Journal articles: 'Macrophage heterogeneity'

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Gordon, Siamon. "Macrophage Heterogeneity." Arteriosclerosis, Thrombosis, and Vascular Biology 32, no. 6 (June 2012): 1339–42. http://dx.doi.org/10.1161/atvbaha.111.238139.

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Nolte, Anna, Johannes Junginger, Berit Baum, and Marion Hewicker-Trautwein. "Heterogeneity of macrophages in canine histiocytic ulcerative colitis." Innate Immunity 23, no. 3 (January 18, 2017): 228–39. http://dx.doi.org/10.1177/1753425916686170.

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Histiocytic ulcerative colitis (HUC) is a chronic enteropathy which most notably occurs in Boxer dogs and French bulldogs. The inflamed mucosa is hallmarked by large, foamy, periodic acid–Schiff (PAS)-positive macrophages infiltrating the colonic mucosa. As little is known about their origin and phenotype, an immunohistochemical study was performed using different macrophage markers. Generally, canine colonic macrophages showed high expression of ionised calcium-binding adaptor molecule 1 and MHC class II. In canine HUC, macrophages revealed up-regulation of lysozyme and L1 Ag but decreased CD163 expression compared with controls, suggesting them to be pro-inflammatory cells, whereas the healthy colonic mucosa was characterised by an anti-inflammatory macrophage phenotype. In addition, PAS reaction was used to discriminate macrophage subpopulations. PAS– macrophages displayed higher expression of L1 Ag and CD64, whereas PAS+ cells, which were only present in HUC patients, were characterised by increased expression of lysozyme, inducible nitric oxide synthase and CD204. This indicates PAS+ cells to be mature macrophages contributing to the inflammatory process, which are most likely maintained by differentiation of immature PAS– macrophages continuously recruited from blood monocytes. In summary, macrophage heterogeneity in canine HUC probably illustrates their different maturation states and functions compared with the healthy animals.

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Boorsma, Carian E., Christina Draijer, and Barbro N. Melgert. "Macrophage Heterogeneity in Respiratory Diseases." Mediators of Inflammation 2013 (2013): 1–19. http://dx.doi.org/10.1155/2013/769214.

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Macrophages are among the most abundant cells in the respiratory tract, and they can have strikingly different phenotypes within this environment. Our knowledge of the different phenotypes and their functions in the lung is sketchy at best, but they appear to be linked to the protection of gas exchange against microbial threats and excessive tissue responses. Phenotypical changes of macrophages within the lung are found in many respiratory diseases including asthma, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis. This paper will give an overview of what macrophage phenotypes have been described, what their known functions are, what is known about their presence in the different obstructive and restrictive respiratory diseases (asthma, COPD, pulmonary fibrosis), and how they are thought to contribute to the etiology and resolution of these diseases.

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OLIVER, A. M. "Macrophage heterogeneity in human fetal tissue. Fetal macrophages." Clinical & Experimental Immunology 80, no. 3 (June 28, 2008): 454–59. http://dx.doi.org/10.1111/j.1365-2249.1990.tb03309.x.

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Stremmel, Christopher, Konstantin Stark, and Christian Schulz. "Heterogeneity of Macrophages in Atherosclerosis." Thrombosis and Haemostasis 119, no. 08 (June 26, 2019): 1237–46. http://dx.doi.org/10.1055/s-0039-1692665.

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AbstractAtherosclerosis is a prevalent inflammatory condition and a frequent cause of morbidity and mortality worldwide. Macrophages are among the key immune cells driving lesion formation in the arterial wall. They have therefore evolved as potential targets for therapeutic strategies. Understanding of the different macrophage phenotypes and functions seems to be of pivotal importance for the development of treatments to target these immune cells. This review highlights the complexity of the mononuclear phagocyte system and summarizes important features of macrophage biology contributing to atherosclerosis.

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Seu, Katie Giger, Julien Papoin, Rose Fessler, Jimmy Hom, Gang Huang, Narla Mohandas, Lionel Blanc, and Theodosia A. Kalfa. "Unravelling Macrophage Heterogeneity in Erythroblastic Islands Between Species." Blood 128, no. 22 (December 2, 2016): 2436. http://dx.doi.org/10.1182/blood.v128.22.2436.2436.

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Abstract Erythroblastic islands (EBIs) are a hallmark of mammalian erythropoiesis consisting of a central macrophage surrounded by and interacting closely with maturing erythroblasts. While it is generally accepted that the island macrophages play an important role in erythropoiesis, the inability to identify and isolate this macrophage subpopulation has limited our understanding of their functional involvement. Previous studies have relied on immunohistochemistry/immunofluorescence in situ or in vitro. More recently, flow cytometry was used to characterize EBI formation and the immunophenotype of the central macrophages in murine erythroblastic islands. These approaches provide either morphological/structural information or high-throughput quantification, but not both, and often carry the expectation that all EBI macrophages have similar phenotype (F4/80+/CD169+/VCAM1+ for example), and thus potentially overlook critical information about the nature and biology of the islands and the central macrophages. We have developed a novel method for analysis and characterization of EBI macrophages from hematopoietic tissues using multispectral imaging flow cytometry, which combines the high-throughput advantage of flow cytometry with the morphology and fluorescence details obtained from microscopy. This method allows automated, non-biased evaluation of the EBIs recovered from a sample, their number, mean size, as well as structural and morphological details of the central macrophages and associated erythroblasts. Most importantly, the images, combined with the fluorescence similarity feature, enables the evaluation of co-expression of any phenotypic markers that may be used to identify the macrophages which is crucial since some antigens used to identify macrophages (e.g. CD45, CD11b) may also be expressed on non-erythroid cells associated with the islands instead of, or in addition to, the central macrophage itself. We used this method to confirm the expression of various markers previously reported to be expressed on the erythroblastic island macrophages by flow, including CD11b, VCAM1, F4/80, CD169, and CD163, in mouse, rat, and human bone marrow. Indeed, while a large number of studies have focused on murine erythropoiesis, the identity and role of the EBIs in other species is much less known. We confirmed expression of CD169 and VCAM1 on the F4/80+ central macrophages of murine EBIs and also identified a population of VCAM+/F4/80- central cells associated with developing erythroblasts. CD11b is abundantly expressed by non-erythroid, non-macrophage cells associated with the islands, but is not expressed significantly on the central macrophages (Figure 1). CD163, a marker of EBI macrophages in rat and human, was not detected in the murine EBIs by imaging flow cytometry, but this may be due to limitation of the antibodies tested. In contrast, anti-CD163 stained well rat and human EBI macrophages but CD11b or VCAM1 were not detected in EBIs from rat and human bone marrow respectively, raising the question of a species-specificity regarding the macrophage heterogeneity and satellite cells present within erythroblastic islands. In summary, the data presented herein demonstrate the effectiveness of this method for the analysis and characterization of EBIs and establish a new tool for future investigations of EBIs and their central macrophages in the nurturing of erythropoiesis. Figure 1 Representative image of an erythroblastic island harvested from murine bone marrow stained with F4/80-AF488 (green), CD11b-PE (blue), and CD71-BV421 (red) and analyzed by imaging flow cytometry. Figure 1. Representative image of an erythroblastic island harvested from murine bone marrow stained with F4/80-AF488 (green), CD11b-PE (blue), and CD71-BV421 (red) and analyzed by imaging flow cytometry. Disclosures No relevant conflicts of interest to declare.

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Mori, M., Y. Sadahira, S. Kawasaki, T. Hayashi, and M. Awai. "Macrophage heterogeneity in bone marrow culture in vitro." Journal of Cell Science 95, no. 3 (March 1, 1990): 481–85. http://dx.doi.org/10.1242/jcs.95.3.481.

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Macrophages in mouse bone marrow cultures were investigated with macrophage-specific monoclonal antibody F4/80 and anti-Forssman glycosphingolipid (GSL) antibody, which was specific for macrophages in hematopoietic foci. Antibody F4/80 stained two types of cells, small macrophages and large flat macrophages associated with hematopoietic cells. The cytochemical and phagocytotic characteristics were similar between these two types of cells, but Forssman GSL was positive only for the large flat macrophages associated with hematopoietic cells. The data suggest that Forssman GSL positive macrophages, derived from resident bone marrow macrophages, play an important role in hematopoiesis and are clearly distinguished from small macrophages in vitro.

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Gordon, Siamon, and Philip R. Taylor. "Monocyte and macrophage heterogeneity." Nature Reviews Immunology 5, no. 12 (December 2005): 953–64. http://dx.doi.org/10.1038/nri1733.

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Gombozhapova, A. E., Yu V. Rogovskaya, M. S. Rebenkova, J. G. Kzhyshkowska, and V. V. Ryabov. "PHENOTYPIC HETEROGENEITY OF CARDIAC MACROPHAGES DURING WOUND HEALING FOLLOWING MYOCARDIAL INFARCTION: PERSPECTIVES IN CLINICAL RESEARCH." Siberian Medical Journal 33, no. 2 (July 14, 2018): 70–76. http://dx.doi.org/10.29001/2073-8552-2018-33-2-70-76.

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Purpose. Myocardial regeneration is one of the most ambitious goals in prevention of adverse cardiac remodeling. Macrophages play a key role in transition from inflammatory to regenerative phase during wound healing following myocardial infarction (MI). We have accumulated data on macrophage properties ex vivo and in cell culture. However, there is no clear information about phenotypic heterogeneity of cardiac macrophages in patients with MI. The purpose of the project was to assess cardiac macrophage infiltration during wound healing following myocardial infarction in clinical settings taking into consideration experimental knowledge.Material and Methods. The study included 41 patients with fatal MI type 1. In addition to routine analysis, macrophages infiltration was assessed by immunohistochemistry. We used CD68 as a marker for the cells of the macrophage lineage, while CD163, CD206, and stabilin-1 were considered as M2 macrophage biomarkers. Nine patients who died from noncardiovascular causes comprised the control group.Results. The intensity of cardiac macrophage infiltration was higher during the regenerative phase than during the inflammatory phase. Results of immunohistochemical analysis demonstrated the presence of phenotypic heterogeneity of cardiac macrophages in patients with MI. We noticed that numbers of CD68+, CD163+, CD206+, and stabilin-1+ macrophages depended on MI phase.Conclusion. Our study supports prospects for implementation of macrophage phenotyping in clinic practice. Improved understanding of phenotypic heterogeneity might become the basis of a method to predict adverse cardiac remodeling and the first step in developing myocardial regeneration target therapy.

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Rojas, Joselyn, Juan Salazar, María Sofía Martínez, Jim Palmar, Jordan Bautista, Mervin Chávez-Castillo, Alexis Gómez, and Valmore Bermúdez. "Macrophage Heterogeneity and Plasticity: Impact of Macrophage Biomarkers on Atherosclerosis." Scientifica 2015 (2015): 1–17. http://dx.doi.org/10.1155/2015/851252.

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Cardiovascular disease (CVD) is a global epidemic, currently representing the worldwide leading cause of morbidity and mortality. Atherosclerosis is the fundamental pathophysiologic component of CVD, where the immune system plays an essential role. Monocytes and macrophages are key mediators in this aspect: due to their heterogeneity and plasticity, these cells may act as either pro- or anti-inflammatory mediators. Indeed, monocytes may develop heterogeneous functional phenotypes depending on the predominating pro- or anti-inflammatory microenvironment within the lesion, resulting in classic, intermediate, and non-classic monocytes, each with strikingly differing features. Similarly, macrophages may also adopt heterogeneous profiles being mainly M1 and M2, the former showing a proinflammatory profile while the latter demonstrates anti-inflammatory traits; they are further subdivided in several subtypes with more specialized functions. Furthermore, macrophages may display plasticity by dynamically shifting between phenotypes in response to specific signals. Each of these distinct cell profiles is associated with diverse biomarkers which may be exploited for therapeutic intervention, including IL-10, IL-13, PPAR-γ, LXR, NLRP3 inflammasomes, and microRNAs. Direct modulation of the molecular pathways concerning these potential macrophage-related targets represents a promising field for new therapeutic alternatives in atherosclerosis and CVD.

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Dijrstra, Christine D., and Jan G. M. C. Damoiseaux. "Macrophage Heterogeneity Established by Immunocytochemistiry." Progress in Histochemistry and Cytochemistry 27, no. 2 (January 1993): III—65. http://dx.doi.org/10.1016/s0079-6336(11)80067-7.

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Verdeguer, Francisco, and Myriam Aouadi. "Macrophage heterogeneity and energy metabolism." Experimental Cell Research 360, no. 1 (November 2017): 35–40. http://dx.doi.org/10.1016/j.yexcr.2017.03.043.

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Erwig, L. P. "Macrophage heterogeneity in renal inflammation." Nephrology Dialysis Transplantation 18, no. 10 (October 1, 2003): 1962–65. http://dx.doi.org/10.1093/ndt/gfg313.

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Gordon, Siamon. "Macrophage heterogeneity and tissue lipids." Journal of Clinical Investigation 117, no. 1 (January 2, 2007): 1–4. http://dx.doi.org/10.1172/jci30992.

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Johnson, Jason L., and Andrew C. Newby. "Macrophage heterogeneity in atherosclerotic plaques." Current Opinion in Lipidology 20, no. 5 (October 2009): 370–78. http://dx.doi.org/10.1097/mol.0b013e3283309848.

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Johnson, G. D. "Macrophage heterogeneity established by immunocytochemistry." Journal of Immunological Methods 170, no. 1 (March 1994): 138. http://dx.doi.org/10.1016/0022-1759(94)90254-2.

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den Haan, Joke M. M., and Luisa Martinez-Pomares. "Macrophage heterogeneity in lymphoid tissues." Seminars in Immunopathology 35, no. 5 (April 12, 2013): 541–52. http://dx.doi.org/10.1007/s00281-013-0378-4.

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Liddiard, Kate, Marcela Rosas, Luke C. Davies, Simon A. Jones, and Philip R. Taylor. "Macrophage heterogeneity and acute inflammation." European Journal of Immunology 41, no. 9 (August 26, 2011): 2503–8. http://dx.doi.org/10.1002/eji.201141743.

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Wang, Zhanchao, Huiqiao Wu, Yu Chen, Huajiang Chen, Wen Yuan, and Xinwei Wang. "The Heterogeneity of Infiltrating Macrophages in Metastatic Osteosarcoma and Its Correlation with Immunotherapy." Journal of Oncology 2021 (July 21, 2021): 1–13. http://dx.doi.org/10.1155/2021/4836292.

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Background. Metastatic osteosarcoma is a common and fatal bone tumor. Several studies have found that tumor-infiltrating immune cells play pivotal roles in the progression of metastatic osteosarcoma. However, the heterogeneity of infiltrating immune cells across metastatic and primary osteosarcoma remains unclear. Methods. Immune infiltration analysis was carried out via the “ESTIMATE” and “xCell” algorithms in primary and metastatic osteosarcoma. Then, we evaluated the prognostic value of infiltrating immune cells in 85 osteosarcomas through the Kaplan–Meier (K-M) and receiver operating characteristic (ROC) curve. Infiltrations of macrophage M1 and M2 were evaluated in metastatic osteosarcoma, as well as their correlation with immune checkpoints. Macrophage-related prognostic genes were identified through Weighted Gene Coexpression Network Analysis (WGCNA), Lasso analysis, and Random Forest algorithm. Finally, a macrophage-related risk model had been constructed and validated. Results. Macrophages, especially the macrophage M1, sparingly infiltrated in metastatic compared with the primary osteosarcoma and predicted the worse overall survival (OS) and disease-free survival (DFS). Macrophage M1 was positively correlated with immune checkpoints PDCD1, CD274 (PD-L1), PDCD1LG2, CTLA4, and TIGIT. In addition, four macrophage-related prognostic genes (IL10, VAV1, CD14, and CCL2) had been identified, and the macrophage-related risk model had been validated to be reliable for evaluating prognosis in osteosarcoma. Simultaneously, the risk score showed a strong correlation with several immune checkpoints. Conclusion. Macrophages potentially contribute to the regulation of osteosarcoma metastasis. It can be used as a candidate marker for metastatic osteosarcoma’ prognosis and immune checkpoints blockades (ICBs) therapy. We constructed a macrophage-related risk model through machine-learning, which might help us evaluate patients’ prognosis and response to ICBs therapy.

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Morales-Nebreda, Luisa, Alexander V. Misharin, Harris Perlman, and G. R. Scott Budinger. "The heterogeneity of lung macrophages in the susceptibility to disease." European Respiratory Review 24, no. 137 (August 31, 2015): 505–9. http://dx.doi.org/10.1183/16000617.0031-2015.

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Alveolar macrophages are specialised resident phagocytes in the alveolus, constituting the first line of immune cellular defence in the lung. As the lung microenvironment is challenged and remodelled by inhaled pathogens and air particles, so is the alveolar macrophage pool altered by signals that maintain and/or replace its composition. The signals that induce the recruitment of circulating monocytes to the injured lung, as well as their distinct gene expression profile and susceptibility to epigenetic reprogramming by the local environment remain unclear. In this review, we summarise the unique characteristics of the alveolar macrophage pool ontogeny, phenotypic heterogeneity and plasticity during homeostasis, tissue injury and normal ageing. We also discuss new evidence arising from recent studies where investigators described how the epigenetic landscape drives the specific gene expression profile of alveolar macrophages. Altogether, new analysis of macrophages by means of “omic” technologies will allow us to identify key pathways by which these cells contribute to the development and resolution of lung disease in both mice and humans.

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A-Gonzalez, Noelia, Juan A. Quintana, Susana García-Silva, Marina Mazariegos, Arturo González de la Aleja, José A. Nicolás-Ávila, Wencke Walter, et al. "Phagocytosis imprints heterogeneity in tissue-resident macrophages." Journal of Experimental Medicine 214, no. 5 (April 21, 2017): 1281–96. http://dx.doi.org/10.1084/jem.20161375.

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Tissue-resident macrophages display varying phenotypic and functional properties that are largely specified by their local environment. One of these functions, phagocytosis, mediates the natural disposal of billions of cells, but its mechanisms and consequences within living tissues are poorly defined. Using a parabiosis-based strategy, we identified and isolated macrophages from multiple tissues as they phagocytosed blood-borne cellular material. Phagocytosis was circadianally regulated and mediated by distinct repertoires of receptors, opsonins, and transcription factors in macrophages from each tissue. Although the tissue of residence defined the core signature of macrophages, phagocytosis imprinted a distinct antiinflammatory profile. Phagocytic macrophages expressed CD206, displayed blunted expression of Il1b, and supported tissue homeostasis. Thus, phagocytosis is a source of macrophage heterogeneity that acts together with tissue-derived factors to preserve homeostasis.

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Trembicki, K. A., M. A. Qureshi, and R. R. Dietert. "Monoclonal Antibodies Reactive with Chicken Peritoneal Macrophages: Identification of Macrophage Heterogeneity." Experimental Biology and Medicine 183, no. 1 (October 1, 1986): 28–41. http://dx.doi.org/10.3181/00379727-183-42382.

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NAITO, Makoto. "Macrophage Heterogeneity in Development and Differentiation." Archives of Histology and Cytology 56, no. 4 (1993): 331–51. http://dx.doi.org/10.1679/aohc.56.331.

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A. Hamilton, John. "Colony stimulating factors and macrophage heterogeneity." Inflammation and Regeneration 31, no. 3 (2011): 228–36. http://dx.doi.org/10.2492/inflammregen.31.228.

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Khan, Arshad, Vipul Kumar Singh, Robert L. Hunter, and Chinnaswamy Jagannath. "Macrophage heterogeneity and plasticity in tuberculosis." Journal of Leukocyte Biology 106, no. 2 (April 2, 2019): 275–82. http://dx.doi.org/10.1002/jlb.mr0318-095rr.

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Gordon, Siamon, and Annette Plűddemann. "Tissue macrophage heterogeneity: issues and prospects." Seminars in Immunopathology 35, no. 5 (June 20, 2013): 533–40. http://dx.doi.org/10.1007/s00281-013-0386-4.

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Forlenza, Maria, Inge R. Fink, Geert Raes, and Geert F. Wiegertjes. "Heterogeneity of macrophage activation in fish." Developmental & Comparative Immunology 35, no. 12 (December 2011): 1246–55. http://dx.doi.org/10.1016/j.dci.2011.03.008.

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Rigamonti, Elena, Paola Zordan, Clara Sciorati, Patrizia Rovere-Querini, and Silvia Brunelli. "Macrophage Plasticity in Skeletal Muscle Repair." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/560629.

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Macrophages are one of the first barriers of host defence against pathogens. Beyond their role in innate immunity, macrophages play increasingly defined roles in orchestrating the healing of various injured tissues. Perturbations of macrophage function and/or activation may result in impaired regeneration and fibrosis deposition as described in several chronic pathological diseases. Heterogeneity and plasticity have been demonstrated to be hallmarks of macrophages. In response to environmental cues they display a proinflammatory (M1) or an alternative anti-inflammatory (M2) phenotype. A lot of evidence demonstrated that after acute injury M1 macrophages infiltrate early to promote the clearance of necrotic debris, whereas M2 macrophages appear later to sustain tissue healing. Whether the sequential presence of two different macrophage populations results from a dynamic shift in macrophage polarization or from the recruitment of new circulating monocytes is a subject of ongoing debate. In this paper, we discuss the current available information about the role that different phenotypes of macrophages plays after injury and during the remodelling phase in different tissue types, with particular attention to the skeletal muscle.

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Poh, Ashleigh R., and Matthias Ernst. "Tumor-Associated Macrophages in Pancreatic Ductal Adenocarcinoma: Therapeutic Opportunities and Clinical Challenges." Cancers 13, no. 12 (June 8, 2021): 2860. http://dx.doi.org/10.3390/cancers13122860.

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Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignant disease with a 5-year survival rate of less than 10%. Macrophages are one of the earliest infiltrating cells in the pancreatic tumor microenvironment, and are associated with an increased risk of disease progression, recurrence, metastasis, and shorter overall survival. Pre-clinical studies have demonstrated an unequivocal role of macrophages in PDAC by contributing to chronic inflammation, cancer cell stemness, desmoplasia, immune suppression, angiogenesis, invasion, metastasis, and drug resistance. Several macrophage-targeting therapies have also been investigated in pre-clinical models, and include macrophage depletion, inhibiting macrophage recruitment, and macrophage reprogramming. However, the effectiveness of these drugs in pre-clinical models has not always translated into clinical trials. In this review, we discuss the molecular mechanisms that underpin macrophage heterogeneity within the pancreatic tumor microenvironment, and examine the contribution of macrophages at various stages of PDAC progression. We also provide a comprehensive update of macrophage-targeting therapies that are currently undergoing clinical evaluation, and discuss clinical challenges associated with these treatment modalities in human PDAC patients.

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Ramsey, S., A. Ozinsky, A. Clark, K. D. Smith, P. de Atauri, V. Thorsson, D. Orrell, and H. Bolouri. "Transcriptional noise and cellular heterogeneity in mammalian macrophages." Philosophical Transactions of the Royal Society B: Biological Sciences 361, no. 1467 (February 2006): 495–506. http://dx.doi.org/10.1098/rstb.2005.1808.

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Transcriptional noise is known to play a crucial role in heterogeneity in bacteria and yeast. Mammalian macrophages are known to exhibit cell-to-cell variation in their responses to pathogens, but the source of this heterogeneity is not known. We have developed a detailed stochastic model of gene expression that takes into account scaling effects due to cell size and genome complexity. We report the results of applying this model to simulating gene expression variability in mammalian macrophages, demonstrating a possible molecular basis for heterogeneity in macrophage signalling responses. We note that the nature of predicted transcriptional noise in macrophages is different from that in yeast and bacteria. Some molecular interactions in yeast and bacteria are thought to have evolved to minimize the effects of the high-frequency noise observed in these species. Transcriptional noise in macrophages results in slow changes to gene expression levels and would not require the type of spike-filtering circuits observed in yeast and bacteria.

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Cassetta, Luca, Edana Cassol, and Guido Poli. "Macrophage Polarization in Health and Disease." Scientific World JOURNAL 11 (2011): 2391–402. http://dx.doi.org/10.1100/2011/213962.

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Macrophages are terminally differentiated cells of the mononuclear phagocyte system that also encompasses dendritic cells, circulating blood monocytes, and committed myeloid progenitor cells in the bone marrow. Both macrophages and their monocytic precursors can change their functional state in response to microenvironmental cues exhibiting a marked heterogeneity. However, there are still uncertainties regarding distinct expression patterns of surface markers that clearly define macrophage subsets, particularly in the case of human macrophages. In addition to their tissue distribution, macrophages can be functionally polarized into M1 (proinflammatory) and M2 (alternatively activated) as well as regulatory cells in response to both exogenous infections and solid tumors as well as by systems biology approaches.

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Tai, D. C. "069 Investigation of macrophage heterogeneity in atherosclerosis." Canadian Journal of Cardiology 27, no. 5 (September 2011): S86. http://dx.doi.org/10.1016/j.cjca.2011.07.062.

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DELGADO, L., J. WINCK, J. RODRIGUES, J. RAMOS, and J. FLEMINGTORRINHA. "81 Alveolar macrophage heterogeneity in hypersensitivity pneumonitis." Journal of Allergy and Clinical Immunology 97, no. 1 (January 1996): 203. http://dx.doi.org/10.1016/s0091-6749(96)80299-5.

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Nahrendorf, Matthias, and Filip K. Swirski. "Monocyte and Macrophage Heterogeneity in the Heart." Circulation Research 112, no. 12 (June 7, 2013): 1624–33. http://dx.doi.org/10.1161/circresaha.113.300890.

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Witsell, A. L., and L. B. Schook. "Macrophage heterogeneity occurs through a developmental mechanism." Proceedings of the National Academy of Sciences 88, no. 5 (March 1, 1991): 1963–67. http://dx.doi.org/10.1073/pnas.88.5.1963.

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Hashimoto, Daigo, Jennifer Miller, and Miriam Merad. "Dendritic Cell and Macrophage Heterogeneity In Vivo." Immunity 35, no. 3 (September 2011): 323–35. http://dx.doi.org/10.1016/j.immuni.2011.09.007.

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Tacke, Frank, and Henning W. Zimmermann. "Macrophage heterogeneity in liver injury and fibrosis." Journal of Hepatology 60, no. 5 (May 2014): 1090–96. http://dx.doi.org/10.1016/j.jhep.2013.12.025.

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Wright, Mark D., and Katrina J. Binger. "Macrophage heterogeneity and renin-angiotensin system disorders." Pflügers Archiv - European Journal of Physiology 469, no. 3-4 (February 8, 2017): 445–54. http://dx.doi.org/10.1007/s00424-017-1940-z.

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Parisi, Luca, Elisabetta Gini, Denisa Baci, Marco Tremolati, Matteo Fanuli, Barbara Bassani, Giampietro Farronato, Antonino Bruno, and Lorenzo Mortara. "Macrophage Polarization in Chronic Inflammatory Diseases: Killers or Builders?" Journal of Immunology Research 2018 (2018): 1–25. http://dx.doi.org/10.1155/2018/8917804.

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Macrophages are key cellular components of the innate immunity, acting as the main player in the first-line defence against the pathogens and modulating homeostatic and inflammatory responses. Plasticity is a major feature of macrophages resulting in extreme heterogeneity both in normal and in pathological conditions. Macrophages are not homogenous, and they are generally categorized into two broad but distinct subsets as either classically activated (M1) or alternatively activated (M2). However, macrophages represent a continuum of highly plastic effector cells, resembling a spectrum of diverse phenotype states. Induction of specific macrophage functions is closely related to the surrounding environment that acts as a relevant orchestrator of macrophage functions. This phenomenon, termed polarization, results from cell/cell, cell/molecule interaction, governing macrophage functionality within the hosting tissues. Here, we summarized relevant cellular and molecular mechanisms driving macrophage polarization in “distant” pathological conditions, such as cancer, type 2 diabetes, atherosclerosis, and periodontitis that share macrophage-driven inflammation as a key feature, playing their dual role as killers (M1-like) and/or builders (M2-like). We also dissect the physio/pathological consequences related to macrophage polarization within selected chronic inflammatory diseases, placing polarized macrophages as a relevant hallmark, putative biomarkers, and possible target for prevention/therapy.

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Tan, Hor-Yue, Ning Wang, Sha Li, Ming Hong, Xuanbin Wang, and Yibin Feng. "The Reactive Oxygen Species in Macrophage Polarization: Reflecting Its Dual Role in Progression and Treatment of Human Diseases." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/2795090.

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High heterogeneity of macrophage is associated with its functions in polarization to different functional phenotypes depending on environmental cues. Macrophages remain in balanced state in healthy subject and thus macrophage polarization may be crucial in determining the tissue fate. The two distinct populations, classically M1 and alternatively M2 activated, representing the opposing ends of the full activation spectrum, have been extensively studied for their associations with several disease progressions. Accumulating evidences have postulated that the redox signalling has implication in macrophage polarization and the key roles of M1 and M2 macrophages in tissue environment have provided the clue for the reasons of ROS abundance in certain phenotype. M1 macrophages majorly clearing the pathogens and ROS may be crucial for the regulation of M1 phenotype, whereas M2 macrophages resolve inflammation which favours oxidative metabolism. Therefore how ROS play its role in maintaining the homeostatic functions of macrophage and in particular macrophage polarization will be reviewed here. We also review the biology of macrophage polarization and the disturbance of M1/M2 balance in human diseases. The potential therapeutic opportunities targeting ROS will also be discussed, hoping to provide insights for development of target-specific delivery system or immunomodulatory antioxidant for the treatment of ROS-related diseases.

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Xu, Hailin, Jingxin Jiang, Wuzhen Chen, Wenlu Li, and Zhigang Chen. "Vascular Macrophages in Atherosclerosis." Journal of Immunology Research 2019 (December 1, 2019): 1–14. http://dx.doi.org/10.1155/2019/4354786.

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Atherosclerosis is the main pathological basis for the occurrence of most cardiovascular diseases, the leading global health threat, and a great burden for society. It has been well established that atherosclerosis is not only a metabolic disorder but also a chronic, sterile, and maladaptive inflammatory process encompassing both innate and adaptive immunity. Macrophages, the major immune cell population in atherosclerotic lesions, have been shown to play critical roles in all stages of atherosclerosis, including the initiation and progression of advanced atherosclerosis. Macrophages have emerged as a novel potential target for antiatherosclerosis therapy. In addition, the macrophage phenotype is greatly influenced by microenvironmental stimuli in the plaques and presents complex heterogeneity. This article reviews the functions of macrophages in different stages of atherosclerosis, as well as the phenotypes and functions of macrophage subsets. New treatment strategies based on macrophage-related inflammation are also discussed.

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Liu, Guangwei, Xue-Pei Xia, Shou-Liang Gong, and Yong Zhao. "The macrophage heterogeneity: Difference between mouse peritoneal exudate and splenic F4/80+ macrophages." Journal of Cellular Physiology 209, no. 2 (2006): 341–52. http://dx.doi.org/10.1002/jcp.20732.

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Wang, Ming, Yalong Yang, Dilay Cansever, Yiming Wang, Crystal Kantores, Sébastien Messiaen, Delphine Moison, et al. "Two populations of self-maintaining monocyte-independent macrophages exist in adult epididymis and testis." Proceedings of the National Academy of Sciences 118, no. 1 (December 28, 2020): e2013686117. http://dx.doi.org/10.1073/pnas.2013686117.

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Macrophages are the principal immune cells of the epididymis and testis, but their origins, heterogeneity, development, and maintenance are not well understood. Here, we describe distinct populations of epididymal and testicular macrophages that display an organ-specific cellular identity. Combining in vivo fate-mapping, chimeric and parabiotic mouse models with in-depth cellular analyses, we found that CD64hiMHCIIlo and CD64loMHCIIhi macrophage populations of epididymis and testis arise sequentially from yolk sac erythro-myeloid progenitors, embryonic hematopoiesis, and nascent neonatal monocytes. While monocytes were the major developmental source of both epididymal and testicular macrophages, both populations self-maintain in the steady-state independent of bone marrow hematopoietic precursors. However, after radiation-induced macrophage ablation or during infection, bone marrow-derived circulating monocytes are recruited to the epididymis and testis, giving rise to inflammatory macrophages that promote tissue damage. These results define the layered ontogeny, maintenance and inflammatory response of macrophage populations in the male reproductive organs.

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Ortiz, Alexandra M., Sarah R. DiNapoli, and Jason M. Brenchley. "Macrophages Are Phenotypically and Functionally Diverse across Tissues in Simian Immunodeficiency Virus-Infected and Uninfected Asian Macaques." Journal of Virology 89, no. 11 (March 18, 2015): 5883–94. http://dx.doi.org/10.1128/jvi.00005-15.

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ABSTRACTMacrophages regulate tissue immunity, orchestrating the initiation and resolution of antimicrobial immune responses and repair of damaged tissue architecture. Their dysfunction can, thus, manifest in either pro- and anti-inflammatory responses. Indeed, despite the importance of macrophage function in health and disease, the role of tissue-resident macrophages in human immunodeficiency virus (HIV) disease progression remains incompletely defined. Here, we use flow cytometry to assess the phenotypes and functions of macrophages isolated from the spleens, axillary lymph nodes, colons, jejuna, and livers of healthy and chronically simian immunodeficiency virus (SIV)-infected Asian macaques, the prominent nonhuman primate model for HIV infection. Our data demonstrate that macrophages from healthy animals exhibit considerable phenotypic and functional heterogeneity across tissues and across a variety of stimuli. Further, our analysis reveals changes in the lipopolysaccharide (LPS) responsiveness of macrophages isolated from SIV-infected animals. We anticipate that our findings will inform future research into macrophage-directed immunity across a variety of primate diseases.IMPORTANCEThese findings highlight the functional and phenotypic heterogeneity of tissue macrophages in different anatomic sites and as a result of SIV infection. We believe that our data will lead to novel therapeutic interventions aimed at altering the proinflammatory capacity of tissue macrophages in progressively HIV-infected individuals.

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Dang, Mai, and Malay Haldar. "TBIO-07. SINGLE-CELL TRANSCRIPTOMIC PROFILE REVEALS MACROPHAGE HETEROGENEITY IN SONIC-HEDGEHOG MEDULLOBLASTOMA AND THEIR DISTINCT RESPONSES TO DIFFERENT TREATMENT MODALITIES." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii468. http://dx.doi.org/10.1093/neuonc/noaa222.835.

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Abstract Tumor-associated macrophages (TAMs) are an important component of the tumor microenvironment. Pro-inflammatory macrophages can suppress while anti-inflammatory macrophages can promote tumor growth. Despite their abundance in many tumors, the origins and diversity of TAMs are not well understood, especially in pediatric brain tumors. Using single-cell RNA sequencing in a genetically engineered mouse model (Ptch+/-:p53-/-) of SHH-MB, we identified the dual microglia and monocytic origin of macrophage and their transcriptomic heterogeneity. We demonstrate differential recruitment and function of macrophages under distinct modalities of tumor therapy of molecular targeted hedgehog inhibition versus radiation. We additionally identify a monocytic macrophage population recruited post-radiation that is immune suppressive, suggesting a mechanism for radiation treatment failure. These insights uncover potential strategies for immunomodulation as adjunctive therapy for radiation.

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Takito, Jiro, and Masanori Nakamura. "Heterogeneity and Actin Cytoskeleton in Osteoclast and Macrophage Multinucleation." International Journal of Molecular Sciences 21, no. 18 (September 10, 2020): 6629. http://dx.doi.org/10.3390/ijms21186629.

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Osteoclast signatures are determined by two transcriptional programs, the lineage-determining transcription pathway and the receptor activator of nuclear factor kappa-B ligand (RANKL)-dependent differentiation pathways. During differentiation, mononuclear precursors become multinucleated by cell fusion. Recently, live-cell imaging has revealed a high level of heterogeneity in osteoclast multinucleation. This heterogeneity includes the difference in the differentiation states and the mobility of the fusion precursors, as well as the mode of fusion among the fusion precursors with different numbers of nuclei. In particular, fusion partners often form morphologically distinct actin-based linkages that allow two cells to exchange lipids and proteins before membrane fusion. However, the origin of this heterogeneity remains elusive. On the other hand, osteoclast multinucleation is sensitive to the environmental cues. Such cues promote the reorganization of the actin cytoskeleton, especially the formation and transformation of the podosome, an actin-rich punctate adhesion. This review covers the heterogeneity of osteoclast multinucleation at the pre-fusion stage with reference to the environment-dependent signaling pathway responsible for reorganizing the actin cytoskeleton. Furthermore, we compare osteoclast multinucleation with macrophage fusion, which results in multinucleated giant macrophages.

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Cheng, Wen-Lin, Quan Zhang, Bo Li, Jian-Lei Cao, Lin Jiao, Sheng-Ping Chao, Zhibing Lu, and Fang Zhao. "PAK1 Silencing Attenuated Proinflammatory Macrophage Activation and Foam Cell Formation by Increasing PPARγ Expression." Oxidative Medicine and Cellular Longevity 2021 (September 23, 2021): 1–13. http://dx.doi.org/10.1155/2021/6957900.

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Macrophage polarization in response to environmental cues has emerged as an important event in the development of atherosclerosis. Compelling evidences suggest that P21-activated kinases 1 (PAK1) is involved in a wide variety of diseases. However, the potential role and mechanism of PAK1 in regulation of macrophage polarization remains to be elucidated. Here, we observed that PAK1 showed a dramatically increased expression in M1 macrophages but decreased expression in M2 macrophages by using a well-established in vitro model to study heterogeneity of macrophage polarization. Adenovirus-mediated loss-of-function approach demonstrated that PAK1 silencing induced an M2 macrophage phenotype-associated gene profiles but repressed the phenotypic markers related to M1 macrophage polarization. Additionally, dramatically decreased foam cell formation was found in PAK1 silencing-induced M2 macrophage activation which was accompanied with alternation of marker account for cholesterol efflux or influx from macrophage foam cells. Moderate results in lipid metabolism and foam cell formation were found in M1 macrophage activation mediated by AdshPAK1. Importantly, we presented mechanistic evidence that PAK1 knockdown promoted the expression of PPARγ, and the effect of macrophage activation regulated by PAK1 silencing was largely reversed when a PPARγ antagonist was utilized. Collectively, these findings reveal that PAK1 is an independent effector of macrophage polarization at least partially attributed to regulation of PPARγ expression, which suggested PAK1-PPARγ axis as a novel therapeutic strategy in atherosclerosis management.

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Rhee, Aaron J., and Kory J. Lavine. "New Approaches to Target Inflammation in Heart Failure: Harnessing Insights from Studies of Immune Cell Diversity." Annual Review of Physiology 82, no. 1 (February 10, 2020): 1–20. http://dx.doi.org/10.1146/annurev-physiol-021119-034412.

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Despite mounting evidence implicating inflammation in cardiovascular diseases, attempts at clinical translation have shown mixed results. Recent preclinical studies have reenergized this field and provided new insights into how to favorably modulate cardiac macrophage function in the context of acute myocardial injury and chronic disease. In this review, we discuss the origins and roles of cardiac macrophage populations in the steady-state and diseased heart, focusing on the human heart and mouse models of ischemia, hypertensive heart disease, and aortic stenosis. Specific attention is given to delineating the roles of tissue-resident and recruited monocyte-derived macrophage subsets. We also highlight emerging concepts of monocyte plasticity and heterogeneity among monocyte-derived macrophages, describe possible mechanisms by which infiltrating monocytes acquire unique macrophage fates, and discuss the putative impact of these populations on cardiac remodeling. Finally, we discuss strategies to target inflammatory macrophage populations.

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Stoger, J., Pieter Goossens, and Menno de Winther. "Macrophage Heterogeneity: Relevance and Functional Implications in Atherosclerosis." Current Vascular Pharmacology 8, no. 2 (March 1, 2010): 233–48. http://dx.doi.org/10.2174/157016110790886983.

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Gordon, Siamon, Annette Plüddemann, and Fernando Martinez Estrada. "Macrophage heterogeneity in tissues: phenotypic diversity and functions." Immunological Reviews 262, no. 1 (October 15, 2014): 36–55. http://dx.doi.org/10.1111/imr.12223.

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Journal articles on the topic 'Macrophage heterogeneity'

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