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Journal articles on the topic 'Macrophage labeling'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Diez-Roux, G., M. Argilla, H. Makarenkova, K. Ko, and R. A. Lang. "Macrophages kill capillary cells in G1 phase of the cell cycle during programmed vascular regression." Development 126, no. 10 (1999): 2141–47. http://dx.doi.org/10.1242/dev.126.10.2141.

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Programmed capillary regression occurs during normal development of the eye and serves as a useful model for assessing the forces that drive vascular involution. Using a combination of S-phase labeling and liposome-mediated macrophage elimination, we show that during regression, macrophages induce apoptosis of both pericytes and endothelial cells in a cell cycle stage-dependent manner. Target cells are signaled to die by macrophages approximately 15 hours after S-phase labeling and this corresponds to a point in mid-G1 phase of the cell cycle. The tight correlation between the restriction poin

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2

Saini, Yogesh, Owais Mohammad, Brandon W. Lewis, and Razia Sultana. "Understanding macrophage recruitment to the stressed airspaces." Journal of Immunology 196, no. 1_Supplement (2016): 60.10. http://dx.doi.org/10.4049/jimmunol.196.supp.60.10.

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Abstract The presence of functionally competent macrophages in respiratory airspaces is critical to the normal host immune responses. To determine the effect of altered macrophage (MΦ) populations on macrophage recruitment, we employed LysM+/mTOM\mEGFP+/DTA+ mice, a model of macrophage depletion and mEGFP+ labeling. Since controlled by same promoter (Lysozyme M; LysM) and separate alleles of ROSA locus, the expression of mEGFP and DTA transgenes is simultaneously induced that facilitates mEGFP+ fluorescent labeling of DTA+ cells with LysM+ activity. Flow cytometric and confocal microscopic ana

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3

Cummings, Thomas J., Christine M. Hulette, Sandra H. Bigner, Gregory J. Riggins, and Roger E. McLendon. "HAM56-Immunoreactive Macrophages in Untreated Infiltrating Gliomas." Archives of Pathology & Laboratory Medicine 125, no. 5 (2001): 637–41. http://dx.doi.org/10.5858/2001-125-0637-himiui.

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Abstract Context.—Classic diagnostic neuropathologic teachings have cautioned against making the diagnosis of neoplasia in the presence of a macrophage population. The knowledge of macrophage distribution should prove useful when confronted with an infiltrating glioma containing macrophages. Objective.—To identify macrophages in untreated, infiltrating gliomas using the monoclonal antibody HAM56, and to confirm their presence in an untreated glioblastoma multiforme (GBM) with the serial analysis of gene expression (SAGE) method. Methods.—We evaluated the presence of macrophages in 16 cases of

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4

Tchernychev, Boris, Bruce Furie, and Barbara C. Furie. "Peritoneal macrophages express both P-selectin and PSGL-1." Journal of Cell Biology 163, no. 5 (2003): 1145–55. http://dx.doi.org/10.1083/jcb.200310079.

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Macrophages, phagocytic cells involved in an early phase of host defense, are known to express the P-selectin ligand, PSGL-1. Heretofore, P-selectin has only been found on platelets and endothelial cells. Here, we demonstrate that peritoneal macrophages isolated by peritoneal lavage of unchallenged mice express P-selectin on the plasma membrane. The peritoneal macrophages synthesize P-selectin, as indicated by metabolic labeling experiments. P-Selectin is constitutively expressed on the extracellular surface of macrophages but is only partially colocalized with PSGL-1. P-Selectin is rapidly tr

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Hammer, Daniel X., Anant Agrawal, Ricardo Villanueva, Osamah Saeedi, and Zhuolin Liu. "Label-free adaptive optics imaging of human retinal macrophage distribution and dynamics." Proceedings of the National Academy of Sciences 117, no. 48 (2020): 30661–69. http://dx.doi.org/10.1073/pnas.2010943117.

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Microglia are resident central nervous system macrophages and the first responders to neural injury. Until recently, microglia have been studied only in animal models with exogenous or transgenic labeling. While these studies provided a wealth of information on the delicate balance between neuroprotection and neurotoxicity within which these cells operate, extrapolation to human immune function has remained an open question. Here we examine key characteristics of retinal macrophage cells in live human eyes, both healthy and diseased, with the unique capabilities of our adaptive optics–optical

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Mercurio, A. M., and P. W. Robbins. "Activation of mouse peritoneal macrophages alters the structure and surface expression of protein-bound lactosaminoglycans." Journal of Immunology 135, no. 2 (1985): 1305–12. http://dx.doi.org/10.4049/jimmunol.135.2.1305.

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Abstract We have begun to analyze and compare the surface carbohydrates present on populations of resident and activated mouse peritoneal macrophages. The activated macrophage populations studied include TG-elicited macrophages, BCG-activated macrophages, and resident macrophages cultured for 24 hr in the presence of lymphokines or heterologous serum. Analysis of glycopeptides generated by pronase digestion of surface glycoproteins labeled by the neuraminidase/galactose oxidase/NaB3H4 method indicates that the macrophage surface contains a class of high m.w. carbohydrates susceptible to degrad

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7

Bassiouni, Mohamed, Philipp Arens, Samira Ira Zabaneh, Heidi Olze, David Horst, and Florian Roßner. "The Relationship between the M1/M2 Macrophage Polarization and the Degree of Ossicular Erosion in Human Acquired Cholesteatoma: An Immunohistochemical Study." Journal of Clinical Medicine 11, no. 16 (2022): 4826. http://dx.doi.org/10.3390/jcm11164826.

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The differential involvement of the macrophage activation phenotypes (M1 vs. M2) has been linked to disease severity in various chronic inflammatory disorders. Pharmacologic manipulation of the M1/M2 macrophage polarization has shown therapeutic potential. Cholesteatoma is a destructive chronic middle ear disease with potentially life-threatening complications. The distribution of macrophage polarization phenotypes in middle ear cholesteatoma has not been described. In the present study, human cholesteatoma specimens acquired during tympanomastoidectomy were retrospectively retrieved and immun

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8

Mecham, J. O., M. M. Soong, C. A. Cain, S. Koehm, J. Goff, and W. A. Tompkins. "Binding of calmodulin to the microfilament network correlates with induction of a macrophage tumoricidal response." Journal of Immunology 134, no. 5 (1985): 3516–23. http://dx.doi.org/10.4049/jimmunol.134.5.3516.

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Abstract Induction of mouse peritoneal macrophage cytotoxicity against SV3T3, a line of virally transformed mouse cells correlated with the distribution of cytoplasmic calmodulin in the macrophages. The organization of the cytoskeleton was examined by fluorescent microscopy and by transmission electron microscopy, using immunogold tagging after Triton-X-100 (TX-100) extraction of the macrophages. Macrophages that had been activated to a tumoricidal state in vivo by vaccinia virus or in vitro by lymphokine stimulation displayed cytoskeletal networks that were more extended and weblike than did

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9

Metcalf, D., M. J. Elliott, and N. A. Nicola. "The excess numbers of peritoneal macrophages in granulocyte-macrophage colony-stimulating factor transgenic mice are generated by local proliferation." Journal of Experimental Medicine 175, no. 4 (1992): 877–84. http://dx.doi.org/10.1084/jem.175.4.877.

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Mice transgenic for the hemopoietic growth factor, granulocyte-macrophage colony-stimulating factor (GM-CSF), exhibit a sustained elevation of GM-CSF levels and a 50-100-fold elevation of peritoneal macrophage cell numbers. The excess cell numbers were found to be generated in pre-adult life, with numbers remaining relatively constant thereafter. In the pre-adult period, no abnormalities were noted in the number or composition of blood, bone marrow, or spleen cells, the type or number of GM progenitor cells in the marrow or spleen, or the rate of appearance of newly formed monocytes in the per

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10

Morrissette, N. S., E. S. Gold, J. Guo, et al. "Isolation and characterization of monoclonal antibodies directed against novel components of macrophage phagosomes." Journal of Cell Science 112, no. 24 (1999): 4705–13. http://dx.doi.org/10.1242/jcs.112.24.4705.

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In order to identify novel proteins associated with various stages of macrophage phagocytosis, we have generated monoclonal antibodies that recognize phagosomes. Purified Fc receptor-mediated phagosomes, isolated by feeding IgG-conjugated magnetic beads to LPS-primed murine peritoneal macrophages, were used as the immunogen. An immunofluorescence screen was used to isolate and single-cell clone approximately 150 monoclonal antibodies that recognize mouse macrophage phagosomes as well as labeling other cellular components in patterns which are frequently distinct from those observed with previo

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Leung, Gabriel, Taylor McCann, Camilla Forsberg, and Anna Beaudin. "IL7R regulates fetal tissue resident macrophage development." Journal of Immunology 200, no. 1_Supplement (2018): 43.7. http://dx.doi.org/10.4049/jimmunol.200.supp.43.7.

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Abstract Tissue-resident macrophages play critical roles in tissue homeostasis and disease. Many populations of tissue-resident macrophages derive from fetal progenitors and self-maintain across the lifespan through in situ proliferation, independent of bone marrow hematopoiesis. However, the developmental mechanisms that specify fetal-derived tissue-resident macrophages are poorly understood. Here, we have identified a novel cytokine regulating tissue-resident macrophage development using an IL7Ra-cre lineage tracing model. Adult tissue resident macrophages in the brain, skin, liver, and lung

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Min, Ji Hyun, Sung Tae Kim, Ji Sung Lee, et al. "Labeling of macrophage cell using biocompatible magnetic nanoparticles." Journal of Applied Physics 109, no. 7 (2011): 07B309. http://dx.doi.org/10.1063/1.3563073.

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13

Hsiao, Jong-Kai, Hung-Hao Chu, Yu-Hsiu Wang, et al. "Macrophage physiological function after superparamagnetic iron oxide labeling." NMR in Biomedicine 21, no. 8 (2008): 820–29. http://dx.doi.org/10.1002/nbm.1260.

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14

Araki, Hiroto, Naoyuki Katayama, Yoshihiro Yamashita, et al. "Reprogramming of human postmitotic neutrophils into macrophages by growth factors." Blood 103, no. 8 (2004): 2973–80. http://dx.doi.org/10.1182/blood-2003-08-2742.

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Abstract It is generally recognized that postmitotic neutrophils give rise to polymorphonuclear neutrophils alone. We obtained evidence for a lineage switch of human postmitotic neutrophils into macrophages in culture. When the CD15+CD14- cell population, which predominantly consists of band neutrophils, was cultured with granulocyte macrophage–colony-stimulating factor, tumor necrosis factor-α, interferon-γ, and interleukin-4, and subsequently with macrophage colony-stimulating factor alone, the resultant cells had morphologic, cytochemical, and phenotypic features of macrophages. In contrast

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Rojas, M., L. F. Barrera, G. Puzo, and L. F. Garcia. "Differential induction of apoptosis by virulent Mycobacterium tuberculosis in resistant and susceptible murine macrophages: role of nitric oxide and mycobacterial products." Journal of Immunology 159, no. 3 (1997): 1352–61. http://dx.doi.org/10.4049/jimmunol.159.3.1352.

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Abstract Resistance and susceptibility of macrophages to mycobacteria are under the control of the Bcg/Nramp1 gene, which also controls the NO- production in response to macrophage activators. There is recent evidence indicating that mycobacteria induces apoptosis in infected macrophages. Using murine macrophage lines, congenic at the Bcg/Nramp1 gene, this report shows that B10R are more prone than B10S macrophages to undergo apoptosis after exposure to live virulent Mycobacterium tuberculosis H37Rv (Mtb) or PPD, as determined by cell viability, DNA fragmentation, hypoploidy, and the terminal

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Kingsley, Paul D., Eli T. Rust, Alec J. Kingsley, et al. "Tissue-Resident Macrophages in the Bone Marrow Comprise a Diverse Cellular Population Derived from Hematopoietic Stem Cells." Blood 142, Supplement 1 (2023): 3910. http://dx.doi.org/10.1182/blood-2023-188067.

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In the bone marrow, tissue-resident macrophages serve several specific roles including engulfing senescent neutrophils, maintaining hematopoietic stem cells (HSCs), and comprising an important component of the erythroid microenvironment within erythroblastic islands (EBIs). These latter macrophages are thought to “nurture” maturing erythroblasts with iron and cytokines, and to serve as a sink for erythroblast mitochondria, while simultaneously phagocytosing newly formed pyrenocytes. Here we sought to delineate the developmental origin of marrow macrophages, as well as their cellular heterogene

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Kradin, RL, GW Lynch, JT Kurnick, M. Erikson, RB Colvin, and J. McDonagh. "Factor XIII A is synthesized and expressed on the surface of U937 cells and alveolar macrophages." Blood 69, no. 3 (1987): 778–85. http://dx.doi.org/10.1182/blood.v69.3.778.778.

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Abstract Factor XIII A subunit was detected in U937 cells and human alveolar macrophages by immunohistology and Western blotting. U937 cells synthesize factor XIII A subunit de novo under serum-free, platelet- free conditions, as indicated by 35S-methionine labeling and immunoprecipitation. Thrombin-dependent activity was demonstrated to account for 98% of the total transglutaminase activity in U937 cells (1.5 micrograms per 0.5 X 10(6) cells/mL). Intact U937 cells and alveolar macrophages and homogenates from these cells cross-linked fibrin to form gamma-gamma and alpha-polymers. Factor XIII

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Kradin, RL, GW Lynch, JT Kurnick, M. Erikson, RB Colvin, and J. McDonagh. "Factor XIII A is synthesized and expressed on the surface of U937 cells and alveolar macrophages." Blood 69, no. 3 (1987): 778–85. http://dx.doi.org/10.1182/blood.v69.3.778.bloodjournal693778.

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Factor XIII A subunit was detected in U937 cells and human alveolar macrophages by immunohistology and Western blotting. U937 cells synthesize factor XIII A subunit de novo under serum-free, platelet- free conditions, as indicated by 35S-methionine labeling and immunoprecipitation. Thrombin-dependent activity was demonstrated to account for 98% of the total transglutaminase activity in U937 cells (1.5 micrograms per 0.5 X 10(6) cells/mL). Intact U937 cells and alveolar macrophages and homogenates from these cells cross-linked fibrin to form gamma-gamma and alpha-polymers. Factor XIII A was det

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19

Bogdan, C., H. Thüring, M. Dlaska, M. Röllinghoff, and G. Weiss. "Mechanism of suppression of macrophage nitric oxide release by IL-13: influence of the macrophage population." Journal of Immunology 159, no. 9 (1997): 4506–13. http://dx.doi.org/10.4049/jimmunol.159.9.4506.

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Abstract IL-13 is a cytokine produced by T lymphocytes, mast cells, basophils, and certain B cell lines that up-regulates or inhibits various macrophage functions. In the present study we analyzed the mechanisms of suppression of nitric oxide (NO) release by IL-13 in the macrophage cell line J774A.1 and in thioglycolate-elicited mouse peritoneal macrophages. In both cell types efficient reduction (&gt;80%) of NO production required treatment of the macrophages with IL-13 for at least 7 h before stimulation with IFN-gamma and LPS. In J774A.1 cells, increasing concentrations of IFN-gamma par

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Huang, Xiao-Zhe, and Luther E. Lindler. "The pH 6 Antigen Is an Antiphagocytic Factor Produced by Yersinia pestis Independent of Yersinia Outer Proteins and Capsule Antigen." Infection and Immunity 72, no. 12 (2004): 7212–19. http://dx.doi.org/10.1128/iai.72.12.7212-7219.2004.

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ABSTRACT The pH 6 antigen (pH 6 Ag; PsaA) of Yersinia pestis has been shown to be a virulence factor. In this study, we set out to investigate the possible function of Y. pestis PsaA in a host cell line, RAW264.7 mouse macrophages, in order to better understand the role it might play in virulence. Y. pestis KIM5 derivatives with and without the pCD1 plasmid and their psaA isogenic counterparts and Escherichia coli HB101 and DΗ5α carrying a psaA clone or a vector control were used for macrophage infections. Macrophage-related bacteria and gentamicin-resistant intracellular bacteria generated fr

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Garello, Francesca, Marina Boido, Martina Miglietti, et al. "Imaging of Inflammation in Spinal Cord Injury: Novel Insights on the Usage of PFC-Based Contrast Agents." Biomedicines 9, no. 4 (2021): 379. http://dx.doi.org/10.3390/biomedicines9040379.

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Labeling of macrophages with perfluorocarbon (PFC)-based compounds allows the visualization of inflammatory processes by 19F-magnetic resonance imaging (19F-MRI), due to the absence of endogenous background. Even if PFC-labeling of monocytes/macrophages has been largely investigated and used, information is lacking about the impact of these agents over the polarization towards one of their cell subsets and on the best way to image them. In the present work, a PFC-based nanoemulsion was developed to monitor the course of inflammation in a model of spinal cord injury (SCI), a pathology in which

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Fink, Marc Y., Jenny G. Maloney, and Steven M. Singer. "Myeloid Cells in the Immune Response to Giardia." Journal of Immunology 200, no. 1_Supplement (2018): 52.12. http://dx.doi.org/10.4049/jimmunol.200.supp.52.12.

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Abstract Infection with the protozoan parasite, Giardia, produces symptoms associated with intestinal distress, but does not induce intestinal inflammation. Long-term sequellae of this infection include malnutrition, Irritable Bowel Syndrome and Chronic Fatigue Syndrome. Previous work indicates that T-cells are critical for clearance of this parasite; however, it is unclear which cells are responsible for the activation of T-cells. As such, our goal was to examine the contribution of myeloid cells to Giardia immunity as possible T-cell activators, effector cells and/or immune regulators. Small

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Ding, Yuanyuan, Yu Sun, Hongyan Wang, et al. "Atherosis-associated lnc_000048 activates PKR to enhance STAT1-mediated polarization of THP-1 macrophages to M1 phenotype." Neural Regeneration Research 19, no. 11 (2024): 2488–98. http://dx.doi.org/10.4103/nrr.nrr-d-23-01355.

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JOURNAL/nrgr/04.03/01300535-202419110-00029/figure1/v/2024-03-08T184507Z/r/image-tiff Our previous study has demonstrated that lnc_000048 is upregulated in large-artery atherosclerotic stroke and promotes atherosclerosis in ApoE– / – mice. However, little is known about the role of lnc_000048 in classically activated macrophage (M1) polarization. In this study, we established THP-1-derived testing state macrophages (M0), M1 macrophages, and alternately activated macrophages (M2). Real-time fluorescence quantitative PCR was used to verify the expression of marker genes and the expression of lnc

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Liu, Yaming, Vikas K. Verma, Harmeet Malhi, et al. "Lipopolysaccharide downregulates macrophage-derived IL-22 to modulate alcohol-induced hepatocyte cell death." American Journal of Physiology-Cell Physiology 313, no. 3 (2017): C305—C313. http://dx.doi.org/10.1152/ajpcell.00005.2017.

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Interleukin-22 (IL-22) is a Th17 cell hepatoprotective cytokine that is undergoing clinical trials to treat patients with alcoholic hepatitis (AH). Lipopolysaccharide (LPS) activation of macrophage is implicated in hepatocyte cell death and pathogenesis of AH. The role of IL-22 production from macrophage, its regulation by LPS, and effects on alcohol-induced hepatocyte cell death are unexplored and were examined in this study. Low levels of IL-22 mRNA/protein were detected in macrophage but were significantly upregulated by 6.5-fold in response to the tissue reparative cytokine IL-10. Converse

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Hirano, Hirofumi, Koji Tanioka, Shunichi Yokoyama, Shin-ichi Akiyama, and Jun-ichi Kuratsu. "Angiogenic effect of thymidine phosphorylase on macrophages in glioblastoma multiforme." Journal of Neurosurgery 95, no. 1 (2001): 89–95. http://dx.doi.org/10.3171/jns.2001.95.1.0089.

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Object. Thymidine phosphorylase (TP) and vascular endothelial growth factor (VEGF) are known angiogenic factors; however, there are few reports in which the relationship between these two factors is addressed. The authors compared expression patterns of TP and VEGF and investigated their role in the angiogenesis of glioblastoma multiforme (GBM). Methods. Surgical specimens from 41 cases of GBM were immunohistochemically stained for TP, VEGF, CD68 (a macrophage marker), and CD31 (an endothelial cell marker). Both TP labeling indices and VEGF immunoreactivity displayed significant correlations w

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Nagashima, R., K. Maeda, Y. Imai, and T. Takahashi. "Lamina propria macrophages in the human gastrointestinal mucosa: their distribution, immunohistological phenotype, and function." Journal of Histochemistry & Cytochemistry 44, no. 7 (1996): 721–31. http://dx.doi.org/10.1177/44.7.8675993.

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In this study we systematically investigated the cellular distribution, immunohistochemical phenotype, and mucosal disposal function of macrophages in the lamina propria of the human gastrointestinal mucosa (lamina propria macrophages; LPMs). In all tissues examined, most of these LPMs accumulated beneath the epithelial layer that covered the apex of the lamina propria of the mucosa. These cells expressed normal levels of common macrophage markers such as CD68, LN5, lysozyme, ferritin, and alpha 1-anti-chymotrypsin. In addition, they expressed high levels of 25F9 (a market for a certain subpop

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Jenvey, Caitlin J., Jesse M. Hostetter, Adrienne L. Shircliff, John P. Bannantine, and Judith R. Stabel. "Quantification of Macrophages andMycobacterium avium Subsp. paratuberculosisin Bovine Intestinal Tissue During Different Stages of Johne’s Disease." Veterinary Pathology 56, no. 5 (2019): 671–80. http://dx.doi.org/10.1177/0300985819844823.

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Johne’s disease is an enteric disease caused by the intracellular pathogen Mycobacterium avium subsp. paratuberculosis (MAP). Upon ingestion of MAP, it is translocated across the intestinal epithelium and may be killed by intestinal macrophages, or depending on the bacterial burden and immunological status of the animal, MAP may thwart innate defense mechanisms and persist within the macrophage. This study aimed to determine the numbers of macrophages and MAP present in bovine midileal tissue during different stages of infection. Immunofluorescent (IF) labeling was performed on frozen bovine m

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Huang, Jiang-Hu, Hang He, Yong-Neng Chen та ін. "Exosomes derived from M2 Macrophages Improve Angiogenesis and Functional Recovery after Spinal Cord Injury through HIF-1α/VEGF Axis". Brain Sciences 12, № 10 (2022): 1322. http://dx.doi.org/10.3390/brainsci12101322.

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Exosomes are nano-sized vesicles that contain a variety of mRNAs, miRNAs, and proteins. They are capable of being released by a variety of cells and are essential for cell–cell communication. The exosomes produced by cells have shown protective benefits against spinal cord damage (SCI). Recently, it was discovered that M2 macrophages aid in the angiogenesis of numerous illnesses. However, the functional role of M2 macrophage-derived exosomes on SCI is unclear. Here, we investigate the pro-angiogenesis of M2 macrophage-derived exosomes on SCI. We founded that M2 macrophage exosomes alleviated t

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Dowdell, Alexander S., and Sean P. Colgan. "Microbial trash to metabolic treasure." Immunometabolism 7, no. 3 (2025): e00067. https://doi.org/10.1097/in9.0000000000000067.

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In a recent Nature publication, Lesbats et al uncover the molecular fate of phagocytosed bacterial contents. The authors observed incorporation of bacterial biomolecules (amino acids, metabolites) into those of the host macrophage through stable isotope labeling and mass spectrometry. Further, the authors found that the state of the phagocytosed bacteria, living or dead, dramatically alters the macrophage’s metabolic program toward either a pro-inflammatory or a “recycling” direction, respectively. This commentary summarizes these findings and further discusses the implications of this work in

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Longo, Giorgia, Linda Giro, Laura Fusco, et al. "Exploring the Biomedical Potential of MXenes in Macrophage Phenotype Identification and Tracking." Journal of Immunology 212, no. 1_Supplement (2024): 0281_5822. http://dx.doi.org/10.4049/jimmunol.212.supp.0281.5822.

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Abstract Macrophages are innate immune cells with varying phenotypes and functions that are influenced by their microenvironment. The distinction between the classical M1 and M2 phenotypes has been crucial in understanding their involvement in inflammation. Recently single-cell technologies have revealed a complex range of macrophage activation states, each contributing differently to maintaining physiological balance and affecting the development and progression of diseases. Identifying the origins and function of these macrophage subsets remains a complex challenge. MXenes, a category of two

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Remold-O'Donnell, E. "Regulation of synthesis of macrophage adhesion molecule, a heterodimeric membrane glycoprotein." Journal of Immunology 140, no. 4 (1988): 1244–49. http://dx.doi.org/10.4049/jimmunol.140.4.1244.

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Abstract Macrophage adhesion molecule is a surface molecule of guinea pig macrophages and neutrophils. It is the counterpart of mouse Mac-1 and human CD11b/CD18 (Mol/OKM-1/Mac-1/Leu-CAM) and is member of a family of heterodimer glycoproteins with a common beta-subunit. Macrophage adhesion molecule is a prevalent molecule in nonactivated macrophages, but it is dramatically decreased in macrophages activated in vivo. The experimental system of activated vs nonactivated guinea pig peritoneal macrophages was used to examine the mechanisms that down-regulate synthesis of this heterodimer molecule.

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Herzyk, D. J., J. N. Allen, C. B. Marsh, and M. D. Wewers. "Macrophage and monocyte IL-1 beta regulation differs at multiple sites. Messenger RNA expression, translation, and post-translational processing." Journal of Immunology 149, no. 9 (1992): 3052–58. http://dx.doi.org/10.4049/jimmunol.149.9.3052.

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Abstract Maturation of blood monocytes into macrophages is accompanied by a number of functional changes including decreased IL-1 beta release in response to LPS. This limitation has previously been ascribed to transcriptional regulation. However, in seeming conflict with the observed depression in IL-1 beta mRNA levels, recent work demonstrates increased intracellular IL-1 beta in macrophages. Therefore, the present study sought to explain these differences by comparing IL-1 beta production from autologous alveolar macrophage and blood monocyte pairs at multiple regulatory sites, including en

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Maimaitijiang, Alimujiang, Qingyu Huang, Yurong Wu, Shengjia Sun, and Qiying Chen. "Transglutaminase 2 inhibition ameliorates cardiac fibrosis in myocardial infarction by inducing M2 macrophage polarization in vitro and in vivo." Cytojournal 21 (November 28, 2024): 58. http://dx.doi.org/10.25259/cytojournal_32_2024.

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Objective: Macrophages perform vital functions in cardiac remodeling after myocardial infarction (MI). Transglutaminase 2 (TG2) participates in fibrosis. Nevertheless, the role of TG2 in MI and mechanisms underlying macrophage polarization are unclear. This study aimed to discover the functions and possible mechanisms of TG2 in MI. Material and Methods: C57BL/6 mice were classified into three groups (six mice per group): Sham, MI, and MI+GK921 groups. GK921 acts as a TG2 inhibitor. Cardiac function, myocardial cell apoptosis, fibrosis, and macrophage phenotype in mouse experiments were detecte

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Risco, C., and P. Pinto da Silva. "Binding of bacterial endotoxins to the macrophage surface: visualization by fracture-flip and immunocytochemistry." Journal of Histochemistry & Cytochemistry 41, no. 4 (1993): 601–8. http://dx.doi.org/10.1177/41.4.8450199.

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Endotoxins (lipopolysaccharides, LPS) are surface components of gram-negative bacteria that stimulate macrophage activation and cause endotoxic shock. How LPS is recognized by host cells is still an open question, but it is generally accepted that many effects of endotoxins follow the overproduction of cytokines by macrophages. In the present study, we used fracture-flip and immunolabeling to study the morphology of isolated commercial LPS (C-LPS), the endotoxin release from the bacterial wall in presence of serum (S-LPS), and the distribution of these two endotoxins on the macrophage surface.

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Yang, Yuchun, Xiaohuan Zhou, Jiao Wang, et al. "Metformin-Loaded Alginate Nanoparticles Inhibits Mouse Atherosclerosis by Regulating Macrophage Differentiation by Activating the Adenosine Monophosphate-Activated Protein Kinase/Signal Transducer and Activator of Transcription 3 Pathway." Journal of Biomedical Nanotechnology 18, no. 5 (2022): 1513–20. http://dx.doi.org/10.1166/jbn.2022.3352.

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Objective: By modulating macrophage phenotype and the adenylate-activated protein kinase/signal transducer and activator of transcription 3 (STAT3) signaling pathway, metformin-loaded alginate nanoparticles may prevent atherosclerosis (As). Methods: Flow cytometry was used to determine the percentage of macrophages with distinct phenotypes (CD86 and CD206). Analysis of protein expression levels of iNOS, arginase 1, AMPK, pAMPK, STAT3 and phosphorylated STAT3 were performed by Western Blot. To confirm the in vitro findings, ApoE−/− mice were employed. Results: AMPK activity and the fraction of

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Martínez-Pomares, L., M. Kosco-Vilbois, E. Darley, et al. "Fc chimeric protein containing the cysteine-rich domain of the murine mannose receptor binds to macrophages from splenic marginal zone and lymph node subcapsular sinus and to germinal centers." Journal of Experimental Medicine 184, no. 5 (1996): 1927–37. http://dx.doi.org/10.1084/jem.184.5.1927.

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Ligands for the cysteine-rich (CR) domain of the mannose receptor (MR) were detected by incubating murine tissues with a chimeric protein containing CR fused to the Fc region of human IgG1 (CR-Fc). In naive mice, CR-Fc bound to sialoadhesin+, F4/80low/-, macrosialin+ macrophages (M phi) in spleen marginal zone (metallophilic M phi) and lymph node subcapsular sinus. Labeling was also observed in B cell areas of splenic white pulp. Western blotting analysis of spleen and lymph nodes lysates revealed a restricted number of molecules that interacted specifically with CR-Fc. In immunized mice, labe

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Boddingius, J., and H. P. Dijkman. "Immunogold labeling method for Mycobacterium leprae-specific phenolic glycolipid in glutaraldehyde-osmium-fixed and Araldite-embedded leprosy lesions." Journal of Histochemistry & Cytochemistry 37, no. 4 (1989): 455–62. http://dx.doi.org/10.1177/37.4.2926124.

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Phenolic glycolipid (PGL)-I, a Mycobacterium leprae-specific antigen currently used for serodiagnosis of preclinical leprosy, has thus far not been localized subcellularly in leprosy bacilli and their host cells. In this study, we developed an immunogold-labeling technique for qualitative identification of PGL-I sites in glutaraldehyde-osmium-fixed and Araldite-embedded M. leprae and host macrophages in human skin biopsies. Such "hard-fixed," plastic-embedded skin and nerve biopsies from patients with varying cell-mediated immunity to leprosy are amply available worldwide. Our method involves

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Luciani, N., M. Levy, E. Lancelot, F. Gazeau, and C. Wilhelm. "CMR2009: 11.03: Outcome of magnetic labeling in monocyte/macrophage system." Contrast Media & Molecular Imaging 4, no. 6 (2009): 295–96. http://dx.doi.org/10.1002/cmmi.356.

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Liao, Xiaomin, Xianxian Ruan, Xiubing Chen та ін. "The Long Noncoding RNA Gm9866/Nuclear Factor-κB Axis Promotes Macrophage Polarization". Mediators of Inflammation 2023 (29 січня 2023): 1–10. http://dx.doi.org/10.1155/2023/9991916.

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Macrophages are a type of immune cells with high levels of plasticity and heterogeneity. They can polarize into M1 or M2 functional phenotypes. These two phenotypes exhibit a dynamic balance during polarization-related diseases and play opposing roles. Long noncoding RNAs (lncRNAs) play an important role in biological processes such as cell proliferation, death, and differentiation; however, how long noncoding RNAs affect the cellular functionality of macrophages remains to be studied. Long noncoding RNA Gm9866 was found to be closely related to macrophage polarization through bioinformatics a

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Somodi, Laura, Emőke Horváth, Helga Bárdos, et al. "Cellular FXIII in Human Macrophage-Derived Foam Cells." International Journal of Molecular Sciences 24, no. 5 (2023): 4802. http://dx.doi.org/10.3390/ijms24054802.

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Macrophages express the A subunit of coagulation factor XIII (FXIII-A), a transglutaminase which cross-links proteins through Nε-(γ-L-glutamyl)-L-lysyl iso-peptide bonds. Macrophages are major cellular constituents of the atherosclerotic plaque; they may stabilize the plaque by cross-linking structural proteins and they may become transformed into foam cells by accumulating oxidized LDL (oxLDL). The combination of oxLDL staining by Oil Red O and immunofluorescent staining for FXIII-A demonstrated that FXIII-A is retained during the transformation of cultured human macrophages into foam cells.

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Sano, Gen-ichiro, Yasunari Takada, Shinichi Goto, et al. "Flagella Facilitate Escape of Salmonella from Oncotic Macrophages." Journal of Bacteriology 189, no. 22 (2007): 8224–32. http://dx.doi.org/10.1128/jb.00898-07.

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ABSTRACT The intracellular parasite Salmonella enterica serovar Typhimurium causes a typhoid-like systemic disease in mice. Whereas the survival of Salmonella in phagocytes is well understood, little has been documented about the exit of intracellular Salmonella from host cells. Here we report that in a population of infected macrophages Salmonella induces “oncosis,” an irreversible progression to eukaryotic cell death characterized by swelling of the entire cell body. Oncotic macrophages (OnMφs) are terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling negative and lack

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Martínez-Zamora, María Angeles, Olga Armengol-Badia, Lara Quintas-Marquès, Francisco Carmona, and Daniel Closa. "Macrophage Phenotype Induced by Circulating Small Extracellular Vesicles from Women with Endometriosis." Biomolecules 14, no. 7 (2024): 737. http://dx.doi.org/10.3390/biom14070737.

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Evidence suggests that immune system dysfunction and macrophages are involved in the disease establishment and progression of endometriosis. Among the factors involved in this alteration in macrophage activity, Small Extracellular Vesicles (sEVs) have been described to play a role favoring the switch to a specific phenotype with controversial results. This study aims to investigate the potential effect of circulating sEVs in the plasma of well-characterized patients with endometriosis on the polarization of macrophages. sEVs were isolated from the plasma of patients diagnosed with endometriosi

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Lin, Tian-Yang, Zong-Juan Lian, Cai-Xia Yao, et al. "CdSe quantum dots labeled Staphylococcus aureus for research studies of THP-1 derived macrophage phagocytic behavior." RSC Advances 10, no. 1 (2020): 260–70. http://dx.doi.org/10.1039/c9ra07892d.

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Hu, Xiaoli, Christian S. Buhl, Marie B. Sjogaard, et al. "Structural Changes of Cutaneous Immune Cells in Patients With Type 1 Diabetes and Their Relationship With Diabetic Polyneuropathy." Neurology - Neuroimmunology Neuroinflammation 10, no. 5 (2023): e200144. http://dx.doi.org/10.1212/nxi.0000000000200144.

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Background and ObjectivesDiabetic polyneuropathy (DPN) is a complication of diabetes characterized by pain or lack of peripheral sensation, but the underlying mechanisms are not yet fully understood. Recent evidence showed increased cutaneous macrophage infiltration in patients with type 2 diabetes and painful DPN, and this study aimed to understand whether the same applies to type 1 diabetes.MethodsThe study included 104 participants: 26 healthy controls and 78 participants with type 1 diabetes (participants without DPN [n = 24], participants with painless DPN [n = 29], and participants with

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Laskarin, G., T. Kehler, D. Legović, et al. "AB0075 SYNOVIAL TISSUE MACROPHAGES ARE DOMINANTLY ALTERNATIVELY ACTIVATED IN PATIENTS WITH MATURE OSTEOARTHRITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1337.2–1338. http://dx.doi.org/10.1136/annrheumdis-2020-eular.3896.

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Background:Macrophages are abundant inflammatory cell type in the synovial membrane of knee osteoarthritis (OA) (1). Their quantity is associated with radiographic severity of knee OA and joint symptoms (2), while their functions are set in response to micro-environmental signals (3). Classically activated macrophages M1 support T helper 1 (Th1) driven pro-inflammatory reactions, while alternatively activated macrophages M2 strengthen Th2 inflammatory processes (3).Objectives:To investigate activation status of synovial tissue macrophages in patients with mature OA in terms of M1 / M2 polariza

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Liu, Zhenyu, Ying Du, Rongfu Zhou, Bing Chen, and Peipei Xu. "A Novel Engineering Platelet Platform Target the Macrophages to Inhibit Cytokine Storm in Hemophagocytic Lymphohistiocytosis." Blood 144, Supplement 1 (2024): 1146. https://doi.org/10.1182/blood-2024-206792.

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Introduction: Hemophagocytic lymphohistiocytosis (HLH) is a severe hematologic disorder characterized by abnormally increased macrophage activity due to abnormal immunoregulation. Etoposide (VP16) is the first-line drug for treating HLH, but its therapeutic effect is still unsatisfactory. The team's previous experiments showed that platelets (PLTs) with surface-associated anti-CD41 can be efficiently recognized and phagocytosed by macrophages. Therefore, we proposed to design and construct anti-CD41-PLT-VP16, a novel engineering platelet platform that can precisely target the abnormal macropha

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Yeo, Jia Hao, Bronwyn M. McAllan, and Stuart T. Fraser. "Scanning Electron Microscopy Reveals Two Distinct Classes of Erythroblastic Island Isolated from Adult Mammalian Bone Marrow." Microscopy and Microanalysis 22, no. 2 (2016): 368–78. http://dx.doi.org/10.1017/s1431927616000155.

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AbstractErythroblastic islands are multicellular clusters in which a central macrophage supports the development and maturation of red blood cell (erythroid) progenitors. These clusters play crucial roles in the pathogenesis observed in animal models of hematological disorders. The precise structure and function of erythroblastic islands is poorly understood. Here, we have combined scanning electron microscopy and immuno-gold labeling of surface proteins to develop a better understanding of the ultrastructure of these multicellular clusters. The erythroid-specific surface antigen Ter-119 and t

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Spencer, S. C., and J. W. Fabre. "Characterization of the tissue macrophage and the interstitial dendritic cell as distinct leukocytes normally resident in the connective tissue of rat heart." Journal of Experimental Medicine 171, no. 6 (1990): 1841–51. http://dx.doi.org/10.1084/jem.171.6.1841.

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Immunohistological studies with a mouse anti-rat macrophage mAb (BMAC-5) demonstrated the presence of numerous positive cells in the interstitial connective tissues of many organs. The pattern resembled that seen with anti-MHC class II antibodies, with the striking exception that BMAC-5+ cells were rare or absent in the portal triad, the islets of Langerhans, and the kidney. Double-labeling fluorescence studies were therefore performed in rat heart using the BMAC-5 mAb in combination with rabbit antisera to pure rat class II MHC antigens and pure rat leukocyte common (CD45) antigens. The tissu

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Wise, Andrea F., Timothy M. Williams, Mensiena B. G. Kiewiet, et al. "Human mesenchymal stem cells alter macrophage phenotype and promote regeneration via homing to the kidney following ischemia-reperfusion injury." American Journal of Physiology-Renal Physiology 306, no. 10 (2014): F1222—F1235. http://dx.doi.org/10.1152/ajprenal.00675.2013.

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Mesenchymal stem cells (MSCs) ameliorate injury and accelerate repair in many organs, including the kidney, although the reparative mechanisms and interaction with macrophages have not been elucidated. This study investigated the reparative potential of human bone marrow-derived MSCs and traced their homing patterns following administration to mice with ischemia-reperfusion (IR) injury using whole body bioluminescence imaging. The effect of MSCs on macrophage phenotype following direct and indirect coculture was assessed using qPCR. Human cytokine production was measured using multiplex arrays

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Reilly, J. J., P. Chen, L. Z. Sailor, D. Wilcox, R. W. Mason, and H. A. Chapman. "Cigarette smoking induces an elastolytic cysteine proteinase in macrophages distinct from cathepsin L." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 2 (1991): L41—L48. http://dx.doi.org/10.1152/ajplung.1991.261.2.l41.

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Degradation of the interstitium of the lung by elastolytic enzymes is thought to be a critical component of the pathogenesis of emphysema. Alveolar macrophages are increased in numbers in cigarette smokers and contain the elastolytic cysteine proteinase cathepsin L. We sought to determine if cigarette smoking induces a change in cathepsin L levels in alveolar macrophages which would, in turn, alter the expression of elastolytic activity. Lysates of smokers' macrophages, assayed at pH 5.50, degraded more than seven times as much [3H]elastin as did lysates from nonsmokers' macrophages (44 +/- 20

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