Inflammation and metabolism in tissue repair and regeneration DOI
Sabine A. Eming, Thomas A. Wynn, Paul Martin

et al.

Science, Journal Year: 2017, Volume and Issue: 356(6342), P. 1026 - 1030

Published: June 9, 2017

Tissue repair after injury is a complex, metabolically demanding process. Depending on the tissue’s regenerative capacity and quality of inflammatory response, outcome generally imperfect, with some degree fibrosis, which defined by aberrant accumulation collagenous connective tissue. Inflammatory cells multitask at wound site facilitating debridement producing chemokines, metabolites, growth factors. If this well-orchestrated response becomes dysregulated, can become chronic or progressively fibrotic, both outcomes impairing tissue function, ultimately lead to organ failure death. Here we review current understanding role inflammation cell metabolism in tissue-regenerative responses, highlight emerging concepts that may expand therapeutic perspectives, briefly discuss where important knowledge gaps remain.

Language: Английский

From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation DOI Creative Commons
Paola Italiani, Diana Boraschi

Frontiers in Immunology, Journal Year: 2014, Volume and Issue: 5

Published: Oct. 17, 2014

Studies on monocyte and macrophage biology differentiation have revealed the pleiotropic activities of these cells. Macrophages are tissue sentinels that maintain integrity by eliminating/repairing damaged cells matrices. In this M2-like mode they can also promote tumor growth. Conversely, M1-like macrophages key effector for elimination pathogens, virally infected, cancer Macrophage from monocytes occurs in concomitance with acquisition a functional phenotype depends microenvironmental signals, thereby accounting many apparently opposed functions. Many questions arise. When differentiate into (concomitantly adopting specific program, M1 or M2), do all die during inflammatory reaction, some them survive? Do those survive become quiescent macrophages, able to react as naïve new challenge? Or, monocyte-derived conserve “memory” their past activation? This review will address important under general framework role initiation, development, resolution chronicization inflammation.

Language: Английский

Citations

1797

Network Integration of Parallel Metabolic and Transcriptional Data Reveals Metabolic Modules that Regulate Macrophage Polarization DOI Creative Commons
Abhishek Jha, Stanley Ching‐Cheng Huang, Alexey Sergushichev

et al.

Immunity, Journal Year: 2015, Volume and Issue: 42(3), P. 419 - 430

Published: March 1, 2015

Language: Английский

Citations

1700

Microglial M1/M2 polarization and metabolic states DOI Open Access
Rubén Orihuela, Christopher A. McPherson, G. Jean Harry

et al.

British Journal of Pharmacology, Journal Year: 2015, Volume and Issue: 173(4), P. 649 - 665

Published: March 20, 2015

Microglia are critical nervous system‐specific immune cells serving as tissue‐resident macrophages influencing brain development, maintenance of the neural environment, response to injury and repair. As influenced by their microglia assume a diversity phenotypes retain capability shift functions maintain tissue homeostasis. In comparison with peripheral macrophages, demonstrate similar unique features regards phenotype polarization, allowing for innate immunological functions. can be stimulated LPS or IFN ‐ γ an M 1 expression pro‐inflammatory cytokines IL‐4/IL‐13 2 resolution inflammation Increasing evidence suggests role metabolic reprogramming in regulation inflammatory response. Studies using that polarization is often accompanied from oxidative phosphorylation aerobic glycolysis energy production. More recently, link between mitochondrial metabolism has been considered microglia. Under these conditions, demands would associated functional activities cell survival thus, may serve influence contribution activation various neurodegenerative conditions. This review examines states relationship metabolism. Additional supporting experimental data provided shifts primary BV ‐2 line induced under ( M1 ) IL ‐4/ IL‐13 M2 polarization. Linked Articles article part themed section on Inflammation: maladies, models, mechanisms molecules. To view other articles this visit http://dx.doi.org/10.1111/bph.2016.173.issue-4

Language: Английский

Citations

1602

Metabolic Pathways in Immune Cell Activation and Quiescence DOI Creative Commons
Erika L. Pearce, Edward J. Pearce

Immunity, Journal Year: 2013, Volume and Issue: 38(4), P. 633 - 643

Published: April 1, 2013

Language: Английский

Citations

1415

Tumor-Associated Macrophages as Major Players in the Tumor Microenvironment DOI Open Access
Theerawut Chanmee,

Pawared Ontong,

Kenjiro Konno

et al.

Cancers, Journal Year: 2014, Volume and Issue: 6(3), P. 1670 - 1690

Published: Aug. 13, 2014

During tumor progression, circulating monocytes and macrophages are actively recruited into tumors where they alter the microenvironment to accelerate progression. Macrophages shift their functional phenotypes in response various microenvironmental signals generated from stromal cells. Based on function, divided broadly two categories: classical M1 alternative M2 macrophages. The macrophage is involved inflammatory response, pathogen clearance, antitumor immunity. In contrast, influences an anti-inflammatory wound healing, pro-tumorigenic properties. Tumor-associated (TAMs) closely resemble M2-polarized critical modulators of microenvironment. Clinicopathological studies have suggested that TAM accumulation correlates with a poor clinical outcome. Consistent evidence, experimental animal supported notion TAMs can provide favorable promote development this review article, we present overview mechanisms responsible for recruitment highlight roles regulation angiogenesis, invasion, metastasis, immunosuppression, chemotherapeutic resistance. Finally, discuss TAM-targeting therapy as promising novel strategy indirect cancer therapy.

Language: Английский

Citations

1409

The Immunomodulatory and Anti-Inflammatory Role of Polyphenols DOI Open Access

Nour Yahfoufi,

Nawal Alsadi,

Majed Jambi

et al.

Nutrients, Journal Year: 2018, Volume and Issue: 10(11), P. 1618 - 1618

Published: Nov. 2, 2018

This review offers a systematic understanding about how polyphenols target multiple inflammatory components and lead to anti-inflammatory mechanisms. It provides clear of the molecular mechanisms action phenolic compounds. Polyphenols regulate immunity by interfering with immune cell regulation, proinflammatory cytokines’ synthesis, gene expression. They inactivate NF-κB (nuclear factor kappa-light-chain-enhancer activated B cells) modulate mitogen-activated protein Kinase (MAPk) arachidonic acids pathways. Polyphenolic compounds inhibit phosphatidylinositide 3-kinases/protein kinase (PI3K/AkT), inhibitor kappa kinase/c-Jun amino-terminal kinases (IKK/JNK), mammalian rapamycin complex 1 (mTORC1) which is that controls JAK/STAT. can suppress toll-like receptor (TLR) pro-inflammatory genes’ Their antioxidant activity ability enzymes involved in production eicosanoids contribute as well their anti-inflammation properties. certain reactive oxygen species ROS like xanthine oxidase NADPH (NOX) while they upregulate other endogenous superoxide dismutase (SOD), catalase, glutathione (GSH) peroxidase (Px). Furthermore, phospholipase A2 (PLA2), cyclooxygenase (COX) lipoxygenase (LOX) leading reduction prostaglandins (PGs) leukotrienes (LTs) inflammation antagonism. The effects these biologically active on system are associated extended health benefits for different chronic diseases. Studies plant extracts show play beneficial role prevention progress diseases related such diabetes, obesity, neurodegeneration, cancers, cardiovascular diseases, among conditions.

Language: Английский

Citations

1357

The cellular and molecular origin of tumor-associated macrophages DOI Open Access
Ruth A. Franklin,

Will Liao,

Abira Sarkar

et al.

Science, Journal Year: 2014, Volume and Issue: 344(6186), P. 921 - 925

Published: May 9, 2014

Long recognized as an evolutionarily ancient cell type involved in tissue homeostasis and immune defense against pathogens, macrophages are being rediscovered regulators of several diseases, including cancer. Here we show that mice, mammary tumor growth induces the accumulation tumor-associated (TAMs) phenotypically functionally distinct from (MTMs). TAMs express adhesion molecule Vcam1 proliferate upon their differentiation inflammatory monocytes, but do not exhibit “alternatively activated” phenotype. TAM terminal depends on transcriptional regulator Notch signaling, RBPJ; TAM, MTM, depletion restores tumor-infiltrating cytotoxic T responses suppresses growth. These findings reveal ontogeny a discrete tumor-elicited response, which may provide new opportunities for cancer immunotherapy.

Language: Английский

Citations

1254

The Role of Macrophages in Acute and Chronic Wound Healing and Interventions to Promote Pro-wound Healing Phenotypes DOI Creative Commons

Paulina Krzyszczyk,

Rene Schloss, Andre F. Palmer

et al.

Frontiers in Physiology, Journal Year: 2018, Volume and Issue: 9

Published: May 1, 2018

Macrophages play key roles in all phases of adult wound healing, which are inflammation, proliferation and remodeling. As wounds heal, the local macrophage population transitions from predominantly pro-inflammatory (M1-like phenotypes) to anti-inflammatory (M2-like phenotypes). Non-healing chronic wounds, such as pressure, arterial, venous diabetic ulcers indefinitely remain inflammation—the first stage healing. Thus, macrophages retain characteristics. This review discusses physiology monocytes acute healing different phenotypes described literature for both vitro vivo models. We also discuss aberrations that occur populations attempts restore function by therapeutic approaches. These include endogenous M1 attenuation, exogenous M2 supplementation modulation/M2 promotion via mesenchymal stem cells, growth factors, biomaterials, heme oxygenase-1 (HO-1) expression oxygen therapy. recognize challenges controversies exist this field, standardization phenotype nomenclature, definition their distinct understanding is optimal order promote wounds.

Language: Английский

Citations

1206

Nanoparticle uptake: The phagocyte problem DOI Creative Commons
Heather H. Gustafson, Dolly Holt‐Casper, David W. Grainger

et al.

Nano Today, Journal Year: 2015, Volume and Issue: 10(4), P. 487 - 510

Published: Aug. 1, 2015

Language: Английский

Citations

1161

Role of Human Macrophage Polarization in Inflammation during Infectious Diseases DOI Open Access
Chiraz Atri, Fatma Z. Guerfali, Dhafer Laouini

et al.

International Journal of Molecular Sciences, Journal Year: 2018, Volume and Issue: 19(6), P. 1801 - 1801

Published: June 19, 2018

Experimental models have often been at the origin of immunological paradigms such as M1/M2 dichotomy following macrophage polarization. However, this clear in animal is not obvious humans, and separating line between M1-like M2-like macrophages rather represented by a continuum, where boundaries are still unclear. Indeed, human infectious diseases, characterized either back forth or mixed profile pro-inflammatory microenvironment (dominated interleukin (IL)-1β, IL-6, IL-12, IL-23 Tumor Necrosis Factor (TNF)-α cytokines) tissue injury driven classically activated (M1-like) wound healing alternatively (M2-like) an anti-inflammatory environment IL-10, Transforming growth factor (TGF)-β, chemokine ligand (CCL)1, CCL2, CCL17, CCL18, CCL22). This review brews complexity situation during diseases stressing on continuum extremes. We first discuss basic biology polarization, function, role inflammatory process its resolution. Secondly, we relevance polarization neglected possibility to interfere with activation states promising therapeutic strategy treatment diseases.

Language: Английский

Citations

1125