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Artykuły w czasopismach na temat „Macrophage”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Rodriguez, Eric, Frederic Boudard, Michele Mallié, Jean-Marie Bastide, and Madeleine Bastide. "Murine macrophage elastolytic activity induced by Aspergillus fumigatus strains in vitro: evidence of the expression of two macrophage-induced protease genes." Canadian Journal of Microbiology 43, no. 7 (1997): 649–57. http://dx.doi.org/10.1139/m97-092.

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The interaction between Aspergillus fumigatus conidia and murine macrophages of various origins was investigated. Cocultures were carried out between A. fumigatus strains and freshly isolated murine pulmonary alveolar macrophages or two murine macrophage cell-lines: murine alveolar cell-line MALU and murine astrocytoma cell-line J774. By measuring the variation of elastolytic activity in the coculture supernatants with two elastin substrates, we demonstrated that either viable or fixed A. fumigatus or C. albicans yeasts or nonspecific particles induced significant macrophage elastolytic activi

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Stojadinović, Marija. "Macrophage polarization and infectious diseases." Biologia Serbica 45, no. 2 (2023): 38–43. https://doi.org/10.5281/zenodo.10402369.

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<strong>Summary. </strong>Macrophages are a heterogeneous cell population present in most mammalian tissues with a wide range of functions. They are an essential component of optimal tissue homeostasis and an essential first line of defense against pathogens. Activated macrophages are typically divided into two phenotypes, M1 macrophages and M2 macrophages, which are influenced by microorganisms, the tissue microenvironment, and cytokine signals from physiological conditions to infections. The management of macrophage polarity is crucial for the prevention and treatment of infections and infla

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Liu, Shuangqing, Huilei Zhang, Yanan Li та ін. "S100A4 enhances protumor macrophage polarization by control of PPAR-γ-dependent induction of fatty acid oxidation". Journal for ImmunoTherapy of Cancer 9, № 6 (2021): e002548. http://dx.doi.org/10.1136/jitc-2021-002548.

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BackgroundThe peroxisome proliferator-activated receptor γ (PPAR-γ)-dependent upregulation of fatty acid oxidation (FAO) mediates protumor (also known as M2-like) polarization of tumor-associated macrophages (TAMs). However, upstream factors determining PPAR-γ upregulation in TAM protumor polarization are not fully identified. S100A4 plays crucial roles in promotion of cancer malignancy and mitochondrial metabolism. The fact that macrophage-derived S100A4 is major source of extracellular S100A4 suggests that macrophages contain a high abundance of intracellular S100A4. However, whether intrace

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Wilson, Justin E., Bhuvana Katkere, and James R. Drake. "Francisella tularensis Induces Ubiquitin-Dependent Major Histocompatibility Complex Class II Degradation in Activated Macrophages." Infection and Immunity 77, no. 11 (2009): 4953–65. http://dx.doi.org/10.1128/iai.00844-09.

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ABSTRACT The intracellular bacterium Francisella tularensis survives and replicates within macrophages, ultimately killing the host cell. Resolution of infection requires the development of adaptive immunity through presentation of F. tularensis antigens to CD4+ and CD8+ T cells. We have previously established that F. tularensis induces macrophage prostaglandin E2 (PGE2) production, leading to skewed T-cell responses. PGE2 can also downregulate macrophage major histocompatibility complex (MHC) class II expression, suggesting that F. tularensis-elicited PGE2 may further alter T-cell responses v

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5

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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6

Careau, Éric, Léa-Isabelle Proulx, Philippe Pouliot, Annie Spahr, Véronique Turmel, and Élyse Y. Bissonnette. "Antigen sensitization modulates alveolar macrophage functions in an asthma model." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 5 (2006): L871—L879. http://dx.doi.org/10.1152/ajplung.00219.2005.

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We have previously demonstrated that adoptive transfer of alveolar macrophages from allergy-resistant rats to alveolar macrophage-depleted allergic rats prevents airway hyperresponsiveness development, suggesting an important role for alveolar macrophages in asthma pathogenesis. Given that ovalbumin sensitization can modulate alveolar macrophage cytokine production, we investigated the role of sensitized and unsensitized alveolar macrophages in an asthma model. Alveolar macrophages from unsensitized or sensitized Brown Norway rats were transferred to alveolar macrophage-depleted sensitized rat

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Xu, Jiawei, Lanya Fu, Junyao Deng, et al. "miR-301a Deficiency Attenuates the Macrophage Migration and Phagocytosis through YY1/CXCR4 Pathway." Cells 11, no. 24 (2022): 3952. http://dx.doi.org/10.3390/cells11243952.

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(1) Background: the miR-301a is well known involving the proliferation and migration of tumor cells. However, the role of miR-301a in the migration and phagocytosis of macrophages is still unclear. (2) Methods: sciatic nerve injury, liver injury models, as well as primary macrophage cultures were prepared from the miR-301a knockout (KO) and wild type (WT) mice to assess the macrophage’s migration and phagocytosis capabilities. Targetscan database analysis, Western blotting, siRNA transfection, and CXCR4 inhibition or activation were performed to reveal miR301a’s potential mechanism. (3) Result

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8

McKenzie, C. G. J., U. Koser, L. E. Lewis, et al. "Contribution of Candida albicans Cell Wall Components to Recognition by and Escape from Murine Macrophages." Infection and Immunity 78, no. 4 (2010): 1650–58. http://dx.doi.org/10.1128/iai.00001-10.

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ABSTRACT The pathogenicity of the opportunistic human fungal pathogen Candida albicans depends on its ability to escape destruction by the host immune system. Using mutant strains that are defective in cell surface glycosylation, cell wall protein synthesis, and yeast-hypha morphogenesis, we have investigated three important aspects of C. albicans innate immune interactions: phagocytosis by primary macrophages and macrophage cell lines, hyphal formation within macrophage phagosomes, and the ability to escape from and kill macrophages. We show that cell wall glycosylation is critically importan

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9

Fahey, T. J., K. J. Tracey, P. Tekamp-Olson, et al. "Macrophage inflammatory protein 1 modulates macrophage function." Journal of Immunology 148, no. 9 (1992): 2764–69. http://dx.doi.org/10.4049/jimmunol.148.9.2764.

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Abstract Macrophage inflammatory protein 1 (MIP 1), initially purified from the conditioned medium of endotoxin-stimulated macrophages, is a low m.w. heparin-binding protein doublet comprising two peptides, MIP 1 alpha and MIP 1 beta. Although native doublet MIP 1 has previously been shown to exert pyrogenic, mitogenic, and proinflammatory effects on other cell types, its actions on its cell of origin, the macrophage, have not been well catalogued. Our study reports several aspects of macrophage function that are modulated by MIP 1. MIP 1 was not directly cytotoxic for WEHI tumor cells, but MI

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Dende, Chaitanya, Mihir Pendse, Daniel Propheter, Gabriella Quinn, and Lora V. Hooper. "Vitamin A regulates phagocytosis by resident macrophages of the small intestine." Journal of Immunology 208, no. 1_Supplement (2022): 113.23. http://dx.doi.org/10.4049/jimmunol.208.supp.113.23.

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Abstract Intestinal Tim4+ CD4+ macrophages are a distinctive macrophage subset that express Tim4, a receptor for phosphatidylserine on dying apoptotic cells, Unlike other macrophage subsets, they do not depend on blood monocytes for their turnover, instead self-maintained in the small intestine. The signal(s) responsible for the self-maintenance and function of Tim4+ CD4+ macrophages is not known. We have discovered that maintenance of the gut resident Tim4+ CD4+ macrophage population depends on dietary vitamin A and its derivative retinoic acid (RA). Retinoic acid receptors, which direct RA-d

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11

Torre, Donato, Luisa Gennero, F. M. Baccino, Filippo Speranza, Gilberto Biondi, and Agostino Pugliese. "Impaired Macrophage Phagocytosis of Apoptotic Neutrophils in Patients with Human Immunodeficiency Virus Type 1 Infection." Clinical and Vaccine Immunology 9, no. 5 (2002): 983–86. http://dx.doi.org/10.1128/cdli.9.5.983-986.2002.

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ABSTRACT Dysfunction of neutrophils (polymorphonuclear leukocytes [PMNL]) and macrophagic cells occurs as a consequence of human immunodeficiency virus type 1 (HIV-1) infection. Macrophages contribute to the resolution of early inflammation ingesting PMNL apoptotic bodies. This study investigated macrophage ability to phagocytose PMNL apoptotic bodies in patients with HIV-1 infection in comparison with uninfected individuals and the effect of HIV Nef protein on apoptotic body phagocytosis to determine if phagocytic activity is impaired by HIV infection. Monocytes/macrophages were isolated from

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12

Vuarchey, Clément, Sushil Kumar, and Reto Schwendener. "Albumin coated liposomes: a novel platform for macrophage specific drug delivery." Nanotechnology Development 1, no. 1 (2011): 2. http://dx.doi.org/10.4081/nd.2011.e2.

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Here we report a new and efficient approach of macrophage specific drug delivery by coating liposomes with albumin. Activated albumin was reacted with liposomes containing polyethylene glycol (PEG) as hydrophilic spacers to create a flexible layer of covalently bound albumin molecules on the liposome surface. Albumin coated liposomes were taken up faster and more efficiently than uncoated liposomes by murine macrophages. Liposome uptake was significantly higher in macropha - ges as compared to other cell types tested (endothelial cells, fibroblasts, tumor cells), suggesting specificity for mac

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13

Doherty, T. M., R. Kastelein, S. Menon, S. Andrade, and R. L. Coffman. "Modulation of murine macrophage function by IL-13." Journal of Immunology 151, no. 12 (1993): 7151–60. http://dx.doi.org/10.4049/jimmunol.151.12.7151.

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Abstract Activated macrophages are important effector cells for immune response to many parasites and immune responses are strongly modulated in part by the effect of Th cell-derived cytokines on macrophages. Th1-derived cytokines such as IFN-gamma are strong stimulators of macrophage activation, while cytokines produced by Th2 cells, including IL-4 and IL-10, have been shown under some conditions to inhibit macrophage activities associated with inflammatory responses. IL-13, a recently described cytokine produced by Th2 cells, is also capable of down-modulating macrophage activity in a manner

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14

Cotechini, Tiziana, Aline Atallah, and Arielle Grossman. "Tissue-Resident and Recruited Macrophages in Primary Tumor and Metastatic Microenvironments: Potential Targets in Cancer Therapy." Cells 10, no. 4 (2021): 960. http://dx.doi.org/10.3390/cells10040960.

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Macrophages within solid tumors and metastatic sites are heterogenous populations with different developmental origins and substantially contribute to tumor progression. A number of tumor-promoting phenotypes associated with both tumor- and metastasis-associated macrophages are similar to innate programs of embryonic-derived tissue-resident macrophages. In contrast to recruited macrophages originating from marrow precursors, tissue-resident macrophages are seeded before birth and function to coordinate tissue remodeling and maintain tissue integrity and homeostasis. Both recruited and tissue-r

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Taylor, Sarah A., Shang-Yang Chen, Gaurav Gadhvi, et al. "Transcriptional profiling of pediatric cholestatic livers identifies three distinct macrophage populations." PLOS ONE 16, no. 1 (2021): e0244743. http://dx.doi.org/10.1371/journal.pone.0244743.

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Background & aims Limited understanding of the role for specific macrophage subsets in the pathogenesis of cholestatic liver injury is a barrier to advancing medical therapy. Macrophages have previously been implicated in both the mal-adaptive and protective responses in obstructive cholestasis. Recently two macrophage subsets were identified in non-diseased human liver; however, no studies to date fully define the heterogeneous macrophage subsets during the pathogenesis of cholestasis. Here, we aim to further characterize the transcriptional profile of macrophages in pediatric cholestatic

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Aziz, Athar, Laurent Vanhille, Peer Mohideen, et al. "Development of Macrophages with Altered Actin Organization in the Absence of MafB." Molecular and Cellular Biology 26, no. 18 (2006): 6808–18. http://dx.doi.org/10.1128/mcb.00245-06.

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ABSTRACT In the hematopoietic system the bZip transcription factor MafB is selectively expressed at high levels in monocytes and macrophages and promotes macrophage differentiation in myeloid progenitors, whereas a dominant-negative allele can inhibit this process. To analyze the requirement of MafB for macrophage development, we generated MafB-deficient mice and, due to their neonatal lethal phenotype, analyzed macrophage differentiation in vitro, in the embryo, and in reconstituted mice. Surprisingly we observed in vitro differentiation of macrophages from E14.5 fetal liver (FL) cells and E1

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Song, Lili, Do-sung Kim, Wenyu Gou, et al. "GRP94 regulates M1 macrophage polarization and insulin resistance." American Journal of Physiology-Endocrinology and Metabolism 318, no. 6 (2020): E1004—E1013. http://dx.doi.org/10.1152/ajpendo.00542.2019.

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Macrophage polarization contributes to obesity-induced insulin resistance. Glucose-regulated protein 94 (GRP94) is an endoplasmic reticulum (ER) chaperone specialized for folding and quality control of secreted and membrane proteins. To determine the role of GRP94 in macrophage polarization and insulin resistance, macrophage-specific GRP94 conditional knockout (KO) mice were challenged with a high-fat diet (HFD). Glucose tolerance, insulin sensitivity, and macrophage composition were compared with control mice. KO mice showed better glucose tolerance and increased insulin sensitivity. Adipose

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18

Pagan, Antonio, Chao-Tsung Yang, Laura Swaim, and Lalita Ramakrishnan. "Replenishment of granuloma macrophages promotes mycobacterial resistance by preventing extracellular bacterial growth (INC7P.410)." Journal of Immunology 192, no. 1_Supplement (2014): 186.11. http://dx.doi.org/10.4049/jimmunol.192.supp.186.11.

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Abstract Pathogenic mycobacteria exploit the early tuberculous granuloma for their expansion by inducing infected macrophage apoptosis and accelerating uninfected macrophage recruitment and infection upon engulfing the dying macrophages. Whether sustained macrophage recruitment to established granulomas is also host-detrimental is unclear. We addressed this question in the zebrafish model of tuberculosis by manipulating the macrophage colony stimulation factor 1 (CSF-1) pathway, which promotes macrophage development. Early granuloma formation was normal in CSF-1 receptor-deficient fish in spit

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Cho, Sun Wook, Young A. Kim, Hyun Jin Sun, et al. "CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma." Endocrine-Related Cancer 23, no. 2 (2015): 113–24. http://dx.doi.org/10.1530/erc-15-0196.

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Macrophages in tumor microenvironment have pivotal roles in tumor growth, metastasis, and angiogenesis. We investigated the interacting mechanism of macrophage actions in human papillary thyroid cancer (PTC). Co-cultures of macrophage/PTC significantly increased the cancer cell migration potentials, compared with the PTC culture alone. Treatment of conditioned medium (CM) of macrophage/PTC co-cultures enhanced cell invasions in 3D invasion assay. Cytokine array analysis demonstrated that CM of macrophage/PTC co-cultures contained a high level of CXCL16, while it was not found in CM of PTC cult

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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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Lee, Hanui, Seong Hee Kang, Gyeong Han Jeong, et al. "Gamma irradiation-engineered macrophage-derived exosomes as potential immunomodulatory therapeutic agents." PLOS ONE 19, no. 6 (2024): e0303434. http://dx.doi.org/10.1371/journal.pone.0303434.

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The modulation of macrophage polarization is a promising strategy for maintaining homeostasis and improving innate and adaptive immunity. Low-dose ionizing radiation has been implicated in macrophage immunomodulatory responses. However, studies on the relationship between exosomes and regulation of macrophage polarization induced by ionizing radiation are limited. Therefore, this study investigated the alterations in macrophages and exosomes induced by gamma irradiation and elucidated the underlying mechanisms. We used the mouse macrophage cell line RAW 264.7 to generate macrophages and perfor

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Deng, Lishuang, Zhijie Jian, Tong Xu, et al. "Macrophage Polarization: An Important Candidate Regulator for Lung Diseases." Molecules 28, no. 5 (2023): 2379. http://dx.doi.org/10.3390/molecules28052379.

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Macrophages are crucial components of the immune system and play a critical role in the initial defense against pathogens. They are highly heterogeneous and plastic and can be polarized into classically activated macrophages (M1) or selectively activated macrophages (M2) in response to local microenvironments. Macrophage polarization involves the regulation of multiple signaling pathways and transcription factors. Here, we focused on the origin of macrophages, the phenotype and polarization of macrophages, as well as the signaling pathways associated with macrophage polarization. We also highl

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Shaw, Maureen A., Zhen Gao, and Eric S. Mullins. "Plasmin(ogen) Mediates Macrophage Migration in a Fibrin(ogen) Dependent Mechanism." Blood 128, no. 22 (2016): 18. http://dx.doi.org/10.1182/blood.v128.22.18.18.

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Abstract Mounting evidence ties both fibrin(ogen) and plasmin(ogen) to inflammatory diseases. Indeed, both fibrin(ogen) and plasmin(ogen) have been linked to critical macrophage functions in multiple disease processes. Migration of macrophages to sites of sterile inflammation is, at least partially, dependent on plasmin(ogen). Mice lacking plasminogen, when challenged with sterile thioglycollate-induced peritonitis, have both diminished overall leukocyte migration and decreased macrophage migration. Additionally, macrophage migration defects have been identified in both mice lacking plasminoge

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Xie, Linglin, M. Teresa Ortega, Silvia Mora, and Stephen K. Chapes. "Interactive Changes between Macrophages and Adipocytes." Clinical and Vaccine Immunology 17, no. 4 (2010): 651–59. http://dx.doi.org/10.1128/cvi.00494-09.

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ABSTRACT Obesity is associated with a proinflammatory state, with macrophage infiltration into adipose tissue. We tested the hypothesis that communication between macrophages and adipocytes affects insulin resistance by disrupting insulin-stimulated glucose transport, adipocyte differentiation, and macrophage function. To test this hypothesis, we cocultured 3T3-L1 adipocytes with C2D macrophages or primary peritoneal mouse macrophages and examined the impacts of macrophages and adipocytes on each other. Adipocytes and preadipocytes did not affect C2D macrophage TNF- α, IL-6, or IL-1 β transcri

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Lu, Chunxia, P. Anil Kumar, Yong Fan, Mark A. Sperling, and Ram K. Menon. "A Novel Effect of Growth Hormone on Macrophage Modulates Macrophage-Dependent Adipocyte Differentiation." Endocrinology 151, no. 5 (2010): 2189–99. http://dx.doi.org/10.1210/en.2009-1194.

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The GH receptor (GHR) is expressed on macrophages. However, the precise role of GH in regulation of macrophage function is unclear. We hypothesized that soluble factors including cytokines produced by macrophages in a GH-dependent manner regulate adipogenesis. We confirmed expression and functional integrity of the GHR in the J774A.1 macrophage cells. Conditioned medium (CM) from macrophages inhibited adipogenesis in a 3T3-L1 adipogenesis assay. CM from GH-treated macrophages decreased the inhibitory effect of CM from macrophages on adipogenesis. This effect on preadipocyte differentiation was

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Mouton, Alan J., Xuan Li, Michael E. Hall, and John E. Hall. "Obesity, Hypertension, and Cardiac Dysfunction." Circulation Research 126, no. 6 (2020): 789–806. http://dx.doi.org/10.1161/circresaha.119.312321.

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Obesity and hypertension, which often coexist, are major risk factors for heart failure and are characterized by chronic, low-grade inflammation, which promotes adverse cardiac remodeling. While macrophages play a key role in cardiac remodeling, dysregulation of macrophage polarization between the proinflammatory M1 and anti-inflammatory M2 phenotypes promotes excessive inflammation and cardiac injury. Metabolic shifting between glycolysis and mitochondrial oxidative phosphorylation has been implicated in macrophage polarization. M1 macrophages primarily rely on glycolysis, whereas M2 macropha

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Snarski, Patricia, Sergiy Sukhanov, Tadashi Yoshida, et al. "Macrophage-Specific IGF-1 Overexpression Reduces CXCL12 Chemokine Levels and Suppresses Atherosclerotic Burden in Apoe-Deficient Mice." Arteriosclerosis, Thrombosis, and Vascular Biology 42, no. 2 (2022): 113–26. http://dx.doi.org/10.1161/atvbaha.121.316090.

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Objective: IGF-1 (insulin-like growth factor 1) exerts pleiotropic effects including promotion of cellular growth, differentiation, survival, and anabolism. We have shown that systemic IGF-1 administration reduced atherosclerosis in Apoe −/ − (apolipoprotein E deficient) mice, and this effect was associated with a reduction in lesional macrophages and a decreased number of foam cells in the plaque. Almost all cell types secrete IGF-1, but the effect of macrophage-derived IGF-1 on the pathogenesis of atherosclerosis is poorly understood. We hypothesized that macrophage-derived IGF-1 will reduce

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Randolph, Gwendalyn J. "Monocyte Trafficking, Inflammation, and Atherosclerosis." Blood 122, no. 21 (2013): SCI—53—SCI—53. http://dx.doi.org/10.1182/blood.v122.21.sci-53.sci-53.

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Abstract Macrophages are central to the progression of atherosclerosis. An increased number of macrophages in plaque are associated with larger, more stenotic lesions. Furthermore, activated plaque macrophages promote rupture, the most significant clinical event affecting mortality. Plaque macrophages derive from monocytes that are recruited from blood. We have thus focused our efforts on understanding the mechanisms that regulate plaque macrophages, with emphasis on how macrophage-burden might be reduced to lower disease risk. We have developed techniques to discern whether macrophage contrac

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García-Rodas, Rocío, Fernando González-Camacho, Juan Luis Rodríguez-Tudela, Manuel Cuenca-Estrella, and Oscar Zaragoza. "The Interaction between Candida krusei and Murine Macrophages Results in Multiple Outcomes, Including Intracellular Survival and Escape from Killing." Infection and Immunity 79, no. 6 (2011): 2136–44. http://dx.doi.org/10.1128/iai.00044-11.

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ABSTRACTCandida kruseiis a fungal pathogen of interest for the scientific community for its intrinsic resistance to fluconazole. Little is known about the interaction of this yeast with host immune cells. In this work, we have characterized the outcome of the interaction betweenC. kruseiand murine macrophages. OnceC. kruseiwas internalized, we observed different phenomena. In a macrophage-like cell line,C. kruseisurvived in a significant number of macrophages and induced filamentation and macrophage explosion. Phagocytosis ofC. kruseiled to actin polymerization around the yeast cells at the si

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Rosa, L. F. B. P. Costa, Y. Cury, and R. Curi. "Hormonal control of macrophage function and glutamine metabolism." Biochemistry and Cell Biology 69, no. 4 (1991): 309–12. http://dx.doi.org/10.1139/o91-047.

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Murine macrophages have been reported to utilize glutamine at high rates. However, the role of glutamine in macrophage function is still unknown. In the present study, the maximum glutaminase activity of macrophages was investigated under several endocrine dysfunctions that are known to cause alterations in macrophage function. The results obtained suggest that glutamine might play an important role in the onset of phagocytosis in inflammatory macrophages. Moreover, the studies show that insulin, glucocorticoids, and thyroid hormones may be responsible for the regulation of glutamine metabolis

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Pervin, Munmun, Mohammad Rabiul Karim, Mizuki Kuramochi, Takeshi Izawa, Mitsuru Kuwamura, and Jyoji Yamate. "Macrophage Populations and Expression of Regulatory Inflammatory Factors in Hepatic Macrophage-depleted Rat Livers under Lipopolysaccharide (LPS) Treatment." Toxicologic Pathology 46, no. 5 (2018): 540–52. http://dx.doi.org/10.1177/0192623318776898.

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To investigate the significance of the appearance of hepatic macrophages and expression of inflammatory factors in normal and macrophage-depleted livers, hepatic macrophages were depleted with liposome (Lipo)-encapsulated clodronate (CLD; 50 mg/kg, i.v.) followed by lipopolysaccharide (LPS) administration (0.1 mg/kg, i.p.) in F344 rats (CLD + LPS). Vehicle control rats (Lipo + LPS) received empty-Lipo before LPS. The low dose of LPS did not result in microscopic changes in the liver in either treatment group but did modulate M1 and M2 macrophage activity in Lipo + LPS rats without altering rep

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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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Li, Xue, Deana Mikhalkova, Erhe Gao, et al. "Myocardial injury after ischemia-reperfusion in mice deficient in Akt2 is associated with increased cardiac macrophage density." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (2011): H1932—H1940. http://dx.doi.org/10.1152/ajpheart.00755.2010.

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Akt2 protein kinase has been shown to promote cell migration and actin polymerization in several cell types, including macrophages. Because migrating macrophages constitute an important inflammatory response after myocardial ischemia, we determined cardiac macrophage expression after ischemia-reperfusion (I/R) injury and cryo-injury in mice lacking Akt2 (Akt2-KO). At 7 days post-I/R, Akt2-KO cardiac tissues showed an increase in immunohistochemical staining for macrophage markers (Galectin 3 and F4/80) compared with wild-type (WT) mice, indicating macrophage density was increased in the injure

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Boutilier, Ava J., and Sherine F. Elsawa. "Macrophage Polarization States in the Tumor Microenvironment." International Journal of Molecular Sciences 22, no. 13 (2021): 6995. http://dx.doi.org/10.3390/ijms22136995.

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The M1/M2 macrophage paradigm plays a key role in tumor progression. M1 macrophages are historically regarded as anti-tumor, while M2-polarized macrophages, commonly deemed tumor-associated macrophages (TAMs), are contributors to many pro-tumorigenic outcomes in cancer through angiogenic and lymphangiogenic regulation, immune suppression, hypoxia induction, tumor cell proliferation, and metastasis. The tumor microenvironment (TME) can influence macrophage recruitment and polarization, giving way to these pro-tumorigenic outcomes. Investigating TME-induced macrophage polarization is critical fo

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Kim, Bo-Young, Ji Hyeon Ryu, Jisu Park, et al. "Fermented Lettuce Extract Induces Immune Responses through Polarization of Macrophages into the Pro-Inflammatory M1-Subtype." Nutrients 15, no. 12 (2023): 2750. http://dx.doi.org/10.3390/nu15122750.

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It has been reported that lettuce and its bioactive compounds enhance the host immune system by acting as immune modulators. This study aimed to identify the immunological effect of fermented lettuce extract (FLE) on macrophages. To evaluate the efficacy of FLE in enhancing macrophage function, we measured and compared the levels of macrophage activation-related markers in FLE- and lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Treatment with FLE activated RAW 264.7 macrophages, increased their phagocytic ability, and increased the production of nitric oxide (NO) and pro-inflammatory cyt

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Hamrick, Terri S., Edward A. Havell, John R. Horton, and Paul E. Orndorff. "Host and Bacterial Factors Involved in the Innate Ability of Mouse Macrophages To Eliminate Internalized UnopsonizedEscherichia coli." Infection and Immunity 68, no. 1 (2000): 125–32. http://dx.doi.org/10.1128/iai.68.1.125-132.2000.

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ABSTRACT In an effort to better understand genetic and cellular factors that influence innate immunity, we examined host and bacterial factors involved in the nonopsonic phagocytosis and killing ofEscherichia coli K-12 by mouse macrophages. Unelicited (resident) peritoneal macrophages from five different mouse strains, BALB/c, C57BL/6, CD-1, C3H/HeJ, and C3H/HeN, were employed. Additional macrophage populations were obtained from CD-1 mice (bone marrow-derived macrophages). Also, for BALB/c and C57BL/6 mice, peritoneal macrophages elicited with either thioglycolate or proteose peptone, bone ma

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Song, Lige, Garyfallia Papaioannou, Hengguang Zhao, et al. "The Vitamin D Receptor Regulates Tissue Resident Macrophage Response to Injury." Endocrinology 157, no. 10 (2016): 4066–75. http://dx.doi.org/10.1210/en.2016-1474.

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Ligand-dependent actions of the vitamin D receptor (VDR) play a pleiotropic role in the regulation of innate and adaptive immunity. The liganded VDR is required for recruitment of macrophages during the inflammatory phase of cutaneous wound healing. Although the number of macrophages in the granulation tissue 2 days after wounding is markedly reduced in VDR knockout (KO) compared with wild-type mice, VDR ablation does not alter macrophage polarization. Parabiosis studies demonstrate that circulatory chimerism with wild-type mice is unable to rescue the macrophage defect in the wounds of VDR KO

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Chen, Peiwen, Hao Zuo, Hu Xiong, et al. "Gpr132 sensing of lactate mediates tumor–macrophage interplay to promote breast cancer metastasis." Proceedings of the National Academy of Sciences 114, no. 3 (2017): 580–85. http://dx.doi.org/10.1073/pnas.1614035114.

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Macrophages are prominent immune cells in the tumor microenvironment that exert potent effects on cancer metastasis. However, the signals and receivers for the tumor–macrophage communication remain enigmatic. Here, we show that G protein-coupled receptor 132 (Gpr132) functions as a key macrophage sensor of the rising lactate in the acidic tumor milieu to mediate the reciprocal interaction between cancer cells and macrophages during breast cancer metastasis. Lactate activates macrophage Gpr132 to promote the alternatively activated macrophage (M2)-like phenotype, which, in turn, facilitates can

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Li, Yingqiu, xiao yu, and Anlong Xu. "The p38-interacting protein negatively regulates monocyte/macrophage differentiation (HEM5P.239)." Journal of Immunology 194, no. 1_Supplement (2015): 120.19. http://dx.doi.org/10.4049/jimmunol.194.supp.120.19.

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Abstract Monocyte/macrophage differentiation is a central event in the immune response. Here, we investigated the role of p38IP (p38-interacting protein) in monocyte/macrophage differentiation. During monocyte/macrophage differentiation, we found that p38IP is downregulated. Forward knockdown of p38IP by RNA interference induced G1/S arrest, promoting monocytes differentiation into macrophages and the maturation of macrophages as well. Further analysis revealed that p38IP negatively regulates monocyte/macrophage differentiation. Moreover, we found that the downregulation of p38IP is caused by

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Martins, Flávia, Rosa Oliveira, Bruno Cavadas, et al. "Hypoxia and Macrophages Act in Concert Towards a Beneficial Outcome in Colon Cancer." Cancers 12, no. 4 (2020): 818. http://dx.doi.org/10.3390/cancers12040818.

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In colon cancer, the prognostic value of macrophages is controversial, and it is still unknown how hypoxia modulates macrophage–cancer cell crosstalk. To unravel this, co-cultures of human primary macrophages and colon cancer cells were performed at 20% and 1% O2, followed by characterization of both cellular components. Different colon cancer patient cohorts were analyzed for hypoxia and immune markers, and their association with patient overall survival was established. A positive correlation between HIF1A and CD68 in colon cancer patients was identified but, unexpectedly, in cases with high

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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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Luo, Qianting, Xingyang Li, Wenchao Zhong, et al. "Dicalcium silicate-induced mitochondrial dysfunction and autophagy-mediated macrophagic inflammation promotes osteogenic differentiation of BMSCs." Regenerative Biomaterials, December 13, 2021. http://dx.doi.org/10.1093/rb/rbab075.

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Abstract Dicalcium silicate (Ca2SiO4, C2S) has osteogenic potential but induces macrophagic inflammation. Mitochondrial function plays a vital role in macrophage polarization and macrophagic inflammation. The mitochondrial function of C2S-treated macrophages is still unclear. This study hypothesized: (1) the C2S modulates mitochondrial function and autophagy in macrophages to regulate macrophagic inflammation, and (2) C2S-induced macrophagic inflammation regulates osteogenesis. We used RAW264.7 cells as a model of macrophage. The C2S (75-150 μg/mL) extract was used to analyze the macrophagic m

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Muhammad, Sajjad, Shafqat Rasul Chaudhry, Gergana Dobreva, Michael T. Lawton, Mika Niemelä, and Daniel Hänggi. "Vascular Macrophages as Therapeutic Targets to Treat Intracranial Aneurysms." Frontiers in Immunology 12 (March 8, 2021). http://dx.doi.org/10.3389/fimmu.2021.630381.

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Aneurysmal subarachnoid hemorrhage (aSAH) is a highly fatal and morbid type of hemorrhagic strokes. Intracranial aneurysms (ICAs) rupture cause subarachnoid hemorrhage. ICAs formation, growth and rupture involves cellular and molecular inflammation. Macrophages orchestrate inflammation in the wall of ICAs. Macrophages generally polarize either into classical inflammatory (M1) or alternatively-activated anti-inflammatory (M2)-phenotype. Macrophage infiltration and polarization toward M1-phenotype increases the risk of aneurysm rupture. Strategies that deplete, inhibit infiltration, ameliorate m

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Bo, Haotian, Ulrich Aymard Ekomi Moure, Yuanmiao Yang, et al. "Mycobacterium tuberculosis-macrophage interaction: Molecular updates." Frontiers in Cellular and Infection Microbiology 13 (March 3, 2023). http://dx.doi.org/10.3389/fcimb.2023.1062963.

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Mycobacterium tuberculosis (Mtb), the causative agent of Tuberculosis (TB), remains a pathogen of great interest on a global scale. This airborne pathogen affects the lungs, where it interacts with macrophages. Acidic pH, oxidative and nitrosative stressors, and food restrictions make the macrophage’s internal milieu unfriendly to foreign bodies. Mtb subverts the host immune system and causes infection due to its genetic arsenal and secreted effector proteins. In vivo and in vitro research have examined Mtb-host macrophage interaction. This interaction is a crucial stage in Mtb infection becau

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Tatano, Yutaka, Toshiaki Shimizu, Chiaki Sano, and Haruaki Tomioka. "Roles of autophagy in killing of mycobacterial pathogens by host macrophages – Effects of some medicinal plants." European Journal of Microbiology and Immunology, February 13, 2024. http://dx.doi.org/10.1556/1886.2023.00062.

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AbstractAutophagy is a cellular stress-induced intracellular process, through which damaged cellular components are decomposed via lysosomal degradation. This process plays important roles in host innate immunity, particularly the elimination of intracellular pathogens inside host macrophages. A more detailed understanding of the roles of autophagic events in the effective manifestation of macrophagic antimycobacterial activity is needed. Furthermore, the effects of medicinal plants on macrophagic autophagy response to mycobacterial infection need to be clarified. We herein examined the signif

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Xiao, Qiuqun, Jinyan Huang, Xing Wang, et al. "Supramolecular Peptide Amphiphile Nanospheres Reprogram Tumor‐associated Macrophage to Reshape the Immune Microenvironment for Enhanced Breast Cancer Immunotherapy." Small, December 15, 2023. http://dx.doi.org/10.1002/smll.202307390.

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AbstractTumor immunotherapy has become a research hotspot in cancer treatment, with macrophages playing a crucial role in tumor development. However, the tumor microenvironment restricts macrophage functionality, limiting their therapeutic potential. Therefore, modulating macrophage function and polarization is essential for enhancing tumor immunotherapy outcomes. Here, a supramolecular peptide amphiphile drug‐delivery system (SPADS) is utilized to reprogram macrophages and reshape the tumor immune microenvironment (TIM) for immune‐based therapies. The approach involved designing highly specif

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Zhang, Lai, Huian Han, Andi Xu, et al. "Lysozyme 1 Inflamed CCR2 ⁺ Macrophages Promote Obesity-Induced Cardiac Dysfunction." Circulation Research, July 26, 2024. http://dx.doi.org/10.1161/circresaha.124.324106.

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BACKGROUND: Macrophages are key players in obesity-associated cardiovascular diseases, which are marked by inflammatory and immune alterations. However, the pathophysiological mechanisms underlying macrophage’s role in obesity-induced cardiac inflammation are incompletely understood. Our study aimed to identify the key macrophage population involved in obesity-induced cardiac dysfunction and investigate the molecular mechanism that contributes to the inflammatory response. METHODS AND RESULTS: Though analyzing in-depth cardiac macrophage clusters identified by single macrophage RNA-sequencing,

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Luque-Campos, Noymar, Felipe A. Bustamante-Barrientos, Carolina Pradenas, et al. "The Macrophage Response Is Driven by Mesenchymal Stem Cell-Mediated Metabolic Reprogramming." Frontiers in Immunology 12 (June 4, 2021). http://dx.doi.org/10.3389/fimmu.2021.624746.

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Mesenchymal stem cells (MSCs) are multipotent adult stromal cells widely studied for their regenerative and immunomodulatory properties. They are capable of modulating macrophage plasticity depending on various microenvironmental signals. Current studies have shown that metabolic changes can also affect macrophage fate and function. Indeed, changes in the environment prompt phenotype change. Therefore, in this review, we will discuss how MSCs orchestrate macrophage’s metabolic plasticity and the impact on their function. An improved understanding of the crosstalk between macrophages and MSCs w

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Umezu, Ryuta, Jun-ichiro Koga, Tetsuya Matoba, et al. "Macrophage (Drp1) Dynamin-Related Protein 1 Accelerates Intimal Thickening After Vascular Injury." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 7 (2020). http://dx.doi.org/10.1161/atvbaha.120.314383.

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Objective: Mitochondria consistently change their morphology in a process regulated by proteins, including Drp1 (dynamin-related protein 1), a protein promoting mitochondrial fission. Drp1 is involved in the mechanisms underlying various cardiovascular diseases, such as myocardial ischemia/reperfusion injury, heart failure, and pulmonary arterial hypertension. However, its role in macrophages, which promote various vascular diseases, is poorly understood. We therefore tested our hypothesis that macrophage Drp1 promotes vascular remodeling after injury. Method and Results: To explore the select

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Orsi, Micaela, Mihaly Palmai-Pallag, Yousof Yakoub, et al. "Monocytic Ontogeny of Regenerated Macrophages Characterizes the Mesotheliomagenic Responses to Carbon Nanotubes." Frontiers in Immunology 12 (June 14, 2021). http://dx.doi.org/10.3389/fimmu.2021.666107.

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Macrophages are not only derived from circulating blood monocytes or embryonic precursors but also expand by proliferation. The origin determines macrophage fate and functions in steady state and pathological conditions. Macrophages predominantly infiltrate fibre-induced mesothelioma tumors and contribute to cancer development. Here, we revealed their ontogeny by comparing the response to needle-like mesotheliomagenic carbon nanotubes (CNT-7) with tangled-like non-mesotheliomagenic CNT-T. In a rat peritoneal cavity model of mesothelioma, both CNT induced a rapid macrophage disappearance reacti

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