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Nathan Goodyear

Regulatory Mechanisms for Adipose Tissue M1 and M2 Macrophages in Diet-Induced Obese Mice - 0 views

diabetes.diabetesjournals.org/...2574.full

obesity overweight weight-loss M1 macrophage M2 ATM inflammation TNF-alpha IL-6

shared by Nathan Goodyear on 03 Jan 12 - No Cached
  • Nathan Goodyear on 03 Jan 12
     
    M1 macrophages (and a high M1/M2 ratio) promote inflammation and insulin resistance in obese individuals; This is in contrast to M2 macrophages.  Obese individuals will see a shift in M2 to M1.  The exact mechanism is yet unknown.  But M2 macrophages have been shown to resolve insulin resistance in this obese mice model
Nathan Goodyear

Different distributions of M1 and M2 macrophages in a mouse model of laser-induced chor... - 0 views

www.ncbi.nlm.nih.gov/...PMC5436148

M2 M1 cancer macrophages

shared by Nathan Goodyear on 26 Jun 19 - No Cached
  • Nathan Goodyear on 26 Jun 19
     
    There are two subtypes of macrophages, M1 and M2 (8,9). M1, or pro-inflammatory macrophages, are considered to be important for the destruction of tumor cells and foreign organisms, whereas M2, or anti-inflammatory macrophages, have been suggested to be primarily involved in angiogenesis, wound healing, chronic infections, tumorigenesis and tumor metastasis
Nathan Goodyear

Inflammation and insulin resistance 10.1016/j.febslet.2007.11.057 : FEBS Letters | Scie... - 0 views

www.sciencedirect.com/...S0014579307012082

inflammation insulin resistance IR PPAR TNF-alpha IL-6 IL-10 IL-1Beta JNK GLT-4 Resistin adiponectin Gherlin NF-kapppB iNOS lkkb obesity TLR-4

shared by Nathan Goodyear on 10 Jan 12 - No Cached
  • A subsequent study by Yuan et al. showed that Tnf treatment of 3T3L1 adipocytes induces insulin resistance and that this could be prevented by pretreatment of cells with aspirin
  • Activation of the Tnf receptor results in stimulation of NFκB signaling via Ikkb
  • Insulin is a pleiotropic hormone
  • ...25 more annotations...
  • the percentage of macrophages in a given adipose tissue depot is positively correlated with adiposity and adipocyte size
  • Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes
  • Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NFκB activation by reducing IKK activity [38]
  • adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression
  • One theory holds that the expansion of adipose tissue leads to adipocyte hypertrophy and hyperplasia and that large adipocytes outstrip the local oxygen supply leading to cell autonomous hypoxia with activation of cellular stress pathways
  • The use of the anti-inflammatory compounds, salicylate and its derivative aspirin, for treating symptoms of T2DM dates back over 100 years
  • elevated levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states
  • overnutrition and obesity are often accompanied by elevations in tissue and circulating FFA concentrations, and saturated FFAs can directly activate pro-inflammatory responses
  • Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity
  • In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter
  • macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the “classically activated” pro-inflammatory macrophage, to the M2 state or the “alternatively activated” non-inflammatory cell
  • saturated fatty acids are the most potent inducers of this inflammatory response
  • Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes iNOS (reviewed in [33]
  • Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes.
  • In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production
  • elevated JNK activity in liver, adipose tissue and skeletal muscle of obese insulin resistant mice, and knockout of Jnk1 (Jnk1−/−) leads to amelioration of insulin resistance in high fat diet
  • Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance
  • C-reactive protein (CRP)
  • these studies highlight the possibility that increased iNOS activity plays a direct role in the pathogenesis of insulin resistance
  • the important role of Ikkb in the development of obesity and inflammation-induced insulin resistance.
  • It is probable that local concentrations of inflammatory mediators, such as FFAs, Tnf or other cytokines/adipokines contribute to this polarity switch
  • Tnf and other cytokines/chemokines are symptomatic of inflammation, and while they propagate and/or maintain the inflammatory state, they are not the initial cause(s) of inflammation
  • Tlr4, in particular, is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria
  • Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system.
  • Tlr4 stimulation results in the activation of both Ikkb/NFκB and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1, etc. (reviewed in [57
  • Nathan Goodyear on 10 Jan 12
     
    Great review of all the known components in the inflammation, insulin resistance link
Nathan Goodyear

Adipose tissue macrophages: p... [Curr Opin Clin Nutr Metab Care. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21587064

adipose tissue macrophages ATMs adipose tissue obesity M2 M1 macrophages

shared by Nathan Goodyear on 04 Jan 13 - No Cached
  • Nathan Goodyear on 04 Jan 13
     
    adipose tissue changes the macrophage type from M2 to M1 dominance.  This reveals the microenvironment found in adipose tissue and the effect on the adipose tissue macrophages.
Nathan Goodyear

American Journal of Obstetrics & Gynecology Home Page - 0 views

www.ajog.org/...fulltext

"Vaginal mesh" immune system

shared by Nathan Goodyear on 31 Aug 18 - No Cached
  • M1 macrophages are characterized by the secretion of reactive oxygen species and proinflammatory cytokines and chemokines and can be identified via the cell surface marker CD86
  • M2 macrophages secrete growth factors and antiinflammatory immune modulators and can be identified by the cell surface marker CD206
  • an overzealous M2 response can also lead to excess tissue deposition and fibrosis
  • ...14 more annotations...
  • Studies of similar meshes that are used in hernia repair have demonstrated that all polypropylene meshes induce a prolonged inflammatory response at the site of implantation
  • the long-term presence of activated inflammatory cells, such as macrophages at the mesh tissue interface, can impact negatively the ability of the mesh to function as intended.
  • All M1 proinflammatory and M2 proremodeling cytokines and chemokines were increased in mesh explants as compared with nonmesh tissue (Table 3Table 3), which indicated a robust, active, and ongoing host response to polypropylene long after implantation
  • Comparison of the ratio of the M2 proremodeling cytokines (IL-10+IL-4) with the M1 proinflammatory cytokines (TNF-α+IL-12p70) revealed a decrease in mesh explants as compared with controls (P = .003), which indicated a shift towards a proinflammatory profile.
  • Mesh explants contained a higher number of total cells/×200 field when compared with controls (682.46 ± 142.61 cells vs 441.63 ± 126.13 cells; P < .001) and a lower ratio of M2:M1 macrophages (0.260 ± 0.161 cells vs 1.772 ± 1.919; P = .001), which supported an ongoing proinflammatory response.
  • the host response was proportional to the amount of material in contact with the host
  • A persistent foreign body response was observed in mesh-tissue complexes that were excised from women who required surgical excision of mesh months to years after mesh implantation
  • The host response was characterized by a predominance of macrophages with an increase in both proinflammatory and proremodeling cytokines/chemokines along with increased tissue degradation, as evidenced by increased MMP-2 and -9
  • Mesh-tissue complexes removed for mesh exposure had increased pro–MMP-9 that indicated a proinflammatory and tissue destruction–type response
  • The presence of macrophages, elevated cytokines, chemokines, and MMPs in tissue-mesh complexes that were excised from patients with exposure or pain suggests that polypropylene mesh elicits an ongoing host inflammatory response
  • In the presence of a permanent foreign body, the implant is surrounded with a fibrotic capsule because it cannot be degraded
  • For hernia meshes, if the fibers are too close (<1 mm), the fibrotic response to neighboring fibers overlaps, or “bridges,” and results in “bridging fibrosis” or encapsulation of the mesh
  • Gynemesh PS has a highly unstable geometry when loaded that resulted in pore collapse and increasing stiffness of the product
  • mesh shrinkage (50-70%) has been described to occur after transvaginal insertion of prolapse meshes
  • Nathan Goodyear on 31 Aug 18
     
    Mesh and the abnormal immune response.
Nathan Goodyear

Hydroxychloroquine induced lung cancer suppression by enhancing chemo-sensitization and... - 0 views

www.ncbi.nlm.nih.gov/...PMC6206903

Tumor associate macrophages hydroxychloroquine M1 macrophages cancer TAMs M2 macrophages

shared by Nathan Goodyear on 03 May 21 - No Cached
  • Nathan Goodyear on 03 May 21
     
    Hydroxychloroquine induces M2 to M1 Macrophage polarization.
Nathan Goodyear

M2 macrophages exhibit higher sensitivity to oxLDL-induced lipotoxicity than other mono... - 0 views

www.lipidworld.com/...1476-511X-10-229.pdf

macrophages obesity overweight weight-loss inflammation M2 M1 oxidized LDL

shared by Nathan Goodyear on 03 Jan 12 - No Cached
  • Nathan Goodyear on 03 Jan 12
     
    macrophages (M1) in obese individuals are more pro-inflammatory than those in lean (M2) individuals. The exact mechanism to explain the switch from M2 to M1 has yet to be determined, but this study proposes that lipotoxic oxidized LDL is a possible target
Nathan Goodyear

M2 to M1; macrophage reprogramming can be done! - 0 views

acir.org/...hage-reprogramming-can-be-done

M1 macrophages M2 macrophages M1 M2

shared by Nathan Goodyear on 05 Oct 20 - No Cached
  • Nathan Goodyear on 05 Oct 20
     
    M2 to M1 polarization is possible.
Nathan Goodyear

Obesity induces a phenotypic switch in adipose tissue macrophage polarization - 0 views

www.ncbi.nlm.nih.gov/...PMC1716210

obesity M1 M2 macrophages inflammation insulin resistance weight-loss overweight

shared by Nathan Goodyear on 03 Jan 12 - No Cached
  • Nathan Goodyear on 03 Jan 12
     
    obesity results in shift from M2 macrophages to M1 macrophages.  This results in inflammation and insulin resistance.  This fits the current hypothesis that obesity is in and of itself an inflammatory condition.
Nathan Goodyear

Obesity is associated with macrophage accumulation in adipose tissue - 0 views

www.ncbi.nlm.nih.gov/...PMC296995

obesity inflammation overweight weight-loss WAT white adipose tissue M1 macrophages

shared by Nathan Goodyear on 16 Jan 12 - No Cached
  • Nathan Goodyear on 16 Jan 12
     
    obesity is associated with dysfunctional immune response to adipose tissue.  The cause is inflammation from White adipose tissue resultant in increased recruitment of macrophages and resultant further inflammation.  M1 macrophages are the predominate culprit.
Nathan Goodyear

A novel mechanism of lung cancer inhibition by methionine enkephalin through remodeling... - 0 views

www.researchgate.net/..._of_the_tumor_microenvironment

M2 macrophages M1 macrophages cancer MET-enkephalins TME MET-5 tumor microenvironment

shared by Nathan Goodyear on 15 Aug 21 - No Cached
  • Nathan Goodyear on 15 Aug 21
     
    MENK increased the infiltration of M1-type macrophages, natural killer cells, CD8+ T cells, CD4+ T cells, and dendritic cells into the TME, and decreased the proportion of myeloid inhibitory cells and M2-type macrophages. Plays particular role in preventing immune escape and immune dysfunction paramount to cancer metastasis
Nathan Goodyear

Hydroxychloroquine induced lung cancer suppression by enhancing chemo-sensitization and... - 0 views

jeccr.biomedcentral.com/...s13046-018-0938-5

hydroxychloroquine M1 macrophages M2 macrophages TME tumor microenvironment cancer repurposed drugs

shared by Nathan Goodyear on 28 Nov 22 - No Cached
  • Nathan Goodyear on 28 Nov 22
     
    hydroxychloroquine induces chemo-sensitivity and pushes M2 to M1 macrophage polarization. Effects occur within the TME to increase CD8+ activity within the TME.
Nathan Goodyear

Inhibition of TGF-β induced lipid droplets switches M2 macrophages to M1 phen... - 0 views

www.sciencedirect.com/...S0887233318307793

M1 macrophages M2 macrophages M2 M1 TGF-beta

shared by Nathan Goodyear on 02 Oct 20 - No Cached
  • Nathan Goodyear on 02 Oct 20
     
    Not specifically on cancer, but inhibition of TGF-beta promotes M2 to M1 polarization. It is one thing to show that TGF-beta stimulates M2 polarization; it is quite another to show the opposite. Significantly relevant in the TME cancer debate.
Nathan Goodyear

Frontiers | Modulators of the Balance between M1 and M2 Macrophages during Pregnancy | ... - 0 views

www.frontiersin.org/...full

immune system tumor microenvironment M1 macrophages M2 macrophages TME M1 Pregnancy M2

shared by Nathan Goodyear on 02 Oct 20 - No Cached
  • Nathan Goodyear on 02 Oct 20
     
    Great review of M1 and M2 polarization in pregnancy. The implication for me is the impact in the TME in cancer and its contribution to physical and immune escape.
Nathan Goodyear

Exploring the basic science of prolapse meshes - 0 views

www.ncbi.nlm.nih.gov/...PMC5161092

vaginal mesh mesh immune system M1 M2 macrophages

shared by Nathan Goodyear on 24 Jan 19 - No Cached
  • Nathan Goodyear on 24 Jan 19
     
    Mesh implantation, here in the vaginal area, increases both M1 and M2 maturation migration. M1 increases pro-inflammatory signaling and processes and M2 promotes remodeling/healing... Both increase, but M1 increases more than M2 proportionally. M2 can increase the bridge scaring that can occur as well as the potential for immune suppression and autoimmune/cancer implications
Nathan Goodyear

JCI - Inflammatory links between obesity and metabolic disease - 0 views

www.jci.org/57132

obesity overweight weight-loss inflammation metabolic disease

shared by Nathan Goodyear on 04 Jan 12 - No Cached
  • metainflammation
  • The chronic nature of obesity produces a tonic low-grade activation of the innate immune system that affects steady-state measures of metabolic homeostasis over time
  • It is clear that inflammation participates in the link between obesity and disease
  • ...25 more annotations...
  • Multiple inflammatory inputs contribute to metabolic dysfunction, including increases in circulating cytokines (10), decreases in protective factors (e.g., adiponectin; ref. 11), and communication between inflammatory and metabolic cells
  • adipose tissue macrophage (ATM)
  • Physiologic enhancement of the M2 pathways (e.g., eosinophil recruitment in parasitic infection) also appears to be capable of reducing metainflammation and improving insulin sensitivity (27).
  • increasing adiposity results in a shift in the inflammatory profile of ATMs as a whole from an M2 state to one in which classical M1 proinflammatory signals predominate (21–23).
  • The M2 activation state is intrinsically linked to the activity of PPARδ and PPARγ
  • well-known regulators of lipid metabolism and mitochondrial activity
  • Independent of obesity, hypothalamic inflammation can impair insulin release from β cells, impair peripheral insulin action, and potentiate hypertension (63–65).
  • inflammation in pancreatic islets can reduce insulin secretion and trigger β cell apoptosis leading to decreased islet mass, critical events in the progression to diabetes (33, 34)
  • Since an estimated excess of 20–30 million macrophages accumulate with each kilogram of excess fat in humans, one could argue that increased adipose tissue mass is de facto a state of increased inflammatory mass
  • JNK, TLR4, ER stress)
  • NAFLD is associated with an increase in M1/Th1 cytokines and quantitative increases in immune cells
  • Upon stimulation by LPS and IFN-γ, macrophages assume a classical proinflammatory activation state (M1) that generates bactericidal or Th1 responses typically associated with obesity
  • DIO, metabolites such as diacylglycerols and ceramides accumulate in the hypothalamus and induce leptin and insulin resistance in the CNS (58, 59)
  • saturated FAs, which activate neuronal JNK and NF-κB signaling pathways with direct effects on leptin and insulin signaling (60)
  • Lipid infusion and a high-fat diet (HFD) activate hypothalamic inflammatory signaling pathways, resulting in increased food intake and nutrient storage (57)
  • Maternal obesity is associated with endotoxemia and ATM accumulation that may affect the developing fetus (73)
  • Placental inflammation is a characteristic of maternal obesity
  • a risk factor for obesity in offspring, and involves inflammatory macrophage infiltration that can alter the maternal-fetal circulation (74
  • Of these PRRs, TLR4 has received the most attention, as this receptor can be activated by free FAs to generate proinflammatory signals and activate NF-κB
  • Nod-like receptor (NLR) family of PRRs
  • ceramides and sphingolipids
  • The adipokine adiponectin has long been recognized to have positive benefits on multiple cell types to promote insulin sensitivity and deactivate proinflammatory pathways.
  • adiponectin stimulates ceramidase activity and modulates the balance between ceramides and sphingosine-1-phosphate
  • Inhibition of ceramide production blocks the ability of saturated FAs to induce insulin resistance (101)
  • NF-κB, obesity also activates JNK in insulin-responsive tissues
  • Nathan Goodyear on 04 Jan 12
     
    must read to see our current knowledge on the link between inflammation and obesity.
Nathan Goodyear

Frontiers | Reprogramming of Tumor-Associated Macrophages with Anticancer Therapies: Ra... - 0 views

www.frontiersin.org/...full

M2 macrophages radiation cancer chemotherapy M1 macrophages

shared by Nathan Goodyear on 16 Feb 21 - No Cached
  • Nathan Goodyear on 16 Feb 21
     
    Chemotherapy and radiation induce M2 macrophage polarization favoring metastasis.
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