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Artykuły w czasopismach na temat „Macrophage activation”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Sharma, Preeti, Shailza Shreshtha, Pradeep Kumar, Rachna Sharma, and T. K. Mahapatra. "A Review on Macrophage Activation Syndrome." Journal of Pure and Applied Microbiology 13, no. 1 (2019): 183–91. http://dx.doi.org/10.22207/jpam.13.1.19.

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Gilbreath, M. J., C. A. Nacy, D. L. Hoover, C. R. Alving, G. M. Swartz, and M. S. Meltzer. "Macrophage activation for microbicidal activity against Leishmania major: inhibition of lymphokine activation by phosphatidylcholine-phosphatidylserine liposomes." Journal of Immunology 134, no. 5 (1985): 3420–25. http://dx.doi.org/10.4049/jimmunol.134.5.3420.

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Abstract Resident peritoneal macrophages from untreated mice develop microbicidal activity against amastigotes of the protozoan parasite Leishmania tropica (current nomenclature = Leishmania major) after in vitro exposure to LK from antigen-stimulated leukocyte culture fluids. This LK-induced macrophage microbicidal activity was completely abrogated by addition of 7:3 phosphatidylcholine: phosphatidylserine liposomes. Liposome inhibition was not due to direct toxic effects against the parasite or macrophage effector cell; factors in LK that induce macrophage microbicidal activity were not adso

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Van Epps, Heather L. "Macrophage activation unveiled." Journal of Experimental Medicine 202, no. 7 (2005): 884. http://dx.doi.org/10.1084/jem.2027fta.

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In the early 1960s, George Mackaness showed that macrophages from mice infected with intracellular bacteria could launch an indiscriminate attack against unrelated bacteria. Thus began an explosion of research on the biology of what Mackaness first termed “macrophage activation.”

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Heidenreich, S., M. Weyers, J. H. Gong, H. Sprenger, M. Nain, and D. Gemsa. "Potentiation of lymphokine-induced macrophage activation by tumor necrosis factor-alpha." Journal of Immunology 140, no. 5 (1988): 1511–18. http://dx.doi.org/10.4049/jimmunol.140.5.1511.

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Abstract In this study, we examined the possible role of TNF-alpha and lymphotoxin (TNF-beta) as cofactors of macrophage activation. The results demonstrate that both TNF were capable of enhancing the cytostatic and cytolytic activity of murine peritoneal macrophages against Eb lymphoma cells. The potentiation of tumor cytotoxicity became apparent when macrophages from DBA/2 mice were suboptimally activated by either a T cell clone-derived macrophage-activating factor or by IFN-gamma plus LPS. Neither TNF-alpha nor TNF-beta could induce tumor cytotoxicity in IFN-gamma-primed macrophages, indic

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5

Zhao, Yu, Yuteng Jiang, Fengmei Wang, et al. "High glucose promotes macrophage switching to the M1 phenotype via the downregulation of STAT-3 mediated autophagy." PLOS ONE 19, no. 12 (2024): e0314974. https://doi.org/10.1371/journal.pone.0314974.

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Aim Imbalanced M1/M2 macrophage phenotype activation is a key point in diabetic kidney disease (DKD). Macrophages mainly exhibit the M1 phenotype, which contributes to inflammation and fibrosis in DKD. Studies have indicated that autophagy plays an important role in M1/M2 activation. However, the mechanism by which autophagy regulates the macrophage M1/M2 phenotype in DKD is unknown. Thus, the aim of the present study was to explore whether high glucose-induced macrophages switch to the M1 phenotype via the downregulation of STAT-3-mediated autophagy. Methods DKD model rats were established in

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McGee, MP, R. Wallin, FB Wheeler, and H. Rothberger. "Initiation of the extrinsic pathway of coagulation by human and rabbit alveolar macrophages: a kinetic study." Blood 74, no. 5 (1989): 1583–90. http://dx.doi.org/10.1182/blood.v74.5.1583.1583.

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Abstract We examined assembly and expression of the factor X activating complex on human and rabbit alveolar macrophages. Kinetic parameters of the factor X activating reaction were determined by functional titrations of factors VII and X with macrophage tissue factor (TF) added. We found rapid activation of factor X to Xa on alveolar macrophage surfaces. Detection of rapid factor Xa formation on macrophages required addition of exogenous factors VII and X. At plasma concentrations of the purified factors, factor Xa was formed on freshly isolated macrophages at approximately 5.4 pmol/min/10(6)

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McGee, MP, R. Wallin, FB Wheeler, and H. Rothberger. "Initiation of the extrinsic pathway of coagulation by human and rabbit alveolar macrophages: a kinetic study." Blood 74, no. 5 (1989): 1583–90. http://dx.doi.org/10.1182/blood.v74.5.1583.bloodjournal7451583.

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We examined assembly and expression of the factor X activating complex on human and rabbit alveolar macrophages. Kinetic parameters of the factor X activating reaction were determined by functional titrations of factors VII and X with macrophage tissue factor (TF) added. We found rapid activation of factor X to Xa on alveolar macrophage surfaces. Detection of rapid factor Xa formation on macrophages required addition of exogenous factors VII and X. At plasma concentrations of the purified factors, factor Xa was formed on freshly isolated macrophages at approximately 5.4 pmol/min/10(6) cells. A

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8

Lewis, Brandon W., Sonika Patial, and Yogesh Saini. "In Vitro Screening Method for Characterization of Macrophage Activation Responses." Methods and Protocols 5, no. 5 (2022): 68. http://dx.doi.org/10.3390/mps5050068.

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Macrophage activation refers to the enhanced functionality of macrophages in response to endogenous or exogenous stimuli. Due to the existence of limitless stimuli and a multitude of receptors on macrophage surfaces, the nature of activation (or acquired functioning) can be specific to the encountering stimulus. This article describes a macrophage-activation screening platform in a 96-well format. The methodology involves the generation of bone marrow-derived macrophages, their activation into two extreme activation states, and screening of activated macrophages for expression of bonafide prot

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Rios, Francisco J., Marianna M. Koga, Mateus Pecenin, Matheus Ferracini, Magnus Gidlund, and S. Jancar. "Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFR." Mediators of Inflammation 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/198193.

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OxLDL is recognized by macrophage scavenger receptors, including CD36; we have recently found that Platelet-Activating Factor Receptor (PAFR) is also involved. Since PAFR in macrophages is associated with suppressor function, we examined the effect of oxLDL on macrophage phenotype. It was found that the presence of oxLDL during macrophage differentiation induced high mRNA levels to IL-10, mannose receptor, PPARγand arginase-1 and low levels of IL-12 and iNOS. When human THP-1 macrophages were pre-treated with oxLDL then stimulated with LPS, the production of IL-10 and TGF-βsignificantly increa

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Valledor, Annabel F., Luís Arpa, Ester Sánchez-Tilló та ін. "IFN-γ–mediated inhibition of MAPK phosphatase expression results in prolonged MAPK activity in response to M-CSF and inhibition of proliferation". Blood 112, № 8 (2008): 3274–82. http://dx.doi.org/10.1182/blood-2007-11-123604.

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Abstract Macrophages have the capacity to proliferate in response to specific growth factors, such as macrophage-colony stimulating factor (M-CSF). In the presence of several cytokines and activating factors, macrophages undergo growth arrest, become activated, and participate in the development of an immune response. We have previously observed that activation of extracellularly regulated kinase 1/2 (ERK-1/2) is required for macrophage proliferation in response to growth factors. A short and early pattern of ERK activity correlated with the proliferative response. In contrast, slightly prolon

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Davis, Spring, Aiko M. Cirone, Janet Menzie, et al. "Phagocytosis-mediated M1 activation by chitin but not by chitosan." American Journal of Physiology-Cell Physiology 315, no. 1 (2018): C62—C72. http://dx.doi.org/10.1152/ajpcell.00268.2017.

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Chitin particles have been used to understand host response to chitin-containing pathogens and allergens and are known to induce a wide range of polarized macrophage activations, depending, at least in part, on particle size. Nonphagocytosable particles larger than a macrophage induce tissue repair M2 activation. In contrast, phagocytosable chitin microparticles (CMPs, 1–10 μm diameters) induce M1 macrophages that kill intracellular microbes and damage tissues. However, chitosan (deacetylated) microparticles (de-CMPs, 1–10 µm) induce poor M1 activation. Toll-like receptor 2 (TLR2) and associat

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Leopold Wager, Chrissy M., Camaron R. Hole, Karen L. Wozniak, Michal A. Olszewski, Mathias Mueller, and Floyd L. Wormley. "STAT1 Signaling within Macrophages Is Required for Antifungal Activity against Cryptococcus neoformans." Infection and Immunity 83, no. 12 (2015): 4513–27. http://dx.doi.org/10.1128/iai.00935-15.

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Cryptococcus neoformans, the predominant etiological agent of cryptococcosis, is an opportunistic fungal pathogen that primarily affects AIDS patients and patients undergoing immunosuppressive therapy. In immunocompromised individuals,C. neoformanscan lead to life-threatening meningoencephalitis. Studies using a virulent strain ofC. neoformansengineered to produce gamma interferon (IFN-γ), denoted H99γ, demonstrated that protection against pulmonaryC. neoformansinfection is associated with the generation of a T helper 1 (Th1)-type immune response and signal transducer and activator of transcri

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13

ONOZAKI, Kikuo. "Macrophage activation by macrophage activation factor, macrophage migration inhibitory factor." Nippon Saikingaku Zasshi 40, no. 5 (1985): 811–17. http://dx.doi.org/10.3412/jsb.40.811.

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Timmer, Anjuli M., та Victor Nizet. "IKKβ/NF-κB and the miscreant macrophage". Journal of Experimental Medicine 205, № 6 (2008): 1255–59. http://dx.doi.org/10.1084/jem.20081056.

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Macrophage activation relies on complex intracellular signaling processes that integrate the need for rapid inflammatory responses to pathogens with the need to resolve inflammation without permanent harm to normal tissues. Patterns of aberrant macrophage activation characterize and sustain disorders of chronic inflammation, infection, and cancer. New studies now show a role for the NF-κB activator IKKβ in promoting an alternative, immunosuppressive pattern of macrophage activation, which limits the cell's tumoricidal and bactericidal capacities. As cancers and pathogens may have evolved multi

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15

Huang, Wei, Itsuko Ishii, Wei-Yang Zhang, Miyahiko Sonobe, and Howard S. Kruth. "PMA activation of macrophages alters macrophage metabolism of aggregated LDL." Journal of Lipid Research 43, no. 8 (2002): 1275–82. http://dx.doi.org/10.1194/jlr.m100436-jlr200.

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Aggregation of LDL may contribute to its retention in atherosclerotic lesions. Previously, we showed that aggregated LDL induces and enters surface-connected compartments (SCCs) in human monocyte-derived macrophages by a process we have named patocytosis. Aggregated LDL was disaggregated and released from SCCs of macrophages when exposed to human lipoprotein-deficient serum. The serum factor that mediated aggregated LDL release and disaggregation was plasmin generated from plasminogen by macrophage urokinase plasminogen activator. We now show that activation of macrophages with PMA inhibits pl

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Wyler, D. J., D. I. Beller, and J. P. Sypek. "Macrophage activation for antileishmanial defense by an apparently novel mechanism." Journal of Immunology 138, no. 4 (1987): 1246–49. http://dx.doi.org/10.4049/jimmunol.138.4.1246.

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Abstract Activation of macrophages by lymphokines (including interferon-gamma; IFN-gamma) is presently considered to be a major host defense mechanism against a number of intracellular microorganisms. In a series of earlier studies that made use of mice undergoing spontaneous resolution of footpad infections with Leishmania major, we obtained evidence suggesting that a subpopulation of Leishmania-sensitized lymph node T lymphocytes could activate antimicrobial effects in Leishmania-infected macrophages by an apparently lymphokine-independent mechanism. These effector lymphocytes are not cytoto

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Stout, R. D., J. Suttles, J. Xu, I. S. Grewal, and R. A. Flavell. "Impaired T cell-mediated macrophage activation in CD40 ligand-deficient mice." Journal of Immunology 156, no. 1 (1996): 8–11. http://dx.doi.org/10.4049/jimmunol.156.1.8.

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Abstract The expression of the ligand for CD40 (CD40L) is critical for induction of T cell-dependent Ab responses. To examine how critical the expression of CD40L is for induction of cell-mediated immune responses, the ability of T cells from CD40L knockout mice to activate macrophage effector function was assessed. CD4+ T cells from CD40L-knockout mice were fourfold less effective than +/+ T cells in activating the nitric oxide response in allogeneic macrophages. CD40L-knockout T cells that were fixed with paraformaldehyde after a 6-h activation period, a time point at which CD40L dominates t

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Yu, Tingting, Yong Zuo, Rong Cai та ін. "SENP1 regulates IFN-γ−STAT1 signaling through STAT3−SOCS3 negative feedback loop". Journal of Molecular Cell Biology 9, № 2 (2016): 144–53. http://dx.doi.org/10.1093/jmcb/mjw042.

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Abstract Interferon-γ (IFN-γ) triggers macrophage for inflammation response by activating the intracellular JAK−STAT1 signaling. Suppressor of cytokine signaling 1 (SOCS1) and protein tyrosine phosphatases can negatively modulate IFN-γ signaling. Here, we identify a novel negative feedback loop mediated by STAT3−SOCS3, which is tightly controlled by SENP1 via de-SUMOylation of protein tyrosine phosphatase 1B (PTP1B), in IFN-γ signaling. SENP1-deficient macrophages show defects in IFN-γ signaling and M1 macrophage activation. PTP1B in SENP1-deficient macrophages is highly SUMOylated, which redu

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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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Oppong-Nonterah, Gertrude O., Omar Lakhdari, Asami Yamamura, Hal M. Hoffman, and Lawrence S. Prince. "TLR Activation Alters Bone Marrow-Derived Macrophage Differentiation." Journal of Innate Immunity 11, no. 1 (2018): 99–108. http://dx.doi.org/10.1159/000494070.

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Early exposure to inflammatory signals may have a lasting impact on immune function. Present throughout embryogenesis, macrophages are key cells providing innate immune protection to the developing fetus and newborn. Here, we have used an established model of macrophage development to test how early inflammatory signals can impact cellular differentiation and function. Bone marrow-derived macrophages were treated with Escherichia coli lipopolysaccharide (LPS) 2 days after initial isolation and culture. LPS treatment during this early stage of differentiation decreased the expression of CSF1R a

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Hardbower, Dana M., Mohammad Asim, Paula B. Luis, et al. "Ornithine decarboxylase regulates M1 macrophage activation and mucosal inflammation via histone modifications." Proceedings of the National Academy of Sciences 114, no. 5 (2017): E751—E760. http://dx.doi.org/10.1073/pnas.1614958114.

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Macrophage activation is a critical step in host responses during bacterial infections. Ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine metabolism, has been well studied in epithelial cells and is known to have essential roles in many different cellular functions. However, its role in regulating macrophage function during bacterial infections is not well characterized. We demonstrate that macrophage-derived ODC is a critical regulator of M1 macrophage activation during bothHelicobacter pyloriandCitrobacter rodentiuminfection. Myeloid-specificOdcdeletion significantly incre

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Serraj Andaloussi, Meriem, Hayat Midyani, Chadia Khalloufi, et al. "Macrophage Activation Syndrome Discovered During Pregnancy: Case Report." Obstetrics Gynecology and Reproductive Sciences 5, no. 7 (2021): 01–04. http://dx.doi.org/10.31579/2578-8965/081.

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Macrophage activation syndrome (MAS) or Haemophagocytic syndrome (HPS) results from an inappropriate stimulation of macrophages in bone marrow and lymphoid organs, leading to haemophagocytosis and hypercytokinemia. HPS may be primitive, essentially in pediatric population, or secondary to malignancy, infection or autoimmune disease. This disease is rare and prognosis is poor. The diagnosis of hemophagocytic syndrome remains a challenge especially during pregnancy. We report a case collected at the Elharouchimaternity service, taken in charge jointly with its intensive care unit, of a 26-year-o

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Seljelid, R. "Macrophage Activation." Scandinavian Journal of Rheumatology 17, sup76 (1988): 67–72. http://dx.doi.org/10.3109/03009748809102954.

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Petit, J. F., and G. Lemaire. "Macrophage activation." Annales de l'Institut Pasteur / Immunologie 137 (January 1986): 191–92. http://dx.doi.org/10.1016/s0771-050x(86)80024-9.

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Pinder, M. "Macrophage activation." Veterinary Immunology and Immunopathology 14, no. 2 (1987): 205–6. http://dx.doi.org/10.1016/0165-2427(87)90055-9.

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Pedicillo, Maria Carmela, Ilenia Sara De Stefano, Rosanna Zamparese, et al. "The Role of Toll-like Receptor-4 in Macrophage Imbalance in Lethal COVID-19 Lung Disease, and Its Correlation with Galectin-3." International Journal of Molecular Sciences 24, no. 17 (2023): 13259. http://dx.doi.org/10.3390/ijms241713259.

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To the current data, there have been 6,955,141 COVID-19-related deaths worldwide, reported to WHO. Toll-like receptors (TLRs) implicated in bacterial and virus sensing could be a crosstalk between activation of persistent innate-immune inflammation, and macrophage’s sub-population alterations, implicated in cytokine storm, macrophage over-activation syndrome, unresolved Acute Respiratory Disease Syndrome (ARDS), and death. The aim of this study is to demonstrate the association between Toll-like-receptor-4 (TLR-4)-induced inflammation and macrophage imbalance in the lung inflammatory infiltrat

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Chen, L., Y. Suzuki, and E. F. Wheelock. "Interferon-gamma synergizes with tumor necrosis factor and with interleukin 1 and requires the presence of both monokines to induce antitumor cytotoxic activity in macrophages." Journal of Immunology 139, no. 12 (1987): 4096–101. http://dx.doi.org/10.4049/jimmunol.139.12.4096.

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Abstract Small concentrations of recombinant murine interferon-gamma (MuIFN-gamma), recombinant human interleukin 1 (HuIL-1), and recombinant murine tumor necrosis factor (MuTNF), added separately to cultures of thioglycolate-elicited peritoneal macrophages, produced no cytotoxic activity against L5178Y cells, a tumor cell line which is resistant to the direct toxic effects of these cytokines, either alone or in combination. However, small concentrations of MuIFN-gamma when combined with small concentrations of either HuIL-1 or MuTNF activated these macrophages to produce cytotoxic effects aga

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Mantuano, Elisabetta, Pardis Azmoon, Coralie Brifault, et al. "Tissue-type plasminogen activator regulates macrophage activation and innate immunity." Blood 130, no. 11 (2017): 1364–74. http://dx.doi.org/10.1182/blood-2017-04-780205.

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Key Points Tissue-type plasminogen activator inhibits the activity of the innate immune system in macrophages in vitro and in vivo in mice. Suppression of macrophage proinflammatory responses by tPA requires the NMDA receptor.

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Liang, Yan, Xiaoli Sun, Mingjie Wang та ін. "PP2Acα promotes macrophage accumulation and activation to exacerbate tubular cell death and kidney fibrosis through activating Rap1 and TNFα production". Cell Death & Differentiation 28, № 9 (2021): 2728–44. http://dx.doi.org/10.1038/s41418-021-00780-5.

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AbstractMacrophage accumulation and activation play an essential role in kidney fibrosis; however, the underlying mechanisms remain to be explored. By analyzing the kidney tissues from patients and animal models with kidney fibrosis, we found a large induction of PP2Acα in macrophages. We then generated a mouse model with inducible macrophage ablation of PP2Acα. The knockouts developed less renal fibrosis, macrophage accumulation, or tubular cell death after unilateral ureter obstruction or ischemic reperfusion injury compared to control littermates. In cultured macrophages, PP2Acα deficiency

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Yamamoto, N., VR Naraparaju, and PJ Orchard. "Defective lymphocyte glycosidases in the macrophage activation cascade of juvenile osteopetrosis." Blood 88, no. 4 (1996): 1473–78. http://dx.doi.org/10.1182/blood.v88.4.1473.bloodjournal8841473.

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Generation of macrophage-activating factor requires a precursor protein, Gc protein (serum vitamin D3-binding protein), as well as participation of beta-galactosidase of inflammation-primed B lymphocytes and sialidase of T lymphocytes. The treatment of human peripheral blood mononuclear cells with an inflammatory lysophospholipid induced beta-galactosidase and sialidase activity of lymphocytes, leading to the generation of macrophage-activating factor and activation of monocytes/macrophages. However, lysophospholipid treatment of peripheral blood mononuclear cells from three infantile patients

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Vieira, Pedro, Angela Castoldi, Pratik Aryal, et al. "CTLA4-Ig treatment improves RBP4-induced adipose tissue inflammation and insulin resistance triggered by MyD88, JNK, ERK and p38 pathways (IRC8P.443)." Journal of Immunology 194, no. 1_Supplement (2015): 129.7. http://dx.doi.org/10.4049/jimmunol.194.supp.129.7.

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Abstract Adipose tissue (AT) inflammation and impaired insulin action is a major cause of type 2 diabetes. RBP4 is an adipocyte- and liver-derived protein that has an important role in insulin resistance, metabolic syndrome and AT inflammation. RBP4 elevation causes AT inflammation by activating innate immunity that elicits an adaptive immune response. Our aims are to determine the signaling pathways involved in RBP4-induced macrophage activation and the resulting antigen presentation and Th1 polarization and whether the blockade of antigen presentation improves AT inflammation and insulin res

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JAWOROWSKI, Anthony, Elizabeth CHRISTY, Permeen YUSOFF, Robert BYRNE, and John A. HAMILTON. "Differences in the kinetics of activation of protein kinases and extracellular signal-related protein kinase 1 in colony-stimulating factor 1-stimulated and lipopolysaccharide-stimulated macrophages." Biochemical Journal 320, no. 3 (1996): 1011–16. http://dx.doi.org/10.1042/bj3201011.

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To determine the relevance of mitogen-activated protein kinase activity to macrophage proliferation, we measured the stimulation of myelin basic protein (MBP) kinase and extracellular signal-related protein kinase (ERK) activity in a macrophage cell line (BAC1.2F5), bone marrow-derived macrophages (BMM) and resident peritoneal macrophages (RPM). By using an ‘in-gel’ MBP kinase assay the activities of renaturable MBP kinases were detected, including several with molecular masses similar to those of ERK-1 and ERK-2. These represented a minor fraction of total activity and were not activated to a

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Bian, Zhen, Lei Shi та Yuan Liu. "Phagocytic plasticity of macrophage towards healthy self cells: inflammatory activation elicit self-attacking phenotype in macrophages lacking SIRPα-CD47 restraint". Journal of Immunology 198, № 1_Supplement (2017): 154.7. http://dx.doi.org/10.4049/jimmunol.198.supp.154.7.

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Abstract The interaction between macrophage signal-regulatory protein alpha (SIRPα) and its ligand CD47 serves as a critical self-recognition mechanism, in which their interaction triggers inhibitory signaling via SIRPα cytoplasmic ITIMs and prevent macrophage phagocytosis toward self-cells. Despite this mechanism being suggestively imperative, CD47−/− mice demonstrate no, or only mild, macrophage phagocytosis toward self-cells, suggesting additional activation and inhibitory mechanisms controlling macrophage behavior. Studying our recently established SIRPα −/− mice, as well as CD47−/− mice,

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Esparza, I., D. Mannel, A. Ruppel, W. Falk та PH Krammer. "Interferon γ and lymphotoxin or tumor necrosis factor act synergistically to induce macrophage killing of tumor cells and schistosomula of schistosoma mansoni". Journal of Experimental Medicine 166, № 2 (1987): 589–94. http://dx.doi.org/10.1084/jem.166.2.589.

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Macrophages play a crucial role in the defense against tumors and parasites. Activation of tumoricidal and microbicidal effector mechanisms requires stimulation of macrophages with macrophage-activating factors (MAF). One such MAF is interferon γ (IFN-γ). In some assays, substantial activity of IFN-γ on murine macrophages, however, is only observed in synergy with lipopolysaccharide (LPS) or other cytokines (1). In addition, certain cytokines have been shown to induce monocyte or macrophage activation in the absence of IFN-γ (2-5). We previously described lymphokines in the supernatant of a mu

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Llauradó Maury, Gabriel, Humberto J. Morris-Quevedo, Annick Heykers, et al. "Differential Induction Pattern Towards Classically Activated Macrophages in Response to an Immunomodulatory Extract from Pleurotus ostreatus Mycelium." Journal of Fungi 7, no. 3 (2021): 206. http://dx.doi.org/10.3390/jof7030206.

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Pleurotus ostreatus mushroom preparations have been investigated because of their ability to modulate the immune function. However, there is still no consensus regarding the activation and polarizing effect on macrophages by Pleurotus-derived bioproducts. This study examined the immune-activating effect of a mycelium-derived P. ostreatus aqueous extract (HW-Pm) on macrophage functions, by means of the determination of nitric oxide (NO) production, the mRNA expression of inducible nitric oxide synthase (iNOS), Arginase-1 and FIZZ and the cytokine levels. The phagocytic activity and the activati

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Leu, R. W., A. Q. Zhou, B. J. Shannon, and M. J. Herriott. "Inhibitors of C1q biosynthesis suppress activation of murine macrophages for both antibody-independent and antibody-dependent tumor cytotoxicity." Journal of Immunology 144, no. 6 (1990): 2281–86. http://dx.doi.org/10.4049/jimmunol.144.6.2281.

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Abstract The inhibitors of C1q biosynthesis and secretion, 3,4-dehydro-DL-proline (DHP) and 2,2'-dipyridyl, were previously shown to suppress murine macrophage FcR-dependent phagocytosis and cytolysis of IgG-opsonized RBC targets. Inasmuch as non-antibody macrophage activators also bind C1q to initiate C1 activation, we determined the effects of these same inhibitors of C1q biosynthesis on activation of macrophages for antibody-independent, nonspecific tumor cytotoxicity by lipid A and a variety of other non-antibody activators. Preexposure of mouse inflammatory peritoneal macrophages to eithe

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Zhao, Yong, Hao Wang, Ming Lu, et al. "Pancreatic Acinar Cells Employ miRNAs as Mediators of Intercellular Communication to Participate in the Regulation of Pancreatitis-Associated Macrophage Activation." Mediators of Inflammation 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/6340457.

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Macrophage activation plays an important role in the inflammatory response in acute pancreatitis. In the present study, the activation of AR42J pancreatic acinar cells was induced by taurolithocholate treatment. The results showed that the culture medium from the activated AR42J cells significantly enhanced NFκB activation in the macrophages compared to that without taurolithocholate treatment. Additionally, the precipitates obtained from ultracentrifugation of the culture media that were rich in exosomes were markedly more potent in activating macrophages compared with the supernatant fractio

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Tekin, Cansu, Hella L. Aberson, Cynthia Waasdorp, et al. "Macrophage-secreted MMP9 induces mesenchymal transition in pancreatic cancer cells via PAR1 activation." Cellular Oncology 43, no. 6 (2020): 1161–74. http://dx.doi.org/10.1007/s13402-020-00549-x.

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Abstract Purpose Targeting tumor-infiltrating macrophages limits progression and improves chemotherapeutic responses in pancreatic ductal adenocarcinoma (PDAC). Protease-activated receptor (PAR)1 drives monocyte/macrophage recruitment, and stromal ablation of PAR1 limits cancer growth and enhances gemcitabine sensitivity in experimental PDAC. However, the functional interplay between PAR1, macrophages and tumor cells remains unexplored. Here we address the PAR1-macrophage-tumor cell crosstalk and assess its contributions to tumor progression. Methods PAR1 expression and macrophage infiltration

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Nedvetzki, Shlomo, Stefanie Sowinski, Robert A. Eagle, et al. "Reciprocal regulation of human natural killer cells and macrophages associated with distinct immune synapses." Blood 109, no. 9 (2007): 3776–85. http://dx.doi.org/10.1182/blood-2006-10-052977.

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AbstractNatural killer (NK) cells directly lyse tumor or viral-infected cells but also an important role for NK cell cytotoxicity in regulating the extent of immune responses is emerging. Here, we show that autologous human macrophages activated NK cell proliferation and cytokine secretion, increased expression of activating receptors, and primed NK cell cytotoxicity against susceptible target cells. Ligation of NK cell 2B4, and not NKp30 (known to be important for DC-mediated NK cell activation), is critical for this macrophage-mediated NK cell activation. Reciprocally, however, NK cells regu

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Maniecki, Maciej Bogdan, Mette Munk Lauridsen, Troels Bygum Knudsen, et al. "A Macrophage Activation Switch (MAcS)-Index for Assessment of Monocyte/Macrophage Activation." Blood 112, no. 11 (2008): 3550. http://dx.doi.org/10.1182/blood.v112.11.3550.3550.

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Abstract BACKGROUND: The monocyte/macrophage system plays important roles in host defense, regulation of immune responses, tissue repair, neovascularization, and inflammation. These diverse roles are performed by specific subpopulations of macrophages that are differently activated by surrounding stimuli, simplified by the M1-M2 dichotomy of classically activated (M1), pro-inflammatory cells and alternatively activated (M2), anti-inflammatory cells. Macrophages, however, display a large degree of flexibility and are able to switch between activation states (1) The hemoglobin scavenger receptor

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Roa-Vidal, Natalia, Adriana S. Rodríguez-Aponte, José A. Lasalde-Dominicci, Coral M. Capó-Vélez, and Manuel Delgado-Vélez. "Cholinergic Polarization of Human Macrophages." International Journal of Molecular Sciences 24, no. 21 (2023): 15732. http://dx.doi.org/10.3390/ijms242115732.

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Macrophages serve as vital defenders, protecting the body by exhibiting remarkable cellular adaptability in response to invading pathogens and various stimuli. These cells express nicotinic acetylcholine receptors, with the α7-nAChR being extensively studied due to its involvement in activating the cholinergic anti-inflammatory pathway. Activation of this pathway plays a crucial role in suppressing macrophages’ production of proinflammatory cytokines, thus mitigating excessive inflammation and maintaining host homeostasis. Macrophage polarization, which occurs in response to specific pathogens

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Yamamoto, N., D. D. Lindsay, V. R. Naraparaju, R. A. Ireland, and S. N. Popoff. "A defect in the inflammation-primed macrophage-activation cascade in osteopetrotic rats." Journal of Immunology 152, no. 10 (1994): 5100–5107. http://dx.doi.org/10.4049/jimmunol.152.10.5100.

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Abstract Macrophages were activated by administration of lysophosphatidylcholine (lyso-Pc) or dodecylglycerol (DDG) to wild-type rats but not in osteopetrotic (op) mutant rats. In vitro treatment of wild-type rat peritoneal cells with lyso-Pc or DDG efficiently activated macrophages whereas treatment of op mutant rat peritoneal cells with lyso-Pc or DDG did not activate macrophages. The inflammation-primed macrophage activation cascade in rats requires participation of B lymphocytes and vitamin D binding protein (DBP). Lyso-Pc-inducible beta-galactosidase of wild-type rat B lymphocytes can con

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TAVARES, ALDO, and ANAMELIA BOCCA. "Dectin-1 restores macrophage anti-Cryptococcus neoformans activity." Journal of Immunology 196, no. 1_Supplement (2016): 60.21. http://dx.doi.org/10.4049/jimmunol.196.supp.60.21.

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Abstract The interaction between macrophages and Cryptococcus neoformans (Cn) can result in fungal killing or intracellular replication. The macrophage optimal response requires the specific recognition of fungal molecular structures by a variety of pattern-recognition receptors (PRRs) receptors, mainly TLRs and CLRs.. We report that zymosan (b-glucan)-stimulated macrophages enhanced the antifungal activity against Cn. This activity depends primarily on Dectin-1 activation, with minor contribution of complement receptor 3 and/or TLR2. b-glucan-stimulation also up-regulates macrophage genes ass

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Yamamoto, N., S. Homma, and I. Millman. "Identification of the serum factor required for in vitro activation of macrophages. Role of vitamin D3-binding protein (group specific component, Gc) in lysophospholipid activation of mouse peritoneal macrophages." Journal of Immunology 147, no. 1 (1991): 273–80. http://dx.doi.org/10.4049/jimmunol.147.1.273.

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Abstract In vitro treatment of mouse peritoneal cells (mixture of adherent and nonadherent cells) with lysophosphatidylcholine (lyso-Pc) in 10% FCS supplemented medium RPMI 1640 results in a greatly enhanced FcR-mediated phagocytic activity of macrophages. This macrophage-activation process requires a serum factor. Fractionation studies with starch block electrophoresis of fetal calf and human sera revealed that alpha 2-globulin fraction contains a serum factor essential for macrophage activation. To identify the serum factor, human serum was precipitated with 50% saturated ammonium sulfate an

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Tang, Hong, JIn Feng, and Chao Zhang. "The innate-like T cells are required to modulate acute inflammatory response (P1050)." Journal of Immunology 190, no. 1_Supplement (2013): 65.26. http://dx.doi.org/10.4049/jimmunol.190.supp.65.26.

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Abstract Macrophages infiltration and activation in myocardium is a pivotal immunopathological lead to hypertensive cardiac micro-injury, but underlying mechanisms remain elusive. We have found that CD8 KO or CD8+ T cells depletion by antibody significantly reduce cardiac pro-fibrotic inflammatory responses induced by angiotensin II (Ang II) infusion, whereas CD8 KO mice reconstituted with CD8+ T cells became sensitive. More importantly, CD8+ T cells are required for macrophage infiltration in myocardium and subsequent activation to express pro-inflammatory cytokines and chemokines, including

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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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Maataoui-Belabbes, Hajar, Hanaa Bencharef, Bouchra Oukkache, Abdellah Madani, and Mouna Lamchahab. "Macrophage activation syndrome revealing Hodgkin lymphoma." Annales Africaines de Medecine 17, no. 3 (2024): e5728-e5733. http://dx.doi.org/10.4314/aamed.v17i3.15.

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Macrophage activation syndrome is an anatomo-clinical entity due to inappropriate stimulation of macrophages. It can be of primary or secondary origin. Blood diseases responsible for reactive macrophage activation syndrome are mainly T or NK lymphomas. The association with Hodgkin lymphoma is exceptional. We report a case of a young adult whose macrophage activation syndrome revealed Hodgkin lymphoma. The diagnosis of macrophage activation syndrome was assured in the light of compatible clinical, biological, and cytological signs. The etiological diagnosis was guided by the bone marrow biopsy

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Jha, Aakanksha, and Erika Moore. "Collagen-derived peptide, DGEA, inhibits pro-inflammatory macrophages in biofunctional hydrogels." Journal of Materials Research 37, no. 1 (2021): 77–87. http://dx.doi.org/10.1557/s43578-021-00423-y.

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AbstractMacrophages are innate immune cells that play important roles in wound healing. Particularly, M1 macrophages are considered pro‐inflammatory and promote initial phases of inflammation. Long-term exposure to inflammatory stimuli causes an increase in M1 macrophages, which contributes to chronic inflammation. Activated M1 macrophages have been shown to upregulate integrin α2β1 expression. To interfere with α2β1 binding, we designed a biofunctional hydrogel utilizing a collagen I-derived peptide, DGEA (Asp-Gly-Glu-Ala). We hypothesize that M1 macrophage activation can be reduced in the pr

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Murray, H. W., G. L. Spitalny, and C. F. Nathan. "Activation of mouse peritoneal macrophages in vitro and in vivo by interferon-gamma." Journal of Immunology 134, no. 3 (1985): 1619–22. http://dx.doi.org/10.4049/jimmunol.134.3.1619.

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Abstract To determine the role of IFN-gamma in the activation of resident mouse peritoneal macrophages, crude macrophage-activating lymphokines were incubated with a monoclonal anti-murine IFN-gamma antibody. This treatment abolished the capacity of mitogen-induced lymphokines to enhance either H2O2 release or activity against the intracellular protozoa Toxoplasma gondii and Leishmania donovani. All macrophage-activating factor detected by these assays was also removed by passing the lymphokines over a Sepharose column to which the monoclonal anti-IFN-gamma antibody had been coupled. Therefore

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Lodyga, Monika, Elizabeth Cambridge, Henna M. Karvonen та ін. "Cadherin-11–mediated adhesion of macrophages to myofibroblasts establishes a profibrotic niche of active TGF-β". Science Signaling 12, № 564 (2019): eaao3469. http://dx.doi.org/10.1126/scisignal.aao3469.

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Macrophages contribute to the activation of fibroblastic cells into myofibroblasts, which secrete collagen and contract the collagen matrix to acutely repair injured tissue. Persistent myofibroblast activation leads to the accumulation of fibrotic scar tissue that impairs organ function. We investigated the key processes that turn acute beneficial repair into destructive progressive fibrosis. We showed that homotypic cadherin-11 interactions promoted the specific binding of macrophages to and persistent activation of profibrotic myofibroblasts. Cadherin-11 was highly abundant at contacts betwe

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