1. Catalog
  2. Nodes
  3. bp(GO:"inflammatory response")

bp(GO:"inflammatory response")

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
inflammatory response
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 22

Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease v1.0.0

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus v1.0.0

Anti-inflammatory activity of anatabine via inhibition of STAT3 phosphorylation v1.0.0

The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0

Alpha-synuclein oligomers: a new hope v1.0.0

In Vivo and In Vitro Characterization of Antalarmin, a Nonpeptide Corticotropin-Releasing Hormone (CRH) Receptor Antagonist: Suppression of Pituitary ACTH Release and Peripheral Inflammation v1.0.0

Tau protein aggregation is associated with cellular senescence in the brain v1.0.0

Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1

TAU and Interaction Partners v1.2.5

TAU Interactions Section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Activation and regulation of the inflammasomes v1.0.0

The role of inflammasome in Alzheimer’s disease v1.0.3

Inflammasome Involvement in Alzheimer’s Disease v1.0.0

Anatabine ameliorates experimental autoimmune thyroiditis. v1.0.0

Chronic Anatabine Treatment Reduces Alzheimer ’ s Disease (AD)-Like Pathology and Improves Socio-Behavioral Deficits in a Transgenic Mouse Model of AD v1.0.0

Molecular Chaperone Functions in Protein Folding and Proteostasis v1.0.0

Molecular chaperones and proteostasis regulation during redox imbalance v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 55

bp(GO:aging) association bp(GO:"inflammatory response") View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

act(a(CHEBI:nicotine)) regulates bp(GO:"inflammatory response") View Subject | View Object

Modulation by nicotine of inflammatory responses in the intestines is much better reported. Early studies found that patients with ulcerative colitis who stopped smoking tobacco developed the disease or exhibited more severe disease progression, which was ameliorated by either returning to smoking (58, 401, 466), or, in some cases, administering nicotine through transdermal patches (313).In contrast, patients with Crohn’s disease experience much more severe disease when smoking (401). PubMed:19126755

Appears in Networks:
Annotations
MeSH
Intestines
Text Location
Review

p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits") regulates bp(GO:"inflammatory response") View Subject | View Object

There is current evidence that nAChRs present in skin cells modulate the responses triggered by inflammatory stimuli applied to the skin (354). Smoking is a welldefined risk factor in delayed wound healing and possibly the development of premature facial wrinkling (226). PubMed:19126755

Appears in Networks:
Annotations
MeSH
Skin
Text Location
Review

p(MGI:App, var("p.Lys670Asn"), var("p.Met671Leu"), var("p.Thr714Ile"), var("p.Val717Ile")) causesNoChange bp(GO:"inflammatory response") View Subject | View Object

In addition, viral transduction did not induce any neuroinflammation, as shown in WT noninjected mice (Fig. 3A and D) PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

a(CHEBI:Anatabine) regulates bp(GO:"inflammatory response") View Subject | View Object

An inhibition of TNFa induced STAT3 (Mann–Whitney U=0, Z=-2.121, P=0.034), and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.121, P=0.034) was observed in these cells following the anatabine treatment (Fig. 4) suggesting that anatabine may also mediate its anti-inflammatory activity independently of nicotinic acetylcholine receptor expression PubMed:23178521

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
HEK293

a(CHEBI:nicotine) regulates bp(GO:"inflammatory response") View Subject | View Object

Nicotine has been shown to modulate inflammation by affecting STAT3 phosphorylation (Chatterjee et al., 2009; Hosur and Loring, 2011) and by opposing NFkB activation (Leite et al., 2010; Zhou et al., 2010) PubMed:23178521

Appears in Networks:

bp(GO:"ubiquitin-dependent protein catabolic process") regulates bp(GO:"inflammatory response") View Subject | View Object

Ubiquitin-mediated proteolysis of a variety of cellular proteins plays an important role in many basic cellular processes. Among these are regulation of cell cycle and division, differentiation and development, involvement in the cellular response to stress and extracellular effectors, morphogenesis of neuronal networks, modulation of cell surface receptors, ion channels and the secretory pathway, DNA repair, transcriptional regulation, transcriptional silencing, long-term memory, circadian rhythms, regulation of the immune and inflammatory responses,and biogenesis of organelles PubMed:14556719

Appears in Networks:

a(HBP:HBP00092) increases bp(GO:"inflammatory response") View Subject | View Object

a report by Hoffmann et al. showed that fibrillar a-syn induced a more pronounced inflammatory response in microglial cells [61]. PubMed:28803412

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Microglia

a(HBP:HBP00093) increases bp(GO:"inflammatory response") View Subject | View Object

Kim et al. demonstrated that a-syn oligomers lead to microglial inflammatory responses via TLR2 activation [74]. PubMed:28803412

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Microglia

a(CHEBI:antalarmin) negativeCorrelation bp(GO:"inflammatory response") View Subject | View Object

These results raise the possibility that pyrrolopyrimidine compounds, such as antalarmin, which antagonize CRH at the level of its own receptor, have therapeutic potential in some forms of inflammation. PubMed:8940412

Appears in Networks:

act(p(RGD:Crh)) positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

Corticotropin-releasing hormone (CRH) secreted from the hypothalamus is the major regulator of pituitary ACTH release and consequent glucocorticoid secretion. CRH secreted in the periphery also acts as a proinflammatory modulator. PubMed:8940412

Appears in Networks:

a(GO:"neurofibrillary tangle") increases bp(GO:"inflammatory response") View Subject | View Object

NFT containing neurons upregulated genes involved in cell survival and viability, inflammation, cell cycle progression and molecular transport and downregulated apoptosis, necrosis and cell death pathways (Figure 1a). NFkB, a pro-survival master transcriptional regulator of inflammation, was the highest predicted upstream regulator of the NFT-gene expression profile. In agreement with inflammatory activation, other predicted upstream regulators included IFNG, TNF, TLR4, IL1B and CXCL1 (Figure 1b) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

bp(GO:"cellular senescence") association bp(GO:"inflammatory response") View Subject | View Object

NFkB regulates the pro-survival, pro-inflammatory SASP gene expression profile characteristic of cellular senescence (Salminen & Kaarniranta, 2011) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

act(p(MGI:Nfkb1)) increases bp(GO:"inflammatory response") View Subject | View Object

NFkB regulates the pro-survival, pro-inflammatory SASP gene expression profile characteristic of cellular senescence (Salminen & Kaarniranta, 2011) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

act(a(MESH:Microglia)) increases bp(GO:"inflammatory response") View Subject | View Object

Activated microglia has a double effect on AD progression (Li et al. 2014). On the one hand, they can release some proinflammatory cytokines, stimulating inflammatory response and ultimately leading to neuronal injuries and death PubMed:29626319

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") increases bp(GO:"inflammatory response") View Subject | View Object

During Abeta-associated inflammation, reactive nitrogen and oxygen species are generated that can cause neuronal dysfunction and death (34-37). Prevalent among these species is peroxynitrite (ONOO-) PubMed:16566606

Appears in Networks:

a(CHEBI:"dimethyl fumarate") decreases bp(GO:"inflammatory response") View Subject | View Object

Messenger RNA analysis of two pro-inflammatory markers such as IL-1β and inducible nitric oxide synthase (iNOS) indicate that TAUP301L expression induce Il-1β (Fig. 6D) and iNOS (Fig. 7D) mRNA expression in both genotypes and DMF treatment decreased this expression only in Nrf2+/+ mice. PubMed:29121589

Appears in Networks:

r(MGI:Il1b) biomarkerFor bp(GO:"inflammatory response") View Subject | View Object

Messenger RNA analysis of two pro-inflammatory markers such as IL-1β and inducible nitric oxide synthase (iNOS) indicate that TAUP301L expression induce Il-1β (Fig. 6D) and iNOS (Fig. 7D) mRNA expression in both genotypes and DMF treatment decreased this expression only in Nrf2+/+ mice. PubMed:29121589

Appears in Networks:

r(MGI:Nos2) biomarkerFor bp(GO:"inflammatory response") View Subject | View Object

Messenger RNA analysis of two pro-inflammatory markers such as IL-1β and inducible nitric oxide synthase (iNOS) indicate that TAUP301L expression induce Il-1β (Fig. 6D) and iNOS (Fig. 7D) mRNA expression in both genotypes and DMF treatment decreased this expression only in Nrf2+/+ mice. PubMed:29121589

Appears in Networks:

p(HGNC:IL1A) increases bp(GO:"inflammatory response") View Subject | View Object

In addition, IL-1α, which also activates IL-1R, could contribute to the inflammatory response in vivo. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL18) increases bp(GO:"inflammatory response") View Subject | View Object

Interleukins, in particular IL-1β and IL-18, are upregulated in AD brain, and the overexpression of IL-1β or IL-18 is critical for the onset of the inflammatory process (Rubio-Perez and Morillas-Ruiz, 2012), and both mediate the expression of a vast array of inflammatory genes (Weber et al., 2010) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Inflammatory response subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL1B) increases bp(GO:"inflammatory response") View Subject | View Object

Interleukins, in particular IL-1β and IL-18, are upregulated in AD brain, and the overexpression of IL-1β or IL-18 is critical for the onset of the inflammatory process (Rubio-Perez and Morillas-Ruiz, 2012), and both mediate the expression of a vast array of inflammatory genes (Weber et al., 2010) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Inflammatory response subgraph
NeuroMMSigDB
Interleukin signaling subgraph

bp(GO:"cytokine secretion") increases bp(GO:"inflammatory response") View Subject | View Object

Pattern recognition receptors such as the TLR4 receptor are expressed in the brain’s own immune cells like microglia and astrocytes that induce inflammation via cytokine secretion [38]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Brain
MeSH
Alzheimer Disease
NeuroMMSigDB
Toll like receptor subgraph

act(p(HGNC:P2RX7)) increases bp(GO:"inflammatory response") View Subject | View Object

P2X7 activation is followed by a number of downstream events, including release of pro-inflammatory mediators, cell death, and proliferation. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Apoptosis signaling subgraph
NeuroMMSigDB
Inflammatory response subgraph

a(CHEBI:Anatabine) decreases bp(GO:"inflammatory response") View Subject | View Object

Furthermore, anatabine has been recently shown to inhibit nuclear factor-kB(NF-kB) activation and reduce neuroinflammation in a mouse model of Alzheimer disease (15). PubMed:22807490

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

a(CHEBI:Anatabine) decreases bp(GO:"inflammatory response") View Subject | View Object

We have shown previously that anatabine displays some anti-inflammatory properties and reduces microgliosis and tau phosphorylation in a pure mouse model of tauopathy. PubMed:26010758

Appears in Networks:

a(CHEBI:Anatabine) decreases bp(GO:"inflammatory response") View Subject | View Object

We have shown previously that anatabine displays some anti-inflammatory properties by reducing the activation of NFκB and STAT3 [17,18]. PubMed:26010758

Appears in Networks:

a(CHEBI:Anatabine) decreases bp(GO:"inflammatory response") View Subject | View Object

We have previously shown that anatabine inhibits STAT3 and NFκB activation [18] resulting in decreased neuroinflammation in a mouse model of multiple sclerosis. PubMed:26010758

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Multiple Sclerosis

bp(HBP:Proteostasis) association bp(GO:"inflammatory response") View Subject | View Object

Additionally, PN regulation is integrated with pathways involved in inflam- mation, response to oxidative stress, caloric restriction/starvation, and longevity. PubMed:23746257

Appears in Networks:

a(CHEBI:"amyloid-beta") increases bp(GO:"inflammatory response") View Subject | View Object

Glial activation, pro-inflammatory gene expression and elevated secretion of IL-1, IL-6 and TNF- are consequences of high A levels [30,31]. PubMed:29179999

Appears in Networks:

a(CHEBI:curcumin) decreases bp(GO:"inflammatory response") View Subject | View Object

Curcumin showed several anti-inflammatory characteristics. It deploys various cytokine-inhibitory, anti-inflammatory activities and decreases the expression levels of COX-2, LOX, and iNOS. Moreover, the expression of the pro-inflammatory cytokines, for instance, TNF-, IL-1, -2,-6, -8, and -12 and the neurotoxic factors were suppressed by curcumin in lipopolysaccharide (LPS)-stimulated monocytes and alveolar macrophages [103]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:44584733) decreases bp(GO:"inflammatory response") View Subject | View Object

Inflammation caused by LPS was reduced with treatment of punicalaginin RAW264.7 macrophages, astrocytes and microglial BV-2 cells PubMed:29179999

Appears in Networks:
Annotations
Cell Ontology (CL)
astrocyte
Cell Ontology (CL)
macrophage
Cell Ontology (CL)
microglial cell

act(p(FPLX:NFkappaB)) association bp(GO:"inflammatory response") View Subject | View Object

Furthermore, A induced NF-B activity in glial and neuronal cells. NF-B is involved in inflammatory responses and is expressed in brains of AD patients [32]. PubMed:29179999

Appears in Networks:
Annotations
Cell Ontology (CL)
glial cell

tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) increases bp(GO:"inflammatory response") View Subject | View Object

ROS activate various downstream signaling molecules, such as PKC and mitogen-activated protein kinases (MAPKs) that induce nuclear translocation of NF-B and the expression of pro-inflammatory genes [41]. PubMed:29179999

Appears in Networks:

p(FPLX:NFkappaB) regulates bp(GO:"inflammatory response") View Subject | View Object

Inflammation is a key pathological hall mark of AD [61,62], NF-κB is considered as a primary regulator of inflammatory processes [10]. PubMed:27288790

Appears in Networks:

act(complex(GO:"NF-kappaB complex")) increases bp(GO:"inflammatory response") View Subject | View Object

Various endogenous and exogenous stimuli activate NF-κB enhancing transactivation of inflammatory molecules and production of free radicals in glial cells PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neuroglia

a(CHEBI:"carbon monoxide") decreases bp(GO:"inflammatory response") View Subject | View Object

Differently from biliverdin and CO, which have anti-inflammatory effects (Otterbein et al., 2000; Baranano et al., 2002), free Fe is highly oxidative and can promote free radicals generation through the Fenton reaction, which catalyzes hydroxyl radicals from the reaction of Fe with H2O2 (Fenton, 1894). PubMed:24904418

Appears in Networks:
Annotations
Text Location
Review

a(CHEBI:"iron(2+)") positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

Importantly, protoporphyrin did not induce TNFα, suggesting a critical proinflammatory role for iron within the heme moiety (supplemental Figure 8). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

a(CHEBI:"iron(2+)") increases bp(GO:"inflammatory response") View Subject | View Object

Another pathogenic mechanism involves the release of iron from cell-free hemoglobin with consecutive radical formation, which in turn can modify lipids, proteins, and DNA, leading to inflammation [39]. PubMed:29956069

Appears in Networks:
Annotations
MeSH
Arteries
MeSH
Sepsis
Text Location
Review

a(CHEBI:heme) positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

As a component of hemoglobin, free heme is released when hemolysis or extensive cell damage occur which results in inflammatory response. PubMed:24464629

Appears in Networks:
Annotations
Text Location
Introduction

a(CHEBI:heme) positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

Hemin induces expression of the adhesion molecules on endothelial cells [7, 8] and enables firm neutrophil attachment to the endothelium and initiation of an inflammatory response [9, 10]. PubMed:28716864

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
Text Location
Introduction

a(CHEBI:heme) increases bp(GO:"inflammatory response") View Subject | View Object

These experiments confirm a number of earlier reports and support the idea that certain solutions derived from purified/crystalline heme have the potential to induce weak TLR4-mediated inflammatory responses in macrophages in the complete absence of plasma derived proteins. PubMed:29610666

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

a(MESH:"Reactive Oxygen Species") positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

As a part of the inflammatory response after injury, oxidative stress due to formation of reactive oxygen species (ROS) is involved both in direct damage of cartilage components and as integral factors in cell signaling leading to cartilage degradation (Henrotin et al., 2003). PubMed:30505280

Appears in Networks:
Annotations
MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

a(MESH:Biliverdine) decreases bp(GO:"inflammatory response") View Subject | View Object

Differently from biliverdin and CO, which have anti-inflammatory effects (Otterbein et al., 2000; Baranano et al., 2002), free Fe is highly oxidative and can promote free radicals generation through the Fenton reaction, which catalyzes hydroxyl radicals from the reaction of Fe with H2O2 (Fenton, 1894). PubMed:24904418

Appears in Networks:
Annotations
Text Location
Review

bp(HM:"macrophage M1 polarization") positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

complex(a(CHEBI:heme), p(HGNC:ALB)) negativeCorrelation bp(GO:"inflammatory response") View Subject | View Object

However, similar to Hb, heme-albumin did not induce an inflammatory response in macrophages or endothelial cells in the presence of low concentrations of serum. PubMed:29610666

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Mitochondria
Text Location
Discussion

p(HGNC:HPX) decreases bp(GO:"inflammatory response") View Subject | View Object

Taken together, these data demonstrate that Hx limits macrophage heme overload and prevents the prooxidant and proinflammatory effects triggered by heme in cellular assays and in vivo. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

p(MGI:Hpx) negativeCorrelation bp(GO:"inflammatory response") View Subject | View Object

Taken together, these data suggest that Hx administration decreases heme-driven proinflammatory activation of macrophages. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

p(MGI:Hpx) negativeCorrelation bp(GO:"inflammatory response") View Subject | View Object

In conclusion, an Hx-based therapy shows beneficial effects, in that it counteracts heme-induced proinflammatory activation of macrophages and attenuates some of its pathophysiologic consequences, such as chronic inflammation, hepatic fibrosis, and apoptosis (Figure 7E). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

p(MGI:Hpx) negativeCorrelation bp(GO:"inflammatory response") View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

p(HGNC:TLR4) positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

Other studies demonstrated that heme can trigger the activation of Toll-like receptor 4 and inflammasomes, thus leading to inflammatory reactions.5,35–37 PubMed:26794659

Appears in Networks:
Annotations
Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Discussion

act(p(HGNC:TLR4)) positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

The released heme can activate the innate immune pattern recognition receptor toll-like receptor 4 (TLR4) on inflammatory cells, platelets and endothelium, promoting a pro-inflammatory and pro-coagulant phenotype, ultimately leading to vaso-occlusion, ischemia-reperfusion physiology, tissue injury, and pain in murine models of SCD [5, 7±10]. PubMed:29694434

Appears in Networks:
Annotations
MeSH
Blood Platelets
MeSH
Anemia, Sickle Cell
Text Location
Introduction

p(HGNC:IL1B) positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

IL-1b participates in a robust inflammatory response. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

path(MESH:"Knee Injuries") positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

Lately, much evidence has emerged to support a central role for participation of local inflammatory pathways in the disease processes (Scanzello, 2017), particularly so after knee injury (Goldring and Otero, 2011). PubMed:30505280

Appears in Networks:
Annotations
MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

path(MESH:Inflammation) positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

Out-Edges 24

bp(GO:"inflammatory response") association bp(GO:aging) View Subject | View Object

Enrichment analysis revealed, however, changes in gene sets involved in immune and inflammatory responses, phospholipid metabolism, extracellular matrix organization, cellular adhesion and endothelial tube morphogenesis, all of which suggest that there are functional alterations in meningeal LECs with age (Fig. 2c). PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

bp(GO:"inflammatory response") causesNoChange path(MESH:"Memory Disorders") View Subject | View Object

We did not detect any glia or microglia activation in WT-APP (Fig. 3C and F) compared with WT-GFP (Fig. 3B and E), meaning that the neuroinflammation does not play a role in the memory deficit we observed PubMed:27522251

Appears in Networks:
Annotations
MeSH
Dentate Gyrus

bp(GO:"inflammatory response") positiveCorrelation act(p(RGD:Crh)) View Subject | View Object

Corticotropin-releasing hormone (CRH) secreted from the hypothalamus is the major regulator of pituitary ACTH release and consequent glucocorticoid secretion. CRH secreted in the periphery also acts as a proinflammatory modulator. PubMed:8940412

Appears in Networks:

bp(GO:"inflammatory response") negativeCorrelation a(CHEBI:antalarmin) View Subject | View Object

These results raise the possibility that pyrrolopyrimidine compounds, such as antalarmin, which antagonize CRH at the level of its own receptor, have therapeutic potential in some forms of inflammation. PubMed:8940412

Appears in Networks:

bp(GO:"inflammatory response") association bp(GO:"cellular senescence") View Subject | View Object

NFkB regulates the pro-survival, pro-inflammatory SASP gene expression profile characteristic of cellular senescence (Salminen & Kaarniranta, 2011) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

bp(GO:"inflammatory response") increases p(HGNC:DKK1) View Subject | View Object

For example, ongoing inflammation can trigger various cell stress-response pathways, including overexpression of the secreted glycoprotein Dickopff-1 (DKK-1). DKK-1 up-regulates GSK-3β activity, promotes tau hyper-phosphorylation, NFT formation and neuronal degeneration. Thus, DKK-1 inhibits Wnt signalling in a manner similar to Aβ, and thereby fosters a self-sustaining feedback loop resulting in cellular injury PubMed:18494933

Appears in Networks:

bp(GO:"inflammatory response") increases a(CHEBI:peroxynitrite) View Subject | View Object

During Abeta-associated inflammation, reactive nitrogen and oxygen species are generated that can cause neuronal dysfunction and death (34-37). Prevalent among these species is peroxynitrite (ONOO-) PubMed:16566606

Appears in Networks:

bp(GO:"inflammatory response") association bp(HBP:Proteostasis) View Subject | View Object

Additionally, PN regulation is integrated with pathways involved in inflam- mation, response to oxidative stress, caloric restriction/starvation, and longevity. PubMed:23746257

Appears in Networks:

bp(GO:"inflammatory response") increases a(CHEBI:"reactive oxygen species") View Subject | View Object

Excessive amounts of ROS may also arise from inflammatory processes [75]. PubMed:24563850

Appears in Networks:

bp(GO:"inflammatory response") association act(p(FPLX:NFkappaB)) View Subject | View Object

Furthermore, A induced NF-B activity in glial and neuronal cells. NF-B is involved in inflammatory responses and is expressed in brains of AD patients [32]. PubMed:29179999

Appears in Networks:
Annotations
Cell Ontology (CL)
glial cell

bp(GO:"inflammatory response") positiveCorrelation a(CHEBI:heme) View Subject | View Object

As a component of hemoglobin, free heme is released when hemolysis or extensive cell damage occur which results in inflammatory response. PubMed:24464629

Appears in Networks:
Annotations
Text Location
Introduction

bp(GO:"inflammatory response") positiveCorrelation a(CHEBI:heme) View Subject | View Object

Hemin induces expression of the adhesion molecules on endothelial cells [7, 8] and enables firm neutrophil attachment to the endothelium and initiation of an inflammatory response [9, 10]. PubMed:28716864

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
Text Location
Introduction

bp(GO:"inflammatory response") positiveCorrelation p(HGNC:IL1B) View Subject | View Object

IL-1b participates in a robust inflammatory response. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

bp(GO:"inflammatory response") positiveCorrelation a(CHEBI:"iron(2+)") View Subject | View Object

Importantly, protoporphyrin did not induce TNFα, suggesting a critical proinflammatory role for iron within the heme moiety (supplemental Figure 8). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

bp(GO:"inflammatory response") negativeCorrelation p(MGI:Hpx) View Subject | View Object

Taken together, these data suggest that Hx administration decreases heme-driven proinflammatory activation of macrophages. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

bp(GO:"inflammatory response") negativeCorrelation p(MGI:Hpx) View Subject | View Object

In conclusion, an Hx-based therapy shows beneficial effects, in that it counteracts heme-induced proinflammatory activation of macrophages and attenuates some of its pathophysiologic consequences, such as chronic inflammation, hepatic fibrosis, and apoptosis (Figure 7E). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

bp(GO:"inflammatory response") negativeCorrelation p(MGI:Hpx) View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

bp(GO:"inflammatory response") positiveCorrelation bp(HM:"macrophage M1 polarization") View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

bp(GO:"inflammatory response") positiveCorrelation path(MESH:Inflammation) View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

bp(GO:"inflammatory response") positiveCorrelation p(HGNC:TLR4) View Subject | View Object

Other studies demonstrated that heme can trigger the activation of Toll-like receptor 4 and inflammasomes, thus leading to inflammatory reactions.5,35–37 PubMed:26794659

Appears in Networks:
Annotations
Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Discussion

bp(GO:"inflammatory response") positiveCorrelation act(p(HGNC:TLR4)) View Subject | View Object

The released heme can activate the innate immune pattern recognition receptor toll-like receptor 4 (TLR4) on inflammatory cells, platelets and endothelium, promoting a pro-inflammatory and pro-coagulant phenotype, ultimately leading to vaso-occlusion, ischemia-reperfusion physiology, tissue injury, and pain in murine models of SCD [5, 7±10]. PubMed:29694434

Appears in Networks:
Annotations
MeSH
Blood Platelets
MeSH
Anemia, Sickle Cell
Text Location
Introduction

bp(GO:"inflammatory response") negativeCorrelation complex(a(CHEBI:heme), p(HGNC:ALB)) View Subject | View Object

However, similar to Hb, heme-albumin did not induce an inflammatory response in macrophages or endothelial cells in the presence of low concentrations of serum. PubMed:29610666

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Mitochondria
Text Location
Discussion

bp(GO:"inflammatory response") positiveCorrelation path(MESH:"Knee Injuries") View Subject | View Object

Lately, much evidence has emerged to support a central role for participation of local inflammatory pathways in the disease processes (Scanzello, 2017), particularly so after knee injury (Goldring and Otero, 2011). PubMed:30505280

Appears in Networks:
Annotations
MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

bp(GO:"inflammatory response") positiveCorrelation a(MESH:"Reactive Oxygen Species") View Subject | View Object

As a part of the inflammatory response after injury, oxidative stress due to formation of reactive oxygen species (ROS) is involved both in direct damage of cartilage components and as integral factors in cell signaling leading to cartilage degradation (Henrotin et al., 2003). PubMed:30505280

Appears in Networks:
Annotations
MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.