI:Cdc42) positiveCorrelation bp(MESH:Phagocytosis) View Subject | View Object

Cdc42 is involved in cell motility and phagocytosis, but is mainly recognized as being a central node in the formation of lamellipodia and filopodia at the leading edge3 PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

path(MESH:Hematoma) negativeCorrelation bp(MESH:Phagocytosis) View Subject | View Object

The hematoma clearance may be via red blood cell (RBC) lysis or phagocytosis. PubMed:27125525

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Annotations
Text Location
Introduction

Out-Edges 13

bp(MESH:Phagocytosis) negativeCorrelation path(MESH:Hematoma) View Subject | View Object

The hematoma clearance may be via red blood cell (RBC) lysis or phagocytosis. PubMed:27125525

Appears in Networks:
Annotations
Text Location
Introduction

bp(MESH:Phagocytosis) negativeCorrelation a(CHEBI:heme) View Subject | View Object

We focused on macrophage effector functions and found that heme pretreatment (15 min, 3–30 μM unless otherwise indicated) led to a strong, dose-dependent reduction of phagocytosis of E. coli by RAW264.7 macrophages compared with DMSO-treated controls (Fig. 3a,b and Supplementary Fig. 2a). PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Blood
MeSH
Sepsis
Text Location
Results

bp(MESH:Phagocytosis) negativeCorrelation a(CHEBI:heme) View Subject | View Object

Induction of hemolysis with phenylhydrazine or addition of heme to whole blood at concentrations mimicking the physiological range of plasma heme in hemolytic patients (5–50 μM)6 led to a dose-dependent impairment of E. coli phagocytosis by neutrophils and monocytes, as compared with DMSO controls (Fig. 3g and Supplementary Fig. 2n,o), indicating that our mouse model was reflective of human hemolytic conditions. PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

bp(MESH:Phagocytosis) negativeCorrelation bp(GO:"actin cytoskeleton reorganization") View Subject | View Object

We quantified these changes by automatic image analysis and found that heme-induced cytoskeleton rearrangement led to a significant increase in cell area and perimeter, as well as a decrease in circularity (form factor) (Fig. 4d,e and Supplementary Fig. 3b–d), indicating that the heme-induced defective phagocytic response was likely tied to cytoskeleton rearrangements. PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

bp(MESH:Phagocytosis) negativeCorrelation bp(GO:"actin cytoskeleton reorganization") View Subject | View Object

Together, these data indicate that heme induces extensive actin cytoskeleton alterations, which results in defective phagocytosis and inflammatory cell migration. PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

bp(MESH:Phagocytosis) positiveCorrelation p(MGI:Cdc42) View Subject | View Object

Cdc42 is involved in cell motility and phagocytosis, but is mainly recognized as being a central node in the formation of lamellipodia and filopodia at the leading edge3 PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

bp(MESH:Phagocytosis) positiveCorrelation a(CHEBI:quinine) View Subject | View Object

The top performing drug identified was the antimalarial compound quinine, which fully restored phagocytosis in the presence of heme, without affecting baseline phagocytosis (Fig. 8a and Supplementary Fig. 8b,c). PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

bp(MESH:Phagocytosis) positiveCorrelation a(CHEBI:quinine) View Subject | View Object

Quinine pretreatment protected RAW264.7 macrophages (Fig. 8b and Supplementary Fig. 8c,d) and human macrophages (Fig. 8c) from heme-induced inhibition of phagocytosis and actin cytoskeleton changes (Supplementary Fig. 8e,f) compared with DMSO-treated cells. PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Results

bp(MESH:Phagocytosis) negativeCorrelation p(MGI:Dock8) View Subject | View Object

Our finding that DOCK8 is necessary for the cytoskeleton changes and disruption of bacterial phagocytosis by heme is consistent with recent studies showing that DOCK8 regulates dendritic cell migration via Cdc42 (refs. 37,44). PubMed:27798618

Appears in Networks:
Annotations
Cell Ontology (CL)
monocyte
MeSH
Blood
MeSH
Sepsis
Text Location
Discussion

bp(MESH:Phagocytosis) increases bp(GO:"macrophage apoptotic process") View Subject | View Object

The causes for RBC-based toxicant exposures are multifactorial; however, following acute transfusion, the most common occurs during the processes of extravascular hemolysis, which includes macrophage erythrophagocytosis followed by macrophage death [1&&], release of iron, transferrin (Tf) saturation and, finally, accumulation of labile plasma iron (LPI) [2]. PubMed:30281034

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

bp(MESH:Phagocytosis) increases a(CHEBI:"iron(2+)") View Subject | View Object

The causes for RBC-based toxicant exposures are multifactorial; however, following acute transfusion, the most common occurs during the processes of extravascular hemolysis, which includes macrophage erythrophagocytosis followed by macrophage death [1&&], release of iron, transferrin (Tf) saturation and, finally, accumulation of labile plasma iron (LPI) [2]. PubMed:30281034

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

bp(MESH:Phagocytosis) increases path(HP:"Elevated transferrin saturation") View Subject | View Object

The causes for RBC-based toxicant exposures are multifactorial; however, following acute transfusion, the most common occurs during the processes of extravascular hemolysis, which includes macrophage erythrophagocytosis followed by macrophage death [1&&], release of iron, transferrin (Tf) saturation and, finally, accumulation of labile plasma iron (LPI) [2]. PubMed:30281034

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

bp(MESH:Phagocytosis) increases a(HM:"Labile iron", loc(MESH:Plasma)) View Subject | View Object

The causes for RBC-based toxicant exposures are multifactorial; however, following acute transfusion, the most common occurs during the processes of extravascular hemolysis, which includes macrophage erythrophagocytosis followed by macrophage death [1&&], release of iron, transferrin (Tf) saturation and, finally, accumulation of labile plasma iron (LPI) [2]. PubMed:30281034

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.