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Journal articles on the topic 'Modulation of macrophage activation'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Stunault, Marion I., Gaël Bories, Rodolphe R. Guinamard, and Stoyan Ivanov. "Metabolism Plays a Key Role during Macrophage Activation." Mediators of Inflammation 2018 (December 10, 2018): 1–10. http://dx.doi.org/10.1155/2018/2426138.

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Monocyte and macrophage diversity is evidenced by the modulation of cell surface markers and differential production of soluble mediators. These immune cells play key roles in controlling tissue homeostasis, infections, and excessive inflammation. Macrophages remove dead cells in a process named efferocytosis, contributing to the healthy tissue maintenance. Recently, it became clear that the main macrophage functions are under metabolic control. Modulation of glucose, fatty acid, and amino acid metabolism is associated with various macrophage activations in response to external stimuli. Deciph

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Sautebin, L., R. Carnuccio, F. D'Acquisto, and M. Di Rosa. "Modulation of macrophage activation by prostaglandins." Mediators of Inflammation 5, no. 1 (1996): 14–17. http://dx.doi.org/10.1155/s0962935196000026.

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The effect of prostaglandtn E2, iloprost and cAMP on both nitric oxide and tumour necrosis factor-α release in J774 macrophages has been studied. Both prostaglandin E2and iloprost inhibited, in a concentration-dependent fashion, the lipopolysaccharide-induced generation of nitric oxide and tumour necrosis factor-α. The inhibitory effect of these prostanoids seems to be mediated by an increase of the second messenger cAMP since it was mimicked by dibutyryl cAMP and potentiated by the selective type IV phosphodiesterase inhibitor RO-20-1724. Our results suggest that the inhibition of nitric oxid

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Searle, S., N. A. Bright, T. I. Roach, et al. "Localisation of Nramp1 in macrophages: modulation with activation and infection." Journal of Cell Science 111, no. 19 (1998): 2855–66. http://dx.doi.org/10.1242/jcs.111.19.2855.

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The murine natural resistance-associated macrophage protein, Nramp1, has multiple pleiotropic effects on macrophage activation and regulates survival of intracellular pathogens including Leishmania, Salmonella and Mycobacterium species. Nramp1 acts as an iron transporter, but precisely how this relates to macrophage activation and/or pathogen survival remains unclear. To gain insight into function, anti-Nramp1 monoclonal and polyclonal antibodies are used here to localise Nramp1 following activation and infection. Confocal microscope analysis in uninfected macrophages demonstrates that both th

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Tseng, Wei-Cheng, Ming-Tsun Tsai, Nien-Jung Chen, and Der-Cherng Tarng. "Trichostatin A Alleviates Renal Interstitial Fibrosis Through Modulation of the M2 Macrophage Subpopulation." International Journal of Molecular Sciences 21, no. 17 (2020): 5966. http://dx.doi.org/10.3390/ijms21175966.

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Mounting evidence indicates that an increase in histone deacetylation contributes to renal fibrosis. Although inhibition of histone deacetylase (HDAC) can reduce the extent of fibrosis, whether HDAC inhibitors exert the antifibrotic effect through modulating the phenotypes of macrophages, the key regulator of renal fibrosis, remains unknown. Moreover, the functional roles of the M2 macrophage subpopulation in fibrotic kidney diseases remain incompletely understood. Herein, we investigated the role of HDAC inhibitors on renal fibrogenesis and macrophage plasticity. We found that HDAC inhibition

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Krishna Vaddi Cheng i Wei. "MODULATION OF MACROPHAGE ACTIVATION BY AMMONIUM METAVANADATE." Journal of Toxicology and Environmental Health 49, no. 6 (1996): 631–45. http://dx.doi.org/10.1080/009841096160673.

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6

Bauerle, Kevin Thomas, Jisu Oh, Amy Elizabeth Riek, et al. "Vitamin D Deficiency Induces Macrophage Pro-Inflammatory Phenotype via ER Stress-Mediated Activation of Renin-Angiotensin System." Journal of the Endocrine Society 5, Supplement_1 (2021): A304—A305. http://dx.doi.org/10.1210/jendso/bvab048.620.

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Abstract Chronic inflammation and local activation of the renin-angiotensin-aldosterone system (RAAS) play a pivotal role in the pathogenesis and progression of diabetic complications. In patients with type 2 diabetes (T2DM), the prevalence of vitamin D deficiency is almost twice that of non-diabetics, and vitamin d deficiency nearly doubles the risk of developing hypertension and cardiovascular complications compared to diabetics with normal vitamin D levels. Interestingly, mice lacking the vitamin D receptor (VDR) in macrophages (KODMAC) develop renin-dependent hypertension, insulin resistan

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Noël, Wim, Gholamreza Hassanzadeh, Geert Raes, et al. "Infection Stage-Dependent Modulation of Macrophage Activation in Trypanosoma congolense-Resistant and -Susceptible Mice." Infection and Immunity 70, no. 11 (2002): 6180–87. http://dx.doi.org/10.1128/iai.70.11.6180-6187.2002.

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ABSTRACT The contribution of cytokines and chemokines to resistance and susceptibility to African trypanosomiasis remains controversial. In the present study, the levels of type I and type II cytokines and of the MCP-1 chemokine were compared during the early and late stages of Trypanosoma congolense infection in susceptible BALB/c and resistant C57BL/6 mice. Moreover, the status of macrophage activation was compared in these animals by analyzing the inducible nitric oxide synthase-arginase balance, tumor necrosis factor secretion, and expression of the FIZZ1 and YM genes. Data show that chang

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Tietzel, Illya. "The modulation of macrophage activation by tyrosine phosphorylation." Frontiers in Bioscience 7, no. 1-3 (2002): d1494. http://dx.doi.org/10.2741/tietzel.

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Mosser, David M. "The modulation of macrophage activation by tyrosine phosphorylation." Frontiers in Bioscience 7, no. 4 (2002): d1494–1502. http://dx.doi.org/10.2741/a856.

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10

Liu, Guangwei, and Hui Yang. "Modulation of macrophage activation and programming in immunity." Journal of Cellular Physiology 228, no. 3 (2012): 502–12. http://dx.doi.org/10.1002/jcp.24157.

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11

Denis, Michel. "Growth of Listeria monocytogenes in murine macrophages and its modulation by cytokines; activation of bactericidal activity by interleukin-4 and interleukin-6." Canadian Journal of Microbiology 37, no. 4 (1991): 253–57. http://dx.doi.org/10.1139/m91-039.

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Bone marrow derived macrophages were infected with a virulent strain of Listeria monocytogenes, and the ability of selected cytokines to modify the intracellular growth was assessed. Macrophage monolayers pretreated with either interferon-γ or tumour necrosis factor were shown to exert a significant listericidal activity. Treatment of monolayers with granulocyte–macrophage colony stimulating factor led to no significant difference in the ability of Listeria to invade and multiply within these cells. Moreover, pulsing of macrophage monolayers with interleukin-6 (IL-6) led to a slight enhancemen

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Swartzwelter, Benjamin J., Alessandro Verde, Laura Rehak, et al. "Interaction between Macrophages and Nanoparticles: In Vitro 3D Cultures for the Realistic Assessment of Inflammatory Activation and Modulation of Innate Memory." Nanomaterials 11, no. 1 (2021): 207. http://dx.doi.org/10.3390/nano11010207.

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Understanding the modes of interaction between human monocytes/macrophages and engineered nanoparticles is the basis for assessing particle safety, in terms of activation of innate/inflammatory reactions, and their possible exploitation for medical applications. In vitro assessment of nanoparticle-macrophage interaction allows for examining the response of primary human cells, but the conventional 2D cultures do not reproduce the three-dimensional spacing of a tissue and the interaction of macrophages with the extracellular tissue matrix, conditions that shape macrophage recognition capacity a

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Pfeifer, Richard W., and Rachel M. Patterson. "Modulation of Lymphokine-Induced Macrophage Activation by Estrogen Metabolites." Journal of Immunopharmacology 7, no. 2 (1985): 247–63. http://dx.doi.org/10.3109/08923978509047637.

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14

Mo, Yosep, Boram Bae, Yuldam Kim, et al. "Antiasthmatic effect of atorvastatin via modulation of macrophage activation." Allergy, Asthma & Respiratory Disease 9, no. 1 (2021): 27. http://dx.doi.org/10.4168/aard.2021.9.1.27.

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Ostriker, Allison, Henrick N. Horita, Joanna Poczobutt, Mary C. M. Weiser-Evans та Raphael A. Nemenoff. "Vascular Smooth Muscle Cell–Derived Transforming Growth Factor-β Promotes Maturation of Activated, Neointima Lesion–Like Macrophages". Arteriosclerosis, Thrombosis, and Vascular Biology 34, № 4 (2014): 877–86. http://dx.doi.org/10.1161/atvbaha.114.303214.

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Objective— To define the contribution of vascular smooth muscle cell (SMC)–derived factors to macrophage phenotypic modulation in the setting of vascular injury. Approach and Results— By flow cytometry, macrophages (M4) were the predominant myeloid cell type recruited to wire-injured femoral arteries, in mouse, compared with neutrophils or eosinophils. Recruited macrophages from injured vessels exhibited a distinct expression profile relative to circulating mononuclear cells (peripheral blood monocytes; increased: interleukin-6, interleukin-10, interleukin-12b, CC chemokine receptor [CCR]3, CC

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Stempin, Cinthia C., Laura R. Dulgerian, Vanina V. Garrido, and Fabio M. Cerban. "Arginase in Parasitic Infections: Macrophage Activation, Immunosuppression, and Intracellular Signals." Journal of Biomedicine and Biotechnology 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/683485.

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A type 1 cytokine-dependent proinflammatory response inducing classically activated macrophages (CaMϕs) is crucial for parasite control during protozoan infections but can also contribute to the development of immunopathological disease symptoms. Type 2 cytokines such as IL-4 and IL-13 antagonize CaMϕs inducing alternatively activated macrophages (AaMϕs) that upregulate arginase-1 expression. During several infections, induction of arginase-1-macrophages was showed to have a detrimental role by limiting CaMϕ-dependent parasite clearance and promoting parasite proliferation. Additionally, the r

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Nasarre, C., J. L. Krahenbuhl, and T. R. Klei. "Down Regulation of Macrophage Activation in Brugia pahangi-Infected Jirds (Meriones unguiculatus)." Infection and Immunity 66, no. 3 (1998): 1063–69. http://dx.doi.org/10.1128/iai.66.3.1063-1069.1998.

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ABSTRACT The macrophage is a major component of the inflammatory response induced by lymphatic tissue-dwelling filariae. Intraperitoneal (i.p.) infections with Brugia pahangi in Mongolian gerbils, or jirds (Meriones unguiculatus), induce a peritoneal inflammatory response characterized by accumulation of numerous macrophages and fewer eosinophils. This inflammatory response is associated with the release of microfilariae by female worms. The aim of this study was to investigate the activation state of the peritoneal macrophages during the course of i.p. infections with either male or female wo

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Aerbajinai, Wulin, Kyung Chin, Hyun Woo Lee, Jianqiong Zhu, and Griffin P. Rodgers. "Glia Maturation Factor-Gamma Negatively Modulates TLR4 Signaling In Macrophages Induced by Lipopolysaccharide (LPS)." Blood 116, no. 21 (2010): 1482. http://dx.doi.org/10.1182/blood.v116.21.1482.1482.

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Abstract Abstract 1482 Toll-like receptor 4 (TLR4) plays a critical role in innate immunity that recognize pathogenic molecules and trigger inflammatory response. However, excessive activation of TLR4 activation may contribute to pathogenesis of autoimmune and inflammatory diseases. Therefore, the negative regulation of TLR4-triggered inflammatory response attracts much attention in recent years. Activation of TLR4 signaling pathways by lipopolysaccharide (LPS) leads to the production of a broad array of cytokines and mediators that coordinate the immune response in macrophages. Glia maturatio

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19

Park, Jin-Woo, Sang-Hyeob Han, and Takao Hanawa. "Effects of Surface Nanotopography and Calcium Chemistry of Titanium Bone Implants on Early Blood Platelet and Macrophage Cell Function." BioMed Research International 2018 (July 4, 2018): 1–10. http://dx.doi.org/10.1155/2018/1362958.

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Early responses of blood platelets and immunoinflammatory cells (macrophages) to titanium (Ti) bone implants affect the subsequent biological healing of implants by modulating early tissue healing-microenvironments via the formation of temporary fibrin matrix scaffolds for stem cell migration and production of growth factors and cytokines. This study investigated the effects of nanoscale surface topography and calcium ion (Ca2+) modification of Ti surfaces on biocompatibility regulated by blood platelets and macrophages, for the future surface design of Ti bone implants with enhanced early ost

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20

GONG, W., K. Guo, and J. Ren. "OP32 Mincle signalling promotes intestinal mucosal inflammation through induction of macrophage pyroptosis and neutrophil chemotaxis in Crohn’s disease." Journal of Crohn's and Colitis 14, Supplement_1 (2020): S031. http://dx.doi.org/10.1093/ecco-jcc/jjz203.031.

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Abstract Background Macrophage-inducible C-type lectin (Mincle) signalling plays a proinflammatory role in different organs such as the brain and liver, but its role in intestinal inflammation remains unknown. Methods We studied the characteristics of Mincle signalling expression in CD patients and experimental colitis. The functional role of Mincle signalling in the intestine was addressed in experimental colitis models in vivo by using mice with Mincle knock out (Mincle−/−), neutralising anti-Mincle antibody, Mincle pharmacologic agonist and RNA-seq genome expression analysis. Bone marrow-de

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Deng, Jiangping, Kuzhali Muthu, Richard Gamelli, Ravi Shankar, and Stephen B. Jones. "Adrenergic modulation of splenic macrophage cytokine release in polymicrobial sepsis." American Journal of Physiology-Cell Physiology 287, no. 3 (2004): C730—C736. http://dx.doi.org/10.1152/ajpcell.00562.2003.

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Enhanced adrenergic stimulation and catecholamine release are important components of the pathophysiology of sepsis. Under physiological conditions, adrenergic stimulation has been shown to be a negative regulator of proinflammatory cytokine production through increasing IL-10 production. Here we have investigated if adrenergic stimulation similarly inhibits TNF-α and IL-6 production by splenic macrophages isolated from a polymicrobial sepsis model. Male B6D2F1mice were subjected to sham (S), laparotomy (Lap), and cecal ligation and puncture (CLP) under anesthesia. Splenic macrophages were iso

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Oda, Tomoyuki, Kiichi Hirota, Kenichiro Nishi, et al. "Activation of hypoxia-inducible factor 1 during macrophage differentiation." American Journal of Physiology-Cell Physiology 291, no. 1 (2006): C104—C113. http://dx.doi.org/10.1152/ajpcell.00614.2005.

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Monocytes/macrophages of the myeloid lineage are the main cellular effectors of innate immunity. Hypoxia-inducible factor 1 (HIF-1) is essential for myeloid cell activation in response to inflammatory stimuli. However, it has not been established whether HIF-1 activity is induced during differentiation from monocyte to macrophage. We demonstrate that macrophage differentiation of THP-1 cells or monocytes from peripheral blood induces increased expression of both HIF-1α and HIF-1β as well as increased HIF-1 transcriptional activity leading to increased expression of HIF-1 target genes. The incr

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Chang, Yung-Chi, Tsui-Ling Hsu, Hsi-Hsien Lin, et al. "Modulation of macrophage differentiation and activation by decoy receptor 3." Journal of Leukocyte Biology 75, no. 3 (2003): 486–94. http://dx.doi.org/10.1189/jlb.0903448.

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Jain, Nikhil, Tamar Shahal, Tslil Gabrieli, et al. "Global modulation in DNA epigenetics during pro-inflammatory macrophage activation." Epigenetics 14, no. 12 (2019): 1183–93. http://dx.doi.org/10.1080/15592294.2019.1638700.

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Meng, Feng-Zhen, Jin-Biao Liu, Xu Wang, et al. "TLR7 Activation of Macrophages by Imiquimod Inhibits HIV Infection through Modulation of Viral Entry Cellular Factors." Biology 10, no. 7 (2021): 661. http://dx.doi.org/10.3390/biology10070661.

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The Toll-like receptor (TLR) 7 is a viral sensor for detecting single-stranded ribonucleic acid (ssRNA), the activation of which can induce intracellular innate immunity against viral infections. Imiquimod, a synthetic ligand for TLR7, has been successfully used for the topical treatment of genital/perianal warts in immunocompetent individuals. We studied the effect of imiquimod on the human immunodeficiency virus (HIV) infection of primary human macrophages and demonstrated that the treatment of cells with imiquimod effectively inhibited infection with multiple strains (Bal, YU2, and Jago) of

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Kang, Sujin, and Atsushi Kumanogoh. "The spectrum of macrophage activation by immunometabolism." International Immunology 32, no. 7 (2020): 467–73. http://dx.doi.org/10.1093/intimm/dxaa017.

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Abstract Macrophages are heterogeneous and plastic, and play several diverse functions in immune responses. Emerging data provide evidence of multiple roles for metabolic pathways in the control of macrophage effector functions. The diverse functions of macrophages are categorized into two main subsets: classical activated macrophages (M1) and alternative activated macrophages (M2). M1 macrophages secrete pro-inflammatory cytokines and reactive oxygen species and migrate into inflamed sites as a part of host defenses. On the other hand, M2 macrophages are involved in immune homeostasis by prod

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Zhang, Ronghua, Tienan Wang, and Qing Lin. "847 Inflammasome activation in M2 macrophage restrain the immune suppressive function." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A900. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0847.

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BackgroundMacrophage is an important component in tumor microenvironment (TME) and plays multiple roles in tumor initiation, progression and metastases. In response to various stimuli within TME, macrophage exhibits high level of functional heterogeneity. There are two distinct groups of macrophages: M1 macrophage exhibits pro-inflammatory phenotype with high levels of TNF-a, IL-6, and IL-1ß, while M2 macrophage displays immune suppressive phenotype with high levels of anti-inflammatory cytokines such as IL-10 and TGF-ß. In response to the M2 cytokines, myeloid cells within the TME further acq

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Gong, Wenbin, Tao Zheng, Kun Guo, et al. "Mincle/Syk Signalling Promotes Intestinal Mucosal Inflammation Through Induction of Macrophage Pyroptosis in Crohn’s Disease." Journal of Crohn's and Colitis 14, no. 12 (2020): 1734–47. http://dx.doi.org/10.1093/ecco-jcc/jjaa088.

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Abstract Background Macrophage-inducible C-type lectin [Mincle] signalling plays a proinflammatory role in different organs such as the brain and liver, but its role in intestinal inflammation, including Crohn’s disease [CD], remains unknown. Methods The characteristics of Mincle signalling expression in CD patients and experimental colitis were examined. The functional role of Mincle signalling in the intestine was addressed in experimental colitis models in vivo by using Mincle knock-out [Mincle-/-] mice. In addition, neutralising anti-Mincle antibody, downstream spleen tyrosine kinase [Syk]

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Gray, Andrea, Rene S. Schloss, and Martin Yarmush. "Donor variability among anti-inflammatory pre-activated mesenchymal stromal cells." TECHNOLOGY 04, no. 03 (2016): 201–15. http://dx.doi.org/10.1142/s2339547816500084.

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Therapeutic mesenchymal stromal cells (MSCs) are attractive in part due to their immunomodulatory properties, achieved by their paracrine secretion of factors including prostaglandin E2 (PGE2). Despite promising pre-clinical data, demonstrating clinical efficacy has proven difficult. The current studies were designed to develop approaches to pre-induce desired functions from naïve MSCs and examine MSC donor variability, two factors contributing to this disconnect. MSCs from six human donors were pre-activated with interleukin 1 beta (IL-1β) at a concentration and duration identified as optimal

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Rupil, Lucía L., Andreza F. de Bem, and German A. Roth. "Diphenyl diselenide-modulation of macrophage activation: Down-regulation of classical and alternative activation markers." Innate Immunity 18, no. 4 (2012): 627–37. http://dx.doi.org/10.1177/1753425911431285.

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Aerbajinai, Wulin, Chutima Kumkhaek, Wenli Liu, and Griffin P. Rodgers. "Glia Maturation Factor-Gamma Regulates Alternative Activation of Macrophage By the Modulation of Iron Homeostasis through HO-1 in Ex Vivo." Blood 128, no. 22 (2016): 3677. http://dx.doi.org/10.1182/blood.v128.22.3677.3677.

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Abstract Macrophages play a key role at the crossroad of iron metabolism and immune function. They store and recycle iron derived from the phagocytosis of senescent erythrocytes. Macrophages iron homeostasis is coupled to their remarkable heterogeneity and functional plasticity. It is well known that the macrophage polarization process dictates expression profiles of genes involved in iron metabolism. M1 macrophages are characterized by increased iron retention, whereas, M2 macrophages showed increased iron recycling. However, the molecular mechanisms underlying iron metabolism link to regulat

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Woods, J. A., J. M. Davis, E. P. Mayer, A. Ghaffar, and R. R. Pate. "Effects of exercise on macrophage activation for antitumor cytotoxicity." Journal of Applied Physiology 76, no. 5 (1994): 2177–85. http://dx.doi.org/10.1152/jappl.1994.76.5.2177.

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Recent evidence suggests that exercise affects macrophage functions and that amount of exercise may be important. We determined effects of moderate (MOD) and exhaustive treadmill running (EXH) on 1) ability of macrophages to become activated for antitumor cytotoxicity after injection of heat-inactivated Propionibacterium acnes in vivo, 2) macrophage responsiveness to activating agents lipopolysaccharide and interferon-gamma, and 3) role of glucocorticoids and various macrophage metabolic products in modulating cytotoxicity in exercised animals. Male C3H/HeN mice were randomly assigned to MOD (

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Han, Xiao, Saihua Huang, Ping Xue, et al. "LncRNA PTPRE-AS1 modulates M2 macrophage activation and inflammatory diseases by epigenetic promotion of PTPRE." Science Advances 5, no. 12 (2019): eaax9230. http://dx.doi.org/10.1126/sciadv.aax9230.

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Long noncoding RNAs (lncRNAs) are important regulators of diverse biological processes; however, their function in macrophage activation is undefined. We describe a new regulatory mechanism, where an unreported lncRNA, PTPRE-AS1, targets receptor-type tyrosine protein phosphatase ε (PTPRE) to regulate macrophage activation. PTPRE-AS1 was selectively expressed in IL-4–stimulated macrophages, and its knockdown promoted M2 macrophage activation via MAPK/ERK 1/2 pathway. In vivo, PTPRE-AS1 deficiency enhanced IL-4–mediated M2 macrophage activation and accelerated pulmonary allergic inflammation wh

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Pignol, B., H. Coulomb, S. Hénane, J. M. Mencia-Huerta, and P. Braquet. "Modulation of Cytotoxic Processes by Platelet-Activating Factor." International Journal of Immunopathology and Pharmacology 5, no. 1 (1992): 1–11. http://dx.doi.org/10.1177/039463209200500101.

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The effect of platelet-activating factor (PAF) on rat NK cell activity, rat macrophage cytotoxicity and TNF production by rat macrophages and human monocytes was investigated. After a 4-h incubation period, PAF enhanced rat NK cell activity at the effector/target cell ratios of 50/1 and 25/1 in a bell-shape fashion and with a peak effect at 1 nM. After 24 h incubation with 1 μM PAF, rat macrophage cytotoxicity, as assessed at the 20/1 effector/target cell ratio, was also increased. Addition of PAF and lipopolysaccharide (LPS) to rat macrophages or human monocytes markedly enhanced TNF producti

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Ayub, Sadia, Mukta Sharma, B. Sivasankar, Monika Katyal, and Nibhriti Das. "Modulation of serum complement and macrophage activation by organophosphate insecticide malation." Immunopharmacology 49, no. 1-2 (2000): 48. http://dx.doi.org/10.1016/s0162-3109(00)80144-7.

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Olivier, Martin, Bertha-Judith Romero-Gallo, Claudine Matte та ін. "Modulation of Interferon-γ-induced Macrophage Activation by Phosphotyrosine Phosphatases Inhibition". Journal of Biological Chemistry 273, № 22 (1998): 13944–49. http://dx.doi.org/10.1074/jbc.273.22.13944.

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He, Yongqun, Sherry Reichow, Sheela Ramamoorthy, et al. "Brucella melitensis Triggers Time-Dependent Modulation of Apoptosis and Down-Regulation of Mitochondrion-Associated Gene Expression in Mouse Macrophages." Infection and Immunity 74, no. 9 (2006): 5035–46. http://dx.doi.org/10.1128/iai.01998-05.

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ABSTRACT Brucella spp. are facultative intracellular bacteria that cause brucellosis in humans and other animals. Brucella spp. are taken up by macrophages, and the outcome of the macrophage-Brucella interaction is a basis for establishment of a chronic Brucella infection. Microarrays were used to analyze the transcriptional response of the murine macrophage-like J774.A1 cell line to infection with virulent Brucella melitensis strain 16M. It was found that most significant changes in macrophage gene transcription happened early following infection, and global macrophage gene expression profile

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Schiavano, Giuditta Fiorella, Sabrina Dominici, Laura Rinaldi, Alfonsina Mariarosaria Cangiano, Giorgio Brandi, and Mauro Magnani. "Modulation of Stat-1 in Human Macrophages Infected with Different Species of Intracellular Pathogenic Bacteria." Journal of Immunology Research 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/5086928.

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The infection of human macrophages by pathogenic bacteria induces different signaling pathways depending on the type of cellular receptors involved in the microorganism entry and on their mechanism(s) of survival and replication in the host cell. It was reported that Stat proteins play an important role in this process. In the present study, we investigate the changes in Stat-1 activation (phosphorylation in p-tyr701) after uptake of two Gram-positive (Listeria monocytogenesandStaphylococcus aureus) and two Gram-negative bacteria (Salmonella typhimuriumandLegionella pneumophila) characterized

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Pradhan, Pooja, Vijith Vijayan, Faikah Gueler, and Stephan Immenschuh. "Interplay of Heme with Macrophages in Homeostasis and Inflammation." International Journal of Molecular Sciences 21, no. 3 (2020): 740. http://dx.doi.org/10.3390/ijms21030740.

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Macrophages are an integral part of the mononuclear phagocyte system that is critical for maintaining immune homeostasis. They play a key role for initiation and modulation of immunological responses in inflammation and infection. Moreover, macrophages exhibit a wide spectrum of tissue-specific phenotypes in steady-state and pathophysiological conditions. Recent clinical and experimental evidence indicates that the ubiquitous compound heme is a crucial regulator of these cells, e.g., in the differentiation of monocytes to tissue-resident macrophages and/ or in activation by inflammatory stimul

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Chiavari, Marta, Gabriella Maria Pia Ciotti, Francesco Canonico, et al. "PDIA3 Expression in Glioblastoma Modulates Macrophage/Microglia Pro-Tumor Activation." International Journal of Molecular Sciences 21, no. 21 (2020): 8214. http://dx.doi.org/10.3390/ijms21218214.

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The glioblastoma (GB) microenvironment includes cells of the innate immune system identified as glioma-associated microglia/macrophages (GAMs) that are still poorly characterized. A potential role on the mechanisms regulating GAM activity might be played by the endoplasmic reticulum protein ERp57/PDIA3 (protein disulfide-isomerase A3), the modulation of which has been reported in a variety of cancers. Moreover, by using The Cancer Genome Atlas database, we found that overexpression of PDIA3 correlated with about 55% reduction of overall survival of glioma patients. Therefore, we analyzed the e

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Schwamb, Janine, Nina Reinart, Daniela Vorholt, et al. "Phagocytic Function of Macrophages Is Impaired By Chronic Lymphocytic Leukemia and high–grade Lymphoma Progression and Can be Highly Effectively Restored for Chemo-Immunotherapy." Blood 124, no. 21 (2014): 2727. http://dx.doi.org/10.1182/blood.v124.21.2727.2727.

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Abstract Macrophage polarity has recently been shown to play a pivotal role in progression and prognosis of human malignancies. In CLL the high dependence of the malignant cell to the tumor microenvironment has revealed macrophages as major mediators of leukemia cell survival. In contrast, macrophage activation also offers novel therapeutic strategies for leukemia cell targeting. Here we analyze the reciprocal relationship of leukemia cells and macrophages and the specific functional impact of phagocytosis in leukemia progression and therapy. We employed the humanized hMB-Lymphoma and the Eµ-T

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Nowakowska, Dominika, Ryan Phennicie, Kevin Kauffman, et al. "PSGL-1 is a novel macrophage checkpoint in immuno-oncology." Journal of Clinical Oncology 38, no. 15_suppl (2020): e15090-e15090. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e15090.

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e15090 Background: Macrophages are both antigen presenting and effector cells of the innate immune system and play an important role in tissue homeostasis as well as in activation and modulation of the adaptive immune response in disease. They display phenotypic heterogeneity in different tissue environments but can be broadly subdivided into pro-inflammatory M1 macrophages, which promote immune response, and anti-inflammatory M2 macrophages, which are associated with immune suppression. Under steady-state conditions, the populations of immune-stimulatory and immune-regulatory macrophages are

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Del Corno, Manuela, Qing-Hua Liu, Dominique Schols, et al. "HIV-1 gp120 and chemokine activation of Pyk2 and mitogen-activated protein kinases in primary macrophages mediated by calcium-dependent, pertussis toxin–insensitive chemokine receptor signaling." Blood 98, no. 10 (2001): 2909–16. http://dx.doi.org/10.1182/blood.v98.10.2909.

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Abstract Human immunodeficiency virus type 1 (HIV-1) uses the chemokine receptors CCR5 and CXCR4 as coreceptors for entry. It was recently demonstrated that HIV-1 glycoprotein 120 (gp120) elevated calcium and activated several ionic signaling responses in primary human macrophages, which are important targets for HIV-1 in vivo. This study shows that chemokine receptor engagement by both CCR5-dependent (R5) and CXCR4-dependent (X4) gp120 led to rapid phosphorylation of the focal adhesion-related tyrosine kinase Pyk2 in macrophages. Pyk2 phosphorylation was also induced by macrophage inflammator

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Ou, Da-Liang, Chia-Wei Chen, Chia-Lang Hsu, et al. "Regorafenib enhances antitumor immunity via inhibition of p38 kinase/Creb1/Klf4 axis in tumor-associated macrophages." Journal for ImmunoTherapy of Cancer 9, no. 3 (2021): e001657. http://dx.doi.org/10.1136/jitc-2020-001657.

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BackgroundRegorafenib and other multikinase inhibitors may enhance antitumor efficacy of anti-program cell death-1 (anti-PD1) therapy in hepatocellular carcinoma (HCC). Its immunomodulatory effects, besides anti-angiogenesis, were not clearly defined.MethodsIn vivo antitumor efficacy was tested in multiple syngeneic liver cancer models. Murine bone marrow–derived macrophages (BMDMs) were tested in vitro for modulation of polarization by regorafenib and activation of cocultured T cells. Markers of M1/M2 polarization were measured by quantitative reverse transcription PCR (RT-PCR), arginase acti

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Rojas, Roxana E., Martha Torres, Jean-Jacques Fournié, Clifford V. Harding та W. Henry Boom. "Phosphoantigen Presentation by Macrophages to Mycobacterium tuberculosis-Reactive Vγ9Vδ2+ T Cells: Modulation by Chloroquine". Infection and Immunity 70, № 8 (2002): 4019–27. http://dx.doi.org/10.1128/iai.70.8.4019-4027.2002.

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ABSTRACT Vγ9Vδ2+ T cells (γδ T cells) are activated by Mycobacterium tuberculosis and recognize mycobacterial nonpeptide phosphoantigens. The role of antigen-presenting cells in the processing and presentation of phosphoantigens to Vγ9Vδ2+ T cells is not understood. We analyzed the role of macrophages for activation of γδ T cells by a new synthetic phosphoantigen bromohydrin pyrophosphate (BrHPP) and M. tuberculosis. Macrophages greatly increased γδ T-cell activation by both BrHPP and M. tuberculosis. Fixation of macrophages before infection demonstrated that uptake of M. tuberculosis was requ

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Bellingan, Geoffrey John, Ping Xu, Helen Cooksley, et al. "Adhesion Molecule–dependent Mechanisms Regulate the Rate of Macrophage Clearance During the Resolution of Peritoneal Inflammation." Journal of Experimental Medicine 196, no. 11 (2002): 1515–21. http://dx.doi.org/10.1084/jem.20011794.

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Macrophage clearance is essential for the resolution of inflammation. Much is known about how monocytes enter the inflammatory site but little is known about how resultant macro-phages are cleared. We have previously demonstrated that macrophage clearance from resolving peritonitis occurs by emigration into draining lymphatics rather than local apoptosis. We now examine mechanisms for this process, in particular by evaluating the hypothesis that modulation of adhesion interactions between macrophages and cells lining the lymphatics regulates the rate of macrophage clearance. We demonstrate in

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Wen, Xia, Dai Xiaoyue, Ding Longkun, et al. "Three main short-chain fatty acids inhibit the activation of THP-1 cells by Mycoplasma pneumoniae." Bioscience, Biotechnology, and Biochemistry 85, no. 4 (2020): 923–30. http://dx.doi.org/10.1093/bbb/zbaa110.

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ABSTRACT The overactivation of macrophages causes chronic inflammatory diseases. Short-chain fatty acids (SCFAs), potential drugs for clinical treatment, are modulators of macrophage inflammatory reaction. Therefore, the modulation of macrophage-mediated cell activity is expected to become a new therapeutic strategy for inflammatory diseases caused by Mycoplasma pneumoniae. In this study, 2 kinds of SCFAs (propionate and butyrate) were found to have anti-inflammatory effects in M. pneumoniae-stimulated THP-1 cells inflammatory. They inhibited the expressions of IL-4, IL-6, ROS, and NLRP3 infla

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Hu, Xuming, Huan Luo, Chunfeng Dou, et al. "Metformin Triggers Apoptosis and Induction of the G0/G1 Switch 2 Gene in Macrophages." Genes 12, no. 9 (2021): 1437. http://dx.doi.org/10.3390/genes12091437.

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Metformin is a widely used antidiabetic drug for the treatment of type 2 diabetes and has been recently demonstrated to possess anti-inflammatory properties via AMPK-mediated modulation of M2 macrophage activation. However, the anti-inflammatory mechanisms of metformin on inflammatory macrophages are still not fully elucidated. In this study, we found that metformin induced apoptosis in macrophages. In particular, metformin induced apoptosis of M1 macrophages, based on M1 marker genes in apoptotic macrophages. Next, we comprehensively screened metformin-responsive genes in macrophages by RNA-s

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Lonardoni, M. V. C., C. L. Barbieri, M. Russo, and S. Jancar. "Modulation ofLeishmania (L.) amazonensisGrowth in Cultured Mouse Macrophages by Prostaglandins and Platelet Activating Factor." Mediators of Inflammation 3, no. 2 (1994): 137–41. http://dx.doi.org/10.1155/s0962935194000177.

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The role of endogenously synthesized PAF and prostaglandins on the infection of mouse macrophages byLetsbmanta (L.) amazonensiswas investigated, as well as the possible correlation between the effects of these inflammatory mediators with nitric oxide production. It was found that pretreatment of macrophages with 10−5M of the PAF antagonists, BN-52021 or WEB-2086, increased macrophage infection by 17 and 59%, respectively. The cyclooxygenase inhibitor, indomethacin (10μg/ml), induced a significant inhibition which was reversed by addition of PGE (10-3 M) to the culture medium. These results sug

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Yuan, Pu-Qing, and Yvette Taché. "Abdominal surgery induced gastric ileus and activation of M1-like macrophages in the gastric myenteric plexus: prevention by central vagal activation in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 313, no. 4 (2017): G320—G329. http://dx.doi.org/10.1152/ajpgi.00121.2017.

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Inflammation plays a role in abdominal surgery (AS)-induced intestinal ileus that is alleviated by electrical vagal stimulation. Intracisternal injection of RX-77368, the stable thyrotropin-releasing hormone agonist, activates dorsal motor nucleus neurons and gastric vagal efferent discharges. We investigated the gastric inflammation induced by AS and the modulation by intracisternal RX-77368 in rats. RX-77368 (50 ng/rat) or saline was injected followed, 1 h later, by laparotomy and small intestinal/cecal manipulation. The sham group had anesthesia alone. After 6 h, gastric emptying (GE) and t

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