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Journal articles on the topic 'Macrophage activity'
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1
Rodriguez, Eric, Frederic Boudard, Michele Mallié, Jean-Marie Bastide, and Madeleine Bastide. "Murine macrophage elastolytic activity induced by Aspergillus fumigatus strains in vitro: evidence of the expression of two macrophage-induced protease genes." Canadian Journal of Microbiology 43, no. 7 (1997): 649–57. http://dx.doi.org/10.1139/m97-092.
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The interaction between Aspergillus fumigatus conidia and murine macrophages of various origins was investigated. Cocultures were carried out between A. fumigatus strains and freshly isolated murine pulmonary alveolar macrophages or two murine macrophage cell-lines: murine alveolar cell-line MALU and murine astrocytoma cell-line J774. By measuring the variation of elastolytic activity in the coculture supernatants with two elastin substrates, we demonstrated that either viable or fixed A. fumigatus or C. albicans yeasts or nonspecific particles induced significant macrophage elastolytic activity. The effect of A. fumigatus supernatant or the purified A. fumigatus galactomannan suggested also the possible involvement of this polysaccharide in macrophage-protease gene expression, release, and activity in invasive aspergillosis. The effect of inhibitory compounds demonstrated the potential implication of a macrophagic metalloprotease and a macrophagic cysteine protease. RNA analysis allowed us to demonstrate the induction of expression of two macrophagic protease genes in stimulated macrophages. Two distinctive mechanisms appeared to be implicated in macrophage protease induction: nonspecific phagocytosis in the earliest times of the coculture and (or) specific galactomannan recognition after its gradual release by the mycelium.Key words: Aspergillus fumigatus, macrophages, proteases, invasive aspergillosis, galactomannan.
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Schumacher, Michael A., Isabella C. Dennis, Cambrian Y. Liu, et al. "NRG4-ErbB4 signaling represses proinflammatory macrophage activity." American Journal of Physiology-Gastrointestinal and Liver Physiology 320, no. 6 (2021): G990—G1001. http://dx.doi.org/10.1152/ajpgi.00296.2020.
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Proinflammatory macrophages are essential drivers of colitis and express the growth factor receptor ErbB4. This study tested the role of ErbB4 and its specific ligand, NRG4, in regulating macrophage function. We show that endogenous NRG4-ErbB4 signaling limits macrophage production of proinflammatory cytokines in vitro and limits colitis severity in vivo and thus is a potential target for therapeutic intervention.
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Lewis, Caitlin V., Antony Vinh, Henry Diep, Chrishan S. Samuel, Grant R. Drummond, and Barbara K. Kemp-Harper. "Distinct Redox Signalling following Macrophage Activation Influences Profibrotic Activity." Journal of Immunology Research 2019 (November 11, 2019): 1–15. http://dx.doi.org/10.1155/2019/1278301.
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Aims. To date, the ROS-generating capacities of macrophages in different activation states have not been thoroughly compared. This study is aimed at determining the nature and levels of ROS generated following stimulation with common activators of M1 and M2 macrophages and investigating the potential for this to impact fibrosis. Results. Human primary and THP-1 macrophages were treated with IFN-γ+LPS or IL-4-activating stimuli, and mRNA expression of established M1 (CXCL11, CCR7, IL-1β) and M2 (MRC-1, CCL18, CCL22) markers was used to confirm activation. Superoxide generation was assessed by L-012-enhanced chemiluminescence and was increased in both M(IFN-γ+LPS) and M(IL-4) macrophages, as compared to unpolarised macrophages (MΦ). This signal was attenuated with NOX2 siRNA. Increased expression of the p47phox and p67phox subunits of the NOX2 oxidase complex was evident in M(IFN-γ+LPS) and M(IL-4) macrophages, respectively. Amplex Red and DCF fluorescence assays detected increased hydrogen peroxide generation following stimulation with IL-4, but not IFN-γ+LPS. Coculture with human aortic adventitial fibroblasts revealed that M(IL-4), but not M(IFN-γ+LPS), enhanced fibroblast collagen 1 protein expression. Macrophage pretreatment with the hydrogen peroxide scavenger, PEG-catalase, attenuated this effect. Conclusion. We show that superoxide generation is not only enhanced with stimuli associated with M1 macrophage activation but also with the M2 stimulus IL-4. Macrophages activated with IL-4 also exhibited enhanced hydrogen peroxide generation which in turn increased aortic fibroblast collagen production. Thus, M2 macrophage-derived ROS is identified as a potentially important contributor to aortic fibrosis.
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Liu, Shuangqing, Huilei Zhang, Yanan Li та ін. "S100A4 enhances protumor macrophage polarization by control of PPAR-γ-dependent induction of fatty acid oxidation". Journal for ImmunoTherapy of Cancer 9, № 6 (2021): e002548. http://dx.doi.org/10.1136/jitc-2021-002548.
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BackgroundThe peroxisome proliferator-activated receptor γ (PPAR-γ)-dependent upregulation of fatty acid oxidation (FAO) mediates protumor (also known as M2-like) polarization of tumor-associated macrophages (TAMs). However, upstream factors determining PPAR-γ upregulation in TAM protumor polarization are not fully identified. S100A4 plays crucial roles in promotion of cancer malignancy and mitochondrial metabolism. The fact that macrophage-derived S100A4 is major source of extracellular S100A4 suggests that macrophages contain a high abundance of intracellular S100A4. However, whether intracellular S100A4 in macrophages also contributes to cancer malignancy by enabling TAMs to acquire M2-like protumor activity remains unknown.MethodsGrowth of tumor cells was evaluated in murine tumor models. TAMs were isolated from the tumor grafts in whole-body S100A4-knockout (KO), macrophage-specific S100A4-KO and transgenic S100A4WT−EGFP mice (expressing enhanced green fluorescent protein (EGFP) under the control of the S100A4 promoter). In vitro induction of macrophage M2 polarization was conducted by interleukin 4 (IL-4) stimulation. RNA-sequencing, real-time quantitative PCR, flow cytometry, western blotting, immunofluorescence staining and mass spectrometry were used to determine macrophage phenotype. Exogenous and endogenous FAO, FA uptake and measurement of lipid content were used to analyze macrophage metabolism.ResultsTAMs contain two subsets based on whether they express S100A4 or not and that S100A4+ subsets display protumor phenotypes. S100A4 can be induced by IL-4, an M2 activator of macrophage polarization. Mechanistically, S100A4 controls the upregulation of PPAR-γ, a transcription factor required for FAO induction during TAM protumor polarization. In S100A4+ TAMs, PPAR-γ mainly upregulates CD36, a FA transporter, to enhance FA absorption as well as FAO. In contrast, S100A4-deficient TAMs exhibited decreased protumor activity because of failure in PPAR-γ upregulation-dependent FAO induction.ConclusionsWe find that macrophagic S100A4 enhances protumor macrophage polarization as a determinant of PPAR-γ-dependent FAO induction. Accordingly, our findings provide an insight into the general mechanisms of TAM polarization toward protumor phenotypes. Therefore, our results strongly suggest that targeting macrophagic S100A4 may be a potential strategy to prevent TAMs from re-differentiation toward a protumor phenotype.
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Leopold Wager, Chrissy M., Camaron R. Hole, Karen L. Wozniak, Michal A. Olszewski, Mathias Mueller, and Floyd L. Wormley. "STAT1 Signaling within Macrophages Is Required for Antifungal Activity against Cryptococcus neoformans." Infection and Immunity 83, no. 12 (2015): 4513–27. http://dx.doi.org/10.1128/iai.00935-15.
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Cryptococcus neoformans, the predominant etiological agent of cryptococcosis, is an opportunistic fungal pathogen that primarily affects AIDS patients and patients undergoing immunosuppressive therapy. In immunocompromised individuals,C. neoformanscan lead to life-threatening meningoencephalitis. Studies using a virulent strain ofC. neoformansengineered to produce gamma interferon (IFN-γ), denoted H99γ, demonstrated that protection against pulmonaryC. neoformansinfection is associated with the generation of a T helper 1 (Th1)-type immune response and signal transducer and activator of transcription 1 (STAT1)-mediated classical (M1) macrophage activation. However, the critical mechanism by which M1 macrophages mediate their anti-C. neoformansactivity remains unknown. The current studies demonstrate that infection withC. neoformansstrain H99γ in mice with macrophage-specific STAT1 ablation resulted in severely increased inflammation of the pulmonary tissue, a dysregulated Th1/Th2-type immune response, increased fungal burden, deficient M1 macrophage activation, and loss of protection. STAT1-deficient macrophages produced significantly less nitric oxide (NO) than STAT1-sufficient macrophages, correlating with an inability to control intracellular cryptococcal proliferation, even in the presence of reactive oxygen species (ROS). Furthermore, macrophages from inducible nitric oxide synthase knockout mice, which had intact ROS production, were deficient in anticryptococcal activity. These data indicate that STAT1 activation within macrophages is required for M1 macrophage activation and anti-C. neoformansactivity via the production of NO.
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Torre, Donato, Luisa Gennero, F. M. Baccino, Filippo Speranza, Gilberto Biondi, and Agostino Pugliese. "Impaired Macrophage Phagocytosis of Apoptotic Neutrophils in Patients with Human Immunodeficiency Virus Type 1 Infection." Clinical and Vaccine Immunology 9, no. 5 (2002): 983–86. http://dx.doi.org/10.1128/cdli.9.5.983-986.2002.
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ABSTRACT Dysfunction of neutrophils (polymorphonuclear leukocytes [PMNL]) and macrophagic cells occurs as a consequence of human immunodeficiency virus type 1 (HIV-1) infection. Macrophages contribute to the resolution of early inflammation ingesting PMNL apoptotic bodies. This study investigated macrophage ability to phagocytose PMNL apoptotic bodies in patients with HIV-1 infection in comparison with uninfected individuals and the effect of HIV Nef protein on apoptotic body phagocytosis to determine if phagocytic activity is impaired by HIV infection. Monocytes/macrophages were isolated from 10 HIV-1-infected patients and from five healthy volunteers, whereas PMNL were isolated from healthy volunteers. Macrophage phagocytosis of apoptotic PMNL was determined by staining of apoptotic bodies with fluorescein-conjugated concanavalin A or with fluorescein-labeled phalloidin. Our data show significant impairment of PMNL apoptotic body macrophage phagocytosis in subjects with HIV-1 infection presenting a concentration of CD4+ T lymphocytes of >200/mm3 and in particular in those with <200 CD4+ T lymphocyte cells/mm3. In addition, HIV-1 recombinant Nef protein is able to decrease phagocytosis of apoptotic PMNL from normal human macrophages in a dose-dependent manner. The results of our study suggest that impaired macrophage phagocytosis of PMNL apoptotic bodies may contribute to the persistence of the inflammatory state in HIV-infected subjects, especially during opportunistic infections that are often favored by defective phagocytic activity.
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Denis, Michel. "Growth of Listeria monocytogenes in murine macrophages and its modulation by cytokines; activation of bactericidal activity by interleukin-4 and interleukin-6." Canadian Journal of Microbiology 37, no. 4 (1991): 253–57. http://dx.doi.org/10.1139/m91-039.
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Bone marrow derived macrophages were infected with a virulent strain of Listeria monocytogenes, and the ability of selected cytokines to modify the intracellular growth was assessed. Macrophage monolayers pretreated with either interferon-γ or tumour necrosis factor were shown to exert a significant listericidal activity. Treatment of monolayers with granulocyte–macrophage colony stimulating factor led to no significant difference in the ability of Listeria to invade and multiply within these cells. Moreover, pulsing of macrophage monolayers with interleukin-6 (IL-6) led to a slight enhancement of Listeria growth in the macrophages, whereas interleukin-4 (IL-4) did not modify Listeria growth. In other sets of experiments, macrophage monolayers were treated with cytokines after phagocytosis of the bacteria. In these conditions, interferon-γ endowed macrophages with only a modest ability to kill Listeria. Conversely, treatment of monolayers with IL-6 or IL-4 at the time of infection led to expression of high bactericidal activity. Collectively, these results suggest that macrophages may respond to different signals, which enhance their antimicrobial activity before or after infection. Furthermore, B-cell stimulatory factors (IL-4 and IL-6) are potent macrophage-activating molecules. Key words: Listeria monocytogenes, cytokines, macrophages.
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Canning, B. J., R. R. Hmieleski, E. W. Spannhake, and G. J. Jakab. "Ozone reduces murine alveolar and peritoneal macrophage phagocytosis: the role of prostanoids." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 4 (1991): L277—L282. http://dx.doi.org/10.1152/ajplung.1991.261.4.l277.
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Continuous ozone exposure (0.5 ppm, 1–14 days) reduced the phagocytic activity of murine alveolar and peritoneal macrophages. The response of peritoneal macrophages to ozone was virtually indistinguishable from the response of alveolar macrophages. When added exogenously, prostaglandin E2 (PGE2) inhibited alveolar and peritoneal macrophage phagocytosis. To test the hypothesis that prostanoids mediated the effects of ozone on macrophages, PGE levels of bronchoalveolar lavage fluid (BALF) and the phagocytic activity of macrophages from ozone-exposed mice pretreated with cyclooxygenase inhibitors were measured. PGE levels in BALF were increased following ozone exposure, with high levels of PGE associated with large decreases in phagocytic activity. Pretreatment with indomethacin and d-naproxen completely inhibited ozone-induced increases in PGE recovered by BAL and the suppression of peritoneal macrophage phagocytic activity. The inactive enantiomer of naproxen, l-naproxen, was without effect. Indomethacin partially inhibited ozone-induced suppression of alveolar macrophage phagocytic activity. These observations suggest that prostanoids play a key role in the response to ozone.
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Lee, Chae Bok, Il Hwan Seo, Myoung-Won Chae, et al. "Anticancer Activity of Liquid Treated with Microwave Plasma-Generated Gas through Macrophage Activation." Oxidative Medicine and Cellular Longevity 2020 (January 31, 2020): 1–13. http://dx.doi.org/10.1155/2020/2946820.
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Reactive nitrogen species (RNS), including nitric oxide (NO⋅) has been known as one of the key regulatory molecules in the immune system. In this study, we generated RNS-containing water treated with microwave plasma-generated gas in which the major component was nitric oxide (PGNO), and the effect on the macrophage polarization was investigated. The RNS-containing water was diluted in complete cell culture media (PGNO-solution) into the concentration that did not induce cell death in RAW 264.7 murine macrophages. PGNO-solution upregulates M1-type macrophage activation and downregulates the characteristics of M2-type macrophage at the transcriptional level. In addition, the PGNO-solution-treated M2-like macrophages had higher potential in killing melanoma cells. The anticancer potential was also investigated in a syngeneic mouse model. Our results show that PGNO-solution has the potential to convert the fate of macrophages, suggesting PGNO-solution treatment as a supportive method for controlling the function of macrophages under the tumor microenvironment.
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Gruden-Movsesijan, Alisa, and Ljiljana Sofronic-Milosavljevic. "Experimental Trichinellosis in rats: Peritoneal macrophage activity." Archives of Biological Sciences 62, no. 1 (2010): 15–22. http://dx.doi.org/10.2298/abs1001015g.
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The influence of Trichinella spiralis infection on macrophage activity in rats during the first 28 days of infection was examined by measuring the production of NO and IL-6, as well as the expression of mannose receptor on the surface of peritoneal macrophages. During the course of a dynamic shift in the 3 life-cycle stages of the parasite, intermittent variations in NO production were observed but ended with increased values that coincided with the highest values for IL-6 release in the final, muscle phase of infection. No change in mannose receptor expression was observed during the course of infection. These results confirm that the Trichinella spiralis infection provokes changes in macrophage activity that could influence not only the course of the parasitic disease but also the overall immune status of the host.
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Zuckerman, Steven H., and Yvonne M. Surprenant. "Induction of Endothelial Cell/Macrophage Procoagulant Activity: Synergistic Stimulation by Gamma Interferon and Granulocyte-Macrophage Colony Stimulating Factor." Thrombosis and Haemostasis 61, no. 02 (1989): 178–82. http://dx.doi.org/10.1055/s-0038-1646555.
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SummaryInflammatory mediators such as endotoxin can stimulate the expression of procoagulant activity on both endothelial cells and macrophages while the monokines Interleukin 1, IL-1, and Tumor Necrosis Factor, TNF induce procoagulant activity on endothelial cells. Incubation of murine peritoneal macrophages with suboptimal concentrations of endotoxin results in a two fold increase in procoagulant activity. Macrophages incubated with gamma interferon, IFN γ, or Granulocyte-Macrophage Colony Stimulating Factor, GM-CSF, for 16 hours prior to endotoxin stimulation demonstrated a synergistic increase in procoagulant activity. A synergistic increase in procoagulant activity was also observed with primary cultures of human umbilical cord endothelial cells incubated with recombinant human IFN γ for 16 hours prior to endotoxin, TNF, or IL-1 stimulation. Human GM-CSF had no stimulatory effect on endotoxin or monokine induced endothelial cell procoagulant activity. The augmentation of macrophage and endothelial cell procoagulant activity by IFN γ and GM-CSF may provide a novel explanation for the role of these cytokines in acute and chronic inflammation.
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Stein, M., S. Keshav, N. Harris, and S. Gordon. "Interleukin 4 potently enhances murine macrophage mannose receptor activity: a marker of alternative immunologic macrophage activation." Journal of Experimental Medicine 176, no. 1 (1992): 287–92. http://dx.doi.org/10.1084/jem.176.1.287.
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Expression of the macrophage mannose receptor is inhibited by interferon gamma (IFN-gamma), a T helper type 1 (Th-1)-derived lymphokine. Interleukin 4 (IL-4), a Th-2 lymphocyte product, upregulates major histocompatibility class II antigen expression but inhibits inflammatory cytokine production by macrophages. We have studied the effect of IL-4 on expression of the macrophage mannose receptor (MMR) by elicited peritoneal macrophages. We found that recombinant murine IL-4 enhances MMR surface expression (10-fold) and activity (15-fold), as measured by the respective binding and degradation of 125I-mannose-bovine serum albumin. Polymerase chain reaction analysis of cDNAs from purified primary macrophage populations revealed that MMR, but not lysozyme or tumor necrosis factor alpha, mRNA levels were markedly increased by IL-4. The above effects were associated with morphologic changes. These data establish IL-4 as a potent and selective enhancer of murine MMR activity in vitro. IL-4 induces inflammatory macrophages to adopt an alternative activation phenotype, distinct from that induced by IFN-gamma, characterized by a high capacity for endocytic clearance of mannosylated ligands, enhanced (albeit restricted) MHC class II antigen expression, and reduced proinflammatory cytokine secretion.
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Schwartz, Y. S., M. I. Dushkin, V. A. Vavilin, et al. "Novel Conjugate of Moxifloxacin and Carboxymethylated Glucan with Enhanced Activity against Mycobacterium tuberculosis." Antimicrobial Agents and Chemotherapy 50, no. 6 (2006): 1982–88. http://dx.doi.org/10.1128/aac.00362-05.
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ABSTRACT Mycobacterium tuberculosis is an intracellular pathogen that persists within macrophages of the human host. One approach to improving the treatment of tuberculosis (TB) is the targeted delivery of antibiotics to macrophages using ligands to macrophage receptors. The moxifloxacin-conjugated dansylated carboxymethylglucan (M-DCMG) conjugate was prepared by chemically linking dansylcadaverine (D) and moxifloxacin (M) to carboxymethylglucan (CMG), a known ligand of macrophage scavenger receptors. The targeted delivery to macrophages and the antituberculosis activity of the conjugate M-DCMG were studied in vitro and in vivo. Using fluorescence microscopy, fluorimetry, and the J774 macrophage cell line, M-DCMG was shown to accumulate in macrophages through scavenger receptors in a dose-dependent (1 to 50 μg/ml) manner. After intravenous administration of M-DCMG into C57BL/6 mice, the fluorescent conjugate was concentrated in the macrophages of the lungs and spleen. Analyses of the pharmacokinetics of the conjugate demonstrated that M-DCMG was more rapidly accumulated and more persistent in tissues than free moxifloxacin. Importantly, therapeutic studies of mycobacterial growth in C57BL/6 mice showed that the M-DCMG conjugate was significantly more potent than free moxifloxacin.
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Wu, Dayong, Casilda Mura, Alison A. Beharka, et al. "Age-associated increase in PGE2 synthesis and COX activity in murine macrophages is reversed by vitamin E." American Journal of Physiology-Cell Physiology 275, no. 3 (1998): C661—C668. http://dx.doi.org/10.1152/ajpcell.1998.275.3.c661.
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We previously showed that increased macrophage and PGE2 production with age is due to enhanced cyclooxygenase (COX) activity and COX-2 expression. This study determined the effect of vitamin E supplementation on macrophage PGE2 synthesis in young and old mice and its underlying mechanism. Mice were fed 30 or 500 parts per million vitamin E for 30 days. Lipopolysaccharide (LPS)-stimulated macrophages from old mice produced significantly more PGE2 than those from young mice. Vitamin E supplementation reversed the increased PGE2 production in old mice but had no effect on macrophage PGE2production in young mice. In both LPS-stimulated and unstimulated macrophages, COX activity was significantly higher in old than in young mice at all intervals. Vitamin E supplementation completely reversed the increased COX activity in old mice to levels comparable to those of young mice but had no effect on macrophage COX activity of young mice or on COX-1 and COX-2 protein or COX-2 mRNA expression in young or old mice. Thus vitamin E reverses the age-associated increase in macrophage PGE2 production and COX activity. Vitamin E exerts its effect posttranslationally, by inhibiting COX activity.
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Tedesco, Scattolini, Albiero, et al. "Mitochondrial Calcium Uptake Is Instrumental to Alternative Macrophage Polarization and Phagocytic Activity." International Journal of Molecular Sciences 20, no. 19 (2019): 4966. http://dx.doi.org/10.3390/ijms20194966.
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Macrophages are highly plastic and dynamic cells that exert much of their function through phagocytosis. Phagocytosis depends on a coordinated, finely tuned, and compartmentalized regulation of calcium concentrations. We examined the role of mitochondrial calcium uptake and mitochondrial calcium uniporter (MCU) in macrophage polarization and function. In primary cultures of human monocyte-derived macrophages, calcium uptake in mitochondria was instrumental for alternative (M2) macrophage polarization. Mitochondrial calcium uniporter inhibition with KB-R7943 or MCU knockdown, which prevented mitochondrial calcium uptake, reduced M2 polarization, while not affecting classical (M1) polarization. Challenging macrophages with E. coli fragments induced spikes of mitochondrial calcium concentrations, which were prevented by MCU inhibition or silencing. In addition, mitochondria remodelled in M2 macrophages during phagocytosis, especially close to sites of E. coli internalization. Remarkably, inhibition or knockdown of MCU significantly reduced the phagocytic capacity of M2 macrophages. KB-R7943, which also inhibits the membrane sodium/calcium exchanger and Complex I, reduced mitochondria energization and cellular ATP levels, but such effects were not observed with MCU silencing. Therefore, phagocytosis inhibition by MCU knockdown depended on the impaired mitochondrial calcium buffering rather than changes in mitochondrial and cellular energy status. These data uncover a new role for MCU in alternative macrophage polarization and phagocytic activity.
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Valledor, Annabel F., Luís Arpa, Ester Sánchez-Tilló та ін. "IFN-γ–mediated inhibition of MAPK phosphatase expression results in prolonged MAPK activity in response to M-CSF and inhibition of proliferation". Blood 112, № 8 (2008): 3274–82. http://dx.doi.org/10.1182/blood-2007-11-123604.
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Abstract Macrophages have the capacity to proliferate in response to specific growth factors, such as macrophage-colony stimulating factor (M-CSF). In the presence of several cytokines and activating factors, macrophages undergo growth arrest, become activated, and participate in the development of an immune response. We have previously observed that activation of extracellularly regulated kinase 1/2 (ERK-1/2) is required for macrophage proliferation in response to growth factors. A short and early pattern of ERK activity correlated with the proliferative response. In contrast, slightly prolonged patterns of activity of these kinases were induced by signals that lead to macrophage activation and growth arrest. IFN-γ is the main endogenous Th1-type macrophage activator. Here we report that stimulation with IFN-γ prolongs the pattern of ERK activity induced by M-CSF in macrophages. These effects correlate with IFN-γ–mediated inhibition of the expression of several members of the MAPK phosphatase family, namely MKP-1, -2, and -4. Moreover, inhibition of MKP-1 expression using siRNA technology or synthetic inhibitors also led to elongated ERK activity and significant blockage of M-CSF–dependent proliferation. These data suggest that subtle changes in the time course of activity of members of the MAPK family contribute to the antiproliferative effects of IFN-γ in macrophages.
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Careau, Éric, Léa-Isabelle Proulx, Philippe Pouliot, Annie Spahr, Véronique Turmel, and Élyse Y. Bissonnette. "Antigen sensitization modulates alveolar macrophage functions in an asthma model." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 5 (2006): L871—L879. http://dx.doi.org/10.1152/ajplung.00219.2005.
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We have previously demonstrated that adoptive transfer of alveolar macrophages from allergy-resistant rats to alveolar macrophage-depleted allergic rats prevents airway hyperresponsiveness development, suggesting an important role for alveolar macrophages in asthma pathogenesis. Given that ovalbumin sensitization can modulate alveolar macrophage cytokine production, we investigated the role of sensitized and unsensitized alveolar macrophages in an asthma model. Alveolar macrophages from unsensitized or sensitized Brown Norway rats were transferred to alveolar macrophage-depleted sensitized rats 24 h before allergen challenge. Airway responsiveness to methacholine and airway inflammation were measured the following day. Methacholine concentration needed to increase lung resistance by 200% was significantly higher in alveolar macrophage-depleted sensitized rats that received unsensitized alveolar macrophages compared with alveolar macrophage-depleted sensitized rats that received sensitized alveolar macrophages. Tumor necrosis factor levels in bronchoalveolar lavage fluid of sensitized rats that received unsensitized alveolar macrophages were significantly lower compared with rats that received sensitized alveolar macrophages. Interestingly, alveolar macrophages of unsensitized animals showed higher phagocytosis activity compared with alveolar macrophages of sensitized rats, suggesting that sensitization modulates alveolar macrophage phagocytosis function. Our data suggest an important role of allergen sensitization on alveolar macrophage function in asthma pathogenesis.
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Nessel, Christopher C., William L. Henry, Balduino Mastrofrancesco, Jonathan S. Reichner, and Jorge E. Albina. "Vestigial respiratory burst activity in wound macrophages." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 6 (1999): R1587—R1594. http://dx.doi.org/10.1152/ajpregu.1999.276.6.r1587.
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Macrophages from experimental wounds in rats were tested for their capacity to generate reactive oxygen intermediates. Measurements of superoxide and H2O2release, [Formula: see text]-dependent lucigenin chemiluminescence, oxygen consumption, hexose monophosphate shunt flux, and NADPH oxidase activity in cell lysates indicated, at best, the presence of a vestigial respiratory burst response in these cells. The inability of wound cells to release[Formula: see text] was not rekindled by priming with endotoxin or interferon-γ in vivo or in vitro. NADPH oxidase activity in a cell-free system demonstrated that wound macrophage membranes, but not their cytosols, were capable of sustaining maximal rates of [Formula: see text] production when mixed with their corresponding counterparts from human neutrophils. Immune detection experiments showed wound macrophages to be particularly deficient in the cytosolic component of the NADPH oxidase p47- phox. Addition of recombinant p47- phox to the human neutrophil-cell membrane/wound macrophage cytosol cell-free oxidase assay, however, failed to support[Formula: see text] production. Present findings indicate an unexpected deficit of wound macrophages in their capacity to generate reactive oxygen intermediates.
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Rosa, L. F. B. P. Costa, Y. Cury, and R. Curi. "Hormonal control of macrophage function and glutamine metabolism." Biochemistry and Cell Biology 69, no. 4 (1991): 309–12. http://dx.doi.org/10.1139/o91-047.
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Murine macrophages have been reported to utilize glutamine at high rates. However, the role of glutamine in macrophage function is still unknown. In the present study, the maximum glutaminase activity of macrophages was investigated under several endocrine dysfunctions that are known to cause alterations in macrophage function. The results obtained suggest that glutamine might play an important role in the onset of phagocytosis in inflammatory macrophages. Moreover, the studies show that insulin, glucocorticoids, and thyroid hormones may be responsible for the regulation of glutamine metabolism and, consequently, of macrophage function.Key words: macrophage, glutamine, insulin, glucocorticoids, thyroid hormones, catecholamines.
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Wilson, Justin E., Bhuvana Katkere, and James R. Drake. "Francisella tularensis Induces Ubiquitin-Dependent Major Histocompatibility Complex Class II Degradation in Activated Macrophages." Infection and Immunity 77, no. 11 (2009): 4953–65. http://dx.doi.org/10.1128/iai.00844-09.
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ABSTRACT The intracellular bacterium Francisella tularensis survives and replicates within macrophages, ultimately killing the host cell. Resolution of infection requires the development of adaptive immunity through presentation of F. tularensis antigens to CD4+ and CD8+ T cells. We have previously established that F. tularensis induces macrophage prostaglandin E2 (PGE2) production, leading to skewed T-cell responses. PGE2 can also downregulate macrophage major histocompatibility complex (MHC) class II expression, suggesting that F. tularensis-elicited PGE2 may further alter T-cell responses via inhibition of class II expression. To test this hypothesis, gamma interferon (IFN-γ)-activated reporter macrophages were exposed to supernatants from F. tularensis-infected macrophages, and the class II levels were measured. Exposure of macrophages to infection supernatants results in essentially complete clearance of surface class II and CD86, compromising the macrophage's ability to present antigens to CD4 T cells. Biochemical analysis revealed that infection supernatants elicit ubiquitin-dependent class II downregulation and degradation within intracellular acidic compartments. By comparison, exposure to PGE2 alone only leads to a minor decrease in macrophage class II expression, demonstrating that a factor distinct from PGE2 is eliciting the majority of class II degradation. However, production of this non-PGE2 factor is dependent on macrophage cyclooxygenase activity and is induced by PGE2. These results establish that F. tularensis induces the production of a PGE2-dependent factor that elicits MHC class II downregulation in IFN-γ-activated macrophages through ubiquitin-mediated delivery of class II to lysosomes, establishing another mechanism for the modulation of macrophage antigen presentation during F. tularensis infection.
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Alford, C. E., T. E. King, and P. A. Campbell. "Role of transferrin, transferrin receptors, and iron in macrophage listericidal activity." Journal of Experimental Medicine 174, no. 2 (1991): 459–66. http://dx.doi.org/10.1084/jem.174.2.459.
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It is not yet known what properties distinguish macrophages which can kill facultative intracellular bacteria, such as Listeria monocytogenes, from those which cannot. Listeria is an organism which requires iron for growth, yet macrophage listericidal mechanisms are also likely to be iron dependent. We show here that resident peritoneal macrophages and thioglycollate-elicited macrophages cannot kill listeria, but proteose peptone-elicited and FCS-elicited macrophages can. All these cell populations phagocytose listeria. Transferrin receptor expression is low on resident cells, intermediate on peptone- and FCS-elicited cells, and high on thioglycollate-elicited cells. Transferrin transports iron into cells via the transferrin receptor: thus, iron content of resident cells is low, of peptone- and FCS-elicited cells is intermediate, and of thioglycollate-elicited cells is high. Moreover, antibody to transferrin, which prevents it binding its receptor, inhibits listericidal macrophages from killing this bacterium. Finally, nonlistericidal cells with high transferrin receptor expression and high intracellular iron become listericidal if they are incubated with apotransferrin, an iron-free ligand which prevents iron uptake by cells. These data suggest that macrophages must have enough available intracellular iron to support listericidal mechanisms, but too much iron favors growth of the bacterium, which no longer can be killed by the macrophage.
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Schwamb, Janine, Nina Reinart, Daniela Vorholt, et al. "Phagocytic Function of Macrophages Is Impaired By Chronic Lymphocytic Leukemia and high–grade Lymphoma Progression and Can be Highly Effectively Restored for Chemo-Immunotherapy." Blood 124, no. 21 (2014): 2727. http://dx.doi.org/10.1182/blood.v124.21.2727.2727.
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Abstract Macrophage polarity has recently been shown to play a pivotal role in progression and prognosis of human malignancies. In CLL the high dependence of the malignant cell to the tumor microenvironment has revealed macrophages as major mediators of leukemia cell survival. In contrast, macrophage activation also offers novel therapeutic strategies for leukemia cell targeting. Here we analyze the reciprocal relationship of leukemia cells and macrophages and the specific functional impact of phagocytosis in leukemia progression and therapy. We employed the humanized hMB-Lymphoma and the Eµ-TCL1 CLL mouse model. Thioglycollate-induced macrophages, bone marrow derived murine macrophages and human monocyte derived macrophages were used for in vitroevaluation of phagocytosis either by bead based approaches or by ADCC. Applying gene-expression profiling of macrophages in Eµ-TCL1 mice we could identify profound transcriptional alterations indicating a re-programming during leukemogenesis. Functional genomic analysis particularly revealed impaired phagocytic function induced during leukemia onset. In vivo and ex vivo phagocytosis assays of primary macrophages showed a significant reduced phagocytic activity during CLL progression. Human macrophages in co-culture with CLL cells in vitro compared to healthy B-cells similarly showed defects in phagocytosis. In the humanized leukemia model we similarly observed impaired phagocytosis resulting in resistance towards therapeutic antibody/macrophage mediated therapy. Resistance was actively induced by increasing leukemia cell infiltration in the bone marrow. Impaired macrophage function could be identified being mediated by secretory crosstalk such as release of PGE2 by leukemia cells and Cholecalciferol. We could restore phagocytic function by combination regimens involving therapeutic antibodies and chemotherapy. Specifically, an acute secretory activating phenotype (ASAP), releasing cytokines from leukemia cells induces macrophage infiltration and phagocytic activity in the bone marrow. Thus, malignant cells can be effectively targeted by modulation of macrophage polarization and function. In conclusion, we have identified decreased phagocytic activity of macrophages as key functional aspect in leukemia and lymphoma associated macrophages. Inversely, enhancing phagocytosis rendered essential for the re-sensitization of refractory niches treatment towards monoclonal antibodies defined by macrophage polarity. Overall macrophage function represents a key therapeutic target in CLL and other B-cell malignancies. Disclosures No relevant conflicts of interest to declare.
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Newman, Simon L., Bindu Bhugra, Angela Holly, and Randal E. Morris. "Enhanced Killing of Candida albicans by Human Macrophages Adherent to Type 1 Collagen Matrices via Induction of Phagolysosomal Fusion." Infection and Immunity 73, no. 2 (2005): 770–77. http://dx.doi.org/10.1128/iai.73.2.770-777.2005.
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ABSTRACT Candida albicans, a component of the normal flora of the alimentary tract and mucocutaneous membranes, is the leading cause of invasive fungal disease in premature infants, diabetics, and surgical patients and of oropharyngeal disease in AIDS patients. As little is known about the regulation of monocyte/macrophage anti-Candida activity, we sought to determine if fungicidal activity might be regulated by extracellular matrix proteins to which monocytes/macrophages are adherent in vivo. Compared to monocyte/macrophages that adhered to plastic, human monocytes and monocyte-derived macrophages that adhered to type 1 collagen matrices, but not to fibronectin, vitronectin, or laminin, demonstrated a significant increase in candidacidal activity. The enhancement of monocyte fungicidal activity was maintained over a 4-h period, whereas macrophage fungicidal activity was maximum at 1 h. Although adherence of monocytes and macrophages to collagen matrices concomitantly enhanced the production of superoxide anion, only the fungicidal activity of collagen-adherent monocytes was partially blocked by superoxide dismutase and catalase. Remarkably, we found that only 10% of the phagosomes in C. albicans-infected macrophages that adhered to plastic fused with lysosomes. In contrast, 80% of yeast-containing phagosomes of collagen-adherent macrophages fused with lysosomes. These data suggest that nonoxidative mechanisms are critical for human macrophage anti-Candida activity and that C. albicans pathogenicity is mediated, in part, by its ability to inhibit phagolysosomal fusion in macrophages.
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PARTRIDGE, Jason, Daniel F. WALLACE, Kishor B. RAJA, James S. DOOLEY, and Ann P. WALKER. "Monocyte–macrophage ferric reductase activity is inhibited by iron and stimulated by cellular differentiation." Biochemical Journal 336, no. 3 (1998): 541–43. http://dx.doi.org/10.1042/bj3360541.
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The enzyme ferric reductase catalyses the reduction of Fe(III) as a prerequisite to its transportation across the cell membrane. Duodenal mucosal biopsies from iron overloaded patients with genetic haemochromatosis (GH) have increased ferric reductase activity and iron absorption compared with controls, yet the GH mucosa is iron deficient. A similar GH-related iron deficiency is also seen in macrophages. The aim of this study was to investigate whether macrophage ferric reductase activity is altered in GH, and to determine ferric reductase activity in monocytes and differentiated macrophages. The erythroleukaemic K562 cell line was studied as a clonal reference cell line. The basal K562 ferric reductase activity is characteristic of a membrane bound enzyme, being both temperature and protease sensitive. Ferric reductase activity was also demonstrated in human leucocyte, monocyte and macrophage preparations. Assays of K562 and macrophage cell supernatants confirmed that the ferric reductase activity was not due to a secreted factor. Assay of ferric reductase in normalized-iron and iron-enriched (100 µM ferric citrate) conditions showed no significant difference between Cys282Tyr (Cys282 → Tyr) homozygous GH macrophages and Cys282-Tyr negative control activities (P> 0.05). However, a 900% increase in ferric reductase activity was observed during monocyte to macrophage differentiation (P< 0.05), possibly reflecting the co-ordinate up-regulation of iron metabolism in these cells. The demonstration of approx. 25% activity after macrophage differentiation at high free-iron concentrations compared with ‘normalized ’ iron is consistent with repression of human ferric reductase activity by iron. The identification of the human ferric reductase gene and its protein will ultimately provide insight into its regulation and role in mammalian iron metabolism.
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Antari, Arlita Leniseptaria, Indah Saraswati, David Pakaya, and Aryoko Widodo. "Macrophage Activity Test of Pulmonary Tuberculosis Patients with Diabetes Mellitus (TB-DM)." Journal of Biomedicine and Translational Research 2, no. 2 (2016): 38. http://dx.doi.org/10.14710/jbtr.v2i2.833.
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Background: Control of pulmonary TB is getting more and more complicated as the number of patients with diabetes mellitus (DM) is increasing. The increasing prevalence of DM is followed by the increasing prevalence of pulmonary TB. Diabetes Mellitus patients have 4,7 times higher risk to develop pulmonary TB compared to patients without DM, since DM can increase the frequency and severity of an infection, including pulmonary TB.Aim: To analyze macrophage activity (phagocytosis, intracellular killing, and TNF-α synthesis) of TB-DM patients.Method: The research is an experimental study using a PBMC cultured sample from TB-DM patient's which undergo observation of macrophage activity (phagocytic, intracellular killing and TNF-α synthesis). The data were taken from microscopic observation of TB-DM patients, colony growth of viable Mycobacterium tuberculosis and the TNF-α level secreted by macrophages.Result: Microscopic observation showed that there are less amount of phagocytosed M. tuberculosis (in macrophage/intracellular level) and there is a little amount of formed vacuoles and giant cells. Furthermore, macrophages in TB-DM patients secrete low level of TNF- α, and there are more viable M. tuberculosis from this macrophage.Conclusions: Macrophages of TB-DM patients are less activated, with reduced phagocytic activity (due to the intrinsic defect of PMN) and reduced antigen presenting activity of phagocytes toward M. tuberculosis. Therefore, there is a need for a further study focused on macrophage activity enhancement on TB-DM patients against M. tuberculosis infection in DM patients.Keywords: macrophage, TB-DM, phagocytosis, intracellular killing, TNF- α.
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Coleman, DL, JA Chodakewitz, AH Bartiss, and JW Mellors. "Granulocyte-macrophage colony-stimulating factor enhances selective effector functions of tissue-derived macrophages." Blood 72, no. 2 (1988): 573–78. http://dx.doi.org/10.1182/blood.v72.2.573.573.
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Abstract Granulocyte-macrophage colony-stimulating factor (GM-CSF) is produced by a variety of cells at sites of exposure to antigens. GM-CSF has a stimulatory effect on a number of neutrophil functions, but the effect on macrophage function is less clear. We investigated the effect of purified murine recombinant GM-CSF on murine peritoneal macrophage oxidative metabolism, Fc-dependent phagocytosis, anti-Toxoplasma activity, and expression of class II major histocompatibility antigen (Iad). GM-CSF significantly increased phorbol myristate acetate- and zymosan-elicited H2O2 release by resident and thioglycollate-elicited macrophages after 48 hours in vitro. The effect of recombinant GM-CSF was blocked by polyclonal anti-GM-CSF antibody and was not altered by lipopolysaccharide (0.01 to 1.0 microgram/mL). GM-CSF also stimulated Fc-dependent phagocytosis by peritoneal macrophages, although the stimulation of resident macrophages (1.4-fold) was less dramatic than that of thioglycollate-elicited cells (2.1-fold). GM-CSF (at doses up to 100 U/mL) had no effect on macrophage anti-Toxoplasma activity or on expression of Iad. In addition to stimulating macrophage growth, GM-CSF selectively promotes the functional capacity of tissue-derived macrophages.
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Coleman, DL, JA Chodakewitz, AH Bartiss, and JW Mellors. "Granulocyte-macrophage colony-stimulating factor enhances selective effector functions of tissue-derived macrophages." Blood 72, no. 2 (1988): 573–78. http://dx.doi.org/10.1182/blood.v72.2.573.bloodjournal722573.
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Granulocyte-macrophage colony-stimulating factor (GM-CSF) is produced by a variety of cells at sites of exposure to antigens. GM-CSF has a stimulatory effect on a number of neutrophil functions, but the effect on macrophage function is less clear. We investigated the effect of purified murine recombinant GM-CSF on murine peritoneal macrophage oxidative metabolism, Fc-dependent phagocytosis, anti-Toxoplasma activity, and expression of class II major histocompatibility antigen (Iad). GM-CSF significantly increased phorbol myristate acetate- and zymosan-elicited H2O2 release by resident and thioglycollate-elicited macrophages after 48 hours in vitro. The effect of recombinant GM-CSF was blocked by polyclonal anti-GM-CSF antibody and was not altered by lipopolysaccharide (0.01 to 1.0 microgram/mL). GM-CSF also stimulated Fc-dependent phagocytosis by peritoneal macrophages, although the stimulation of resident macrophages (1.4-fold) was less dramatic than that of thioglycollate-elicited cells (2.1-fold). GM-CSF (at doses up to 100 U/mL) had no effect on macrophage anti-Toxoplasma activity or on expression of Iad. In addition to stimulating macrophage growth, GM-CSF selectively promotes the functional capacity of tissue-derived macrophages.
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Holsapple, Jason S., Ben Cooper, Susan H. Berry, et al. "Low Intensity Shockwave Treatment Modulates Macrophage Functions Beneficial to Healing Chronic Wounds." International Journal of Molecular Sciences 22, no. 15 (2021): 7844. http://dx.doi.org/10.3390/ijms22157844.
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Extracorporeal Shock Wave Therapy (ESWT) is used clinically in various disorders including chronic wounds for its pro-angiogenic, proliferative, and anti-inflammatory effects. However, the underlying cellular and molecular mechanisms driving therapeutic effects are not well characterized. Macrophages play a key role in all aspects of healing and their dysfunction results in failure to resolve chronic wounds. We investigated the role of ESWT on macrophage activity in chronic wound punch biopsies from patients with non-healing venous ulcers prior to, and two weeks post-ESWT, and in macrophage cultures treated with clinical shockwave intensities (150–500 impulses, 5 Hz, 0.1 mJ/mm2). Using wound area measurements and histological/immunohistochemical analysis of wound biopsies, we show ESWT enhanced healing of chronic ulcers associated with improved wound angiogenesis (CD31 staining), significantly decreased CD68-positive macrophages per biopsy area and generally increased macrophage activation. Shockwave treatment of macrophages in culture significantly boosted uptake of apoptotic cells, healing-associated cytokine and growth factor gene expressions and modulated macrophage morphology suggestive of macrophage activation, all of which contribute to wound resolution. Macrophage ERK activity was enhanced, suggesting one mechanotransduction pathway driving events. Collectively, these in vitro and in vivo findings reveal shockwaves as important regulators of macrophage functions linked with wound healing. This immunomodulation represents an underappreciated role of clinically applied shockwaves, which could be exploited for other macrophage-mediated disorders.
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Vuarchey, Clément, Sushil Kumar, and Reto Schwendener. "Albumin coated liposomes: a novel platform for macrophage specific drug delivery." Nanotechnology Development 1, no. 1 (2011): 2. http://dx.doi.org/10.4081/nd.2011.e2.
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Here we report a new and efficient approach of macrophage specific drug delivery by coating liposomes with albumin. Activated albumin was reacted with liposomes containing polyethylene glycol (PEG) as hydrophilic spacers to create a flexible layer of covalently bound albumin molecules on the liposome surface. Albumin coated liposomes were taken up faster and more efficiently than uncoated liposomes by murine macrophages. Liposome uptake was significantly higher in macropha - ges as compared to other cell types tested (endothelial cells, fibroblasts, tumor cells), suggesting specificity for macrophages. In vivo, splenic macrophages phagocytosed BSA coated liposomes (BSA-L) at faster rates compared to conventional liposomes (L) and PEG liposomes (PEG-L). To prove the effectiveness of this new macrophage specific drug carrier, the bisphosphonates clodronate and zoledronate were encapsulated in BSA-L and compared with conventional liposomes. <em>In vitro</em>, treatment of macrophages with clodronate or zoledronate in BSA-L led to cytotoxic activity within a very short time and to up to 50-fold reduced IC50 concentrations. <em>In vivo</em>, clodronate encapsulated in BSA-L depleted splenic macrophages at a 5-fold lower concentration as conventional clodronate-liposomes. Our results highlight the pharmaceutical benefits of albumin-coated liposomes for macrophage specific drug delivery.
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Liu, Jin-Biao, Li Zhou, Yi-Zhong Wang, et al. "Neuroprotective Activity of (-)-Epigallocatechin Gallate against Lipopolysaccharide-Mediated Cytotoxicity." Journal of Immunology Research 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/4962351.
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Lipopolysaccharide- (LPS-) mediated systemic inflammation plays a critical role in neurodegenerative diseases. The present study was conducted to evaluate the protective effects of epigallocatechin gallate (EGCG), the major component in green tea, on LPS-mediated inflammation and neurotoxicity. LPS treatment of macrophages induced expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6). However, EGCG pretreatment of macrophages significantly inhibited LPS-mediated induction of these cytokines. In addition, EGCG significantly diminished LPS-induced inflammatory cytokines in the peripheral mononuclear blood cells (PBMCs). Supernatant from EGCG-pretreated and LPS-activated macrophage cultures was found to be less cytotoxic to neurons than that from non-EGCG-pretreated and LPS-activated macrophage cultures. Furthermore, EGCG treatment of neurons could inhibit LPS-induced production of reactive oxygen species (ROS). Thus EGCG represents a potent and useful neuroprotective agent for inflammation-mediated neurological disorders.
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Kisseleva, Ekaterina P., Andrei V. Krylov, Olga I. Stepanova, and Victoria I. Lioudyno. "Transplantable Subcutaneous Hepatoma 22a Affects Functional Activity of Resident Tissue Macrophages in Periphery." International Journal of Cell Biology 2011 (2011): 1–14. http://dx.doi.org/10.1155/2011/793034.
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Tumors spontaneously develop central necroses due to inadequate blood supply. Recent data indicate that dead cells and their products are immunogenic to the host. We hypothesized that macrophage tumor-dependent reactions can be mediated differentially by factors released from live or dead tumor cells. In this study, functional activity of resident peritoneal macrophages was investigated in parallel with tumor morphology during the growth of syngeneic nonimmunogenic hepatoma 22a. Morphometrical analysis of tumor necroses, mitoses and leukocyte infiltration was performed in histological sections. We found that inflammatory potential of peritoneal macrophages in tumor-bearing mice significantly varied depending on the stage of tumor growth and exhibited two peaks of activation as assessed by nitroxide and superoxide anion production, 5′-nucleotidase activity and pinocytosis. Increased inflammatory reactions were not followed by the enhancement of angiogenic potential as assessed by Vascular Endothelial Growth Factor mRNA expression. Phases of macrophage activity corresponded to the stages of tumor growth characterized by high proliferative potential. The appearance and further development of necrotic tissue inside the tumor did not coincide with changes in macrophage behavior and therefore indirectly indicated that activation of macrophages was a reaction mostly to the signals produced by live tumor cells.
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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 peripheral blood. Peritoneal macrophages in pre-adult transgenic mice exhibited elevated mitotic activity and, after tritiated thymidine labeling, a more rapid accumulation of labeled progeny. The increase in peritoneal macrophage cell numbers appears, therefore, to be based on a GM-CSF-induced increase in local proliferative activity by peritoneal macrophages. This increased activity declined at the age of 8-10 wk, in parallel with a change in the morphology of the transgenic macrophages and an increase in binucleate and multinucleate macrophages arising by cell fusion. This change in macrophage phenotype was restricted to the transgenic mice and may therefore be a consequence of continued overstimulation by GM-CSF.
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Hamilton, JA, G. Vairo, KR Knight, and BG Cocks. "Activation and proliferation signals in murine macrophages. Biochemical signals controlling the regulation of macrophage urokinase-type plasminogen activator activity by colony-stimulating factors and other agents." Blood 77, no. 3 (1991): 616–27. http://dx.doi.org/10.1182/blood.v77.3.616.616.
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Abstract Purified hematopoietic growth factors such as colony-stimulating factor- 1 (CSF-1) or macrophage CSF, granulocyte-macrophage CSF, and interleukin-3 or multi-CSF, stimulate the urokinase-type plasminogen activator (u-PA) activity of murine bone marrow-derived macrophages (BMM) and resident peritoneal macrophages. Granulocyte-CSF was inactive. The increases in BMM u-PA activity were inhibited by the glucocorticoid dexamethasone, and by agents that raise intracellular cyclic adenosine monophosphate levels, including prostaglandin E2 and cholera toxin. These changes in u-PA activity were paralleled by corresponding changes in u-PA mRNA levels. Evidence was obtained for protein kinase C and phospholipase C-mediated stimulation of BMM u-PA activity and mRNA levels; however, no evidence was found for an involvement of Na+/H+ exchange or Na+, K(+)-ATPase activity, Ca2+ fluxes, or pertussis toxin-sensitive G proteins. Several findings point to a dissociation between macrophage u-PA expression and DNA synthesis.
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Hamilton, JA, G. Vairo, KR Knight, and BG Cocks. "Activation and proliferation signals in murine macrophages. Biochemical signals controlling the regulation of macrophage urokinase-type plasminogen activator activity by colony-stimulating factors and other agents." Blood 77, no. 3 (1991): 616–27. http://dx.doi.org/10.1182/blood.v77.3.616.bloodjournal773616.
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Purified hematopoietic growth factors such as colony-stimulating factor- 1 (CSF-1) or macrophage CSF, granulocyte-macrophage CSF, and interleukin-3 or multi-CSF, stimulate the urokinase-type plasminogen activator (u-PA) activity of murine bone marrow-derived macrophages (BMM) and resident peritoneal macrophages. Granulocyte-CSF was inactive. The increases in BMM u-PA activity were inhibited by the glucocorticoid dexamethasone, and by agents that raise intracellular cyclic adenosine monophosphate levels, including prostaglandin E2 and cholera toxin. These changes in u-PA activity were paralleled by corresponding changes in u-PA mRNA levels. Evidence was obtained for protein kinase C and phospholipase C-mediated stimulation of BMM u-PA activity and mRNA levels; however, no evidence was found for an involvement of Na+/H+ exchange or Na+, K(+)-ATPase activity, Ca2+ fluxes, or pertussis toxin-sensitive G proteins. Several findings point to a dissociation between macrophage u-PA expression and DNA synthesis.
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Eljaszewicz, Andrzej, Lidia Gackowska, Izabela Kubiszewska, et al. "Macrophage activity in tumour development." Współczesna Onkologia 1 (2010): 1–6. http://dx.doi.org/10.5114/wo.2010.971.
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MIWA, Misao, Zwe-Ling KONG, Kazuki SHINOHARA, and Michiko WATANABE. "Macrophage stimulating activity of foods." Agricultural and Biological Chemistry 54, no. 7 (1990): 1863–66. http://dx.doi.org/10.1271/bbb1961.54.1863.
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Miwa, Misao, Zwe-Ling Kong, Kazuki Shinohara, and Michiko Watanabe. "Macrophage Stimulating Activity of Foods." Agricultural and Biological Chemistry 54, no. 7 (1990): 1863–66. http://dx.doi.org/10.1080/00021369.1990.10870220.
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Devaraj, Sridevi, and Ishwarlal Jialal. "Validation of the Circulating Monocyte Being Representative of the Cholesterol-Loaded Macrophage: Biomediator Activity." Archives of Pathology & Laboratory Medicine 132, no. 9 (2008): 1432–35. http://dx.doi.org/10.5858/2008-132-1432-votcmb.
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Abstract Context.—Inflammation is pivotal to atherosclerosis. The monocyte-macrophage, a crucial cell in atherogenesis, is present during all stages of atherosclerosis. However, there is a paucity of data comparing circulating monocytes to cholesterol-laden macrophages (foam cells), with regard to their atherogenic properties, especially in subjects with established risk factors such as hyperlipidemia. Objective.—To determine whether the circulating blood monocyte is representative of the cholesterol-loaded macrophage with regard to its proatherogenicity in healthy controls and hyperlipidemic patients. Design.—Fasting blood was drawn from 32 subjects (n = 16 controls and n = 16 hyperlipidemic patients), and peripheral blood monocytes were obtained. Also, macrophages were cultured and loaded with acetyl low-density lipoprotein on day 10. Day 1 peripheral blood monocytes and day 11 cholesterol-loaded macrophages were assessed for release of superoxide anion and cytokines (interleukin 1, interleukin 6, tumor necrosis factor α); surface expression of CD11b, VLA-4, and CD40; and adhesion to human endothelium. Results.—Monocyte and cholesterol-loaded macrophage superoxide anion release, cytokines, and adhesion of monocytes to human endothelium were significantly increased in hyperlipidemic patients compared with controls. Furthermore, following cholesterol loading, there were no significant differences in monocyte versus cholesterol-loaded macrophage activity (P = .71). Also, CD14 and CD11b surface expression on monocytes was significantly increased in hyperlipidemic patients as compared with controls. The magnitude of change in the monocytes versus cholesterol-loaded macrophages was similar. Conclusions.—From these studies, we can conclude that the monocyte, which is readily accessible, is an appropriate cell to study for modulation of proatherogenic activity, especially with regard to genomic and proteomic analyses/ microarrays.
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Kubelka, C. F., A. Ruppel, P. H. Krammer, and D. Gemsa. "Killing of schistosomula of Schistosoma mansoni by macrophages: induction by T-cell clone-derived lymphokines and interferon-gamma." Parasitology 92, no. 2 (1986): 325–36. http://dx.doi.org/10.1017/s003118200006409x.
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SUMMARYThe induction of schistosomulicidal activity of peritoneal macrophages by concanavalin A-stimulated supernatants from long-term T-cell clones and by interferon-gamma (IFN-γ) was investigated in detail. Optimal conditions of in vitro macrophage activation by T-cell clone supernatants were established. Macrophages from 13-week S. mansoni-infected mice responded to lymphokine activation as well as resident mnacrophages from uninfecteci mice. IFN-γ was shown to play an essential role in induction of schistosomulicidal macrophage activity: recombinant IFN-γ at high concentration could induce schistosomula killing, and an anti-IFN-γ antiserum inhibited the induction ofschistosomulicidal activity by T-cell clone supernatants. Our data also indicate that macrophage activation could be obtained by IFN-γ in synergy with other lymphokines in the supernatant of long-term T-cell clones. Macrophages from mice injected with T-cell clone supernatants were primed in vivo and triggered to kill schistosomula in vitro in the presence of lipopolysaccharide (LPS). The data demonstrate that lymphokines produced by T-cell clones and, in particular, IFN-γ can participate in the activation of schistosomulicidal macrophages.
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Figueroa, Florencia, Gisela Mendoza, Darío Cardozo, Fabián Mohamed, Liliana Oliveros, and Myriam Forneris. "Sympathetic innervation regulates macrophage activity in rats with polycystic ovary." Journal of Endocrinology 238, no. 1 (2018): 33–45. http://dx.doi.org/10.1530/joe-17-0736.
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Polycystic ovarian syndrome (PCOS) is a low-grade inflammatory disease characterized by hyperandrogenism and ovarian hyperinnervation. The aim of this work is to investigate whether in vivo bilateral superior ovarian nerve (SON) section in adult rats with estradiol valerate-induced PCOS (PCO rats) affects macrophage spleen cells (MФ) and modifies the steroidogenic ability of their secretions. Culture media of MФ from PCO rats and PCO rats with SON section (PCO-SON rats) were used to stimulate in vitro intact ovaries. Compared with macrophages PCO, macrophages from PCO-SON rats released less tumor necrosis factor-α and nitric oxide, expressed lower Bax and Nfkb mRNA and showed reduced TUNEL staining. Also, in PCO rats, the SON section decreased kisspeptin and nerve growth factor mRNA expressions, without changes in Trka receptor mRNA levels. Macrophage secretions from PCO-SON rats decreased androstenedione and stimulated progesterone release in PCO ovaries, compared to macrophage secretions from PCO rats. No changes were observed in ovarian estradiol response. These findings emphasize the importance of the SON in spleen MΦ, since its manipulation leads to secondary modifications of immunological and neural mediators, which might influence ovarian steroidogenesis. In PCO ovaries, the reduction of androstenedione and the improvement of progesterone release induced by PCO-SON MΦ secretion, might be beneficial considering the hormonal anomalies characteristic of PCOS. We present functional evidence that modulation of the immune-endocrine function by peripheral sympathetic nervous system might have implications for understanding the pathophysiology of PCOS.
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Li, Cong, Xiao Yan Ding, Dong Mei Xiang, et al. "Enhanced M1 and Impaired M2 Macrophage Polarization and Reduced Mitochondrial Biogenesis via Inhibition of AMP Kinase in Chronic Kidney Disease." Cellular Physiology and Biochemistry 36, no. 1 (2015): 358–72. http://dx.doi.org/10.1159/000430106.
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Background: Macrophage polarization plays a pivotal role in the process of inflammation which is common in chronic kidney disease (CKD). Macrophages polarization under the condition of CKD remains poorly understood. Here we tested the hypothesis that CKD promotes macrophage M1 polarization. Methods: A rat model of CKD was established by reduced renal mass (RRM). Polarization of macrophages was induced in ex vivo macrophages from RRM rats and cultured ones under the condition of uremic serum. The markers were evaluated by RT-PCR, western blot, and flow cytometer. Results: Our data showed that macrophages from RRM rats displayed enhanced M1 and impaired M2 polarization as revealed by increased M1 markers (tumor necrosis factor α, IL-6, IL-12p40, nitric oxide) and decreased M2 markers (IL-10, CD206, arginase activity) in response to LPS and IL-4 induction, respectively. Treatment with uremic sera in peritoneal and bone marrow derived macrophages from normal rats led to similar results. Moreover, macrophages from RRM rats and cultured under the condition of uremic sera had reduced mitochondrial biogenesis. The disturbed macrophage polarization and mitochondrial biogenesis were accompanied by reduced activity of adenosine monophosphate-activated protein (AMP)-activated kinase (AMPK). Enhancing activation of AMPK restored mitochondrial biogenesis and M2 macrophage polarization. Conclusion: These observations suggest that CKD disturbs macrophage polarization and mitochondrial biogenesis through inhibition of AMPK. This might provide a novel therapeutic strategy for intervention of chronic inflammation in CKD.
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Pervin, Munmun, Mohammad Rabiul Karim, Mizuki Kuramochi, Takeshi Izawa, Mitsuru Kuwamura, and Jyoji Yamate. "Macrophage Populations and Expression of Regulatory Inflammatory Factors in Hepatic Macrophage-depleted Rat Livers under Lipopolysaccharide (LPS) Treatment." Toxicologic Pathology 46, no. 5 (2018): 540–52. http://dx.doi.org/10.1177/0192623318776898.
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To investigate the significance of the appearance of hepatic macrophages and expression of inflammatory factors in normal and macrophage-depleted livers, hepatic macrophages were depleted with liposome (Lipo)-encapsulated clodronate (CLD; 50 mg/kg, i.v.) followed by lipopolysaccharide (LPS) administration (0.1 mg/kg, i.p.) in F344 rats (CLD + LPS). Vehicle control rats (Lipo + LPS) received empty-Lipo before LPS. The low dose of LPS did not result in microscopic changes in the liver in either treatment group but did modulate M1 and M2 macrophage activity in Lipo + LPS rats without altering repopulating hepatic macrophages in CLD + LPS rats. LPS treatment in Lipo + LPS rats dramatically increased the M1 (IL-1β, IL-6, TNF-α, and MCP-1) but not M2 macrophage-related factors (IL-4 and CSF-1) compared to CLD + LPS rats. In the CLD + LPS rats, the M2 macrophage-related factors IL-4 and CSF-1 were elevated. In conclusion, low-dose LPS activated hepatic macrophages in rat livers without causing liver injury or stimulating repopulating hepatic macrophages. These data suggest that LPS may alter the liver microenvironment by modulating M1 or M2 macrophage-related inflammatory mediators and macrophage-based hepatotoxicity.
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Smith, Monica R., Theodore J. Standiford, and Raju C. Reddy. "PPARs in Alveolar Macrophage Biology." PPAR Research 2007 (2007): 1–12. http://dx.doi.org/10.1155/2007/23812.
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PPARs, most notably PPAR-γ, play a crucial role in regulating the activation of alveolar macrophages, which in turn occupy a pivotal place in the immune response to pathogens and particulates drawn in with inspired air. In this review, we describe the dual role of the alveolar macrophage as both a first-line defender through its phagocytotic activity and a regulator of the immune response. Depending on its state of activation, the alveolar macrophage may either enhance or suppress different aspects of immune function in the lung. We then review the role of PPAR-γand its ligands in deactivating alveolar macrophages—thus limiting the inflammatory response that, if unchecked, could threaten the essential respiratory function of the alveolus—while upregulating the cell's phagocytotic activity. Finally, we examine the role that inadequate or inappropriate PPAR-γresponses play in specific lung diseases.
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Cabrales, Pedro, Corey Carter, Bryan Oronsky та Tony Reid. "Rrx-001 Is a Phase 3 Small Molecule Dual Inhibitor of CD47 and Sirpα with Activity in Multiple Myeloma". Blood 132, Supplement 1 (2018): 5623. http://dx.doi.org/10.1182/blood-2018-99-116947.
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Abstract Background: CD47 binds to SIRPα on the surface of macrophages delivering a "do not eat" signal to suppress phagocytosis. To evade macrophage-mediated destruction, CD47 is frequently overexpressed in cancers, including multiple myeloma (MM). CD47 inhibition is an area of intense therapeutic interest with three anti-CD47 monoclonal antibodies (mAbs) currently in clinical trials. However, these mAbs have been associated with severe hematologic toxicities. RRx-001 is a minimally toxic small molecule that dually downregulates CD47 on tumor cells and SIRPα on macrophages and triggers tumor associated macrophage phagocytosis of tumor cells in vitro and in vivo. RRx-001 is entering Phase 3 trials for the treatment of multiple cancer indications. Methods: The effect of RRx-001 on the expression of CD47 and SIRPα on macrophages was evaluated with Western blotting and flow cytometry. An in vitro phagocytotic assay was used to determine whether RRx-001 promoted engulfment of multiple myeloma cells by macrophages. Transcriptional mRNA profiling in murine tumor associated macrophages (TAMs) was performed to analyze the cytokine profile of TAMs in the presence or absence of RRx-001. Finally, myeloma bearing mice were treated with RRx-001 in the presence or absence or absence of clodronate to determine the effect of macrophage depletion on RRx-001 anticancer activity. Results: RRx-001 was shown to downregulate CD47 and SIRPα expression on tumor cells and macrophages, respectively, and to promote the phagocytosis of multiple myeloma tumor cells. RRx-001 also stimulated the production of pro-inflammatory cytokines in TAMs. In tumor bearing mice, depletion of macrophages by clodronate reduced the antitumor effects of RRx-001. Conclusions: RRx-001 is a Phase 3-ready small molecule innate immune checkpoint inhibitor, which triggers tumor associated macrophage phagocytosis of high-expressing CD47 tumor cells. Dual downregulation of CD47 and SIRPα by RRx-001 results in TAM repolarization and phagocytosis of tumor cells. Depletion of macrophages by clodronate in tumor-bearing mice reduced the antitumor effects of RRx-001 and further suggests that the target of RRx-001 is the macrophage. Disclosures Cabrales: EpicentRx Inc: Research Funding. Carter:EpicentRx Inc: Employment. Oronsky:EpicentRx Inc: Employment. Reid:EpicentRx Inc: Employment.
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Tsubota, Maho, Tomoyoshi Miyamoto, Saki Hiruma, et al. "Repeated Cold Stress Reduces Cyclophosphamide-Induced Cystitis/Bladder Pain and Macrophage Activity in Mice." Pharmacology 99, no. 5-6 (2017): 286–90. http://dx.doi.org/10.1159/000461588.
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We examined the effect of repeated cold (RC) stress on cyclophosphamide (CPA)-induced cystitis/bladder pain in mice, in relation to macrophage activity. CPA, given i.p. at 400 mg/kg, caused bladder pain symptoms accompanying cystitis in both unstressed and RC-stressed mice, which were prevented by the macrophage inhibitor minocycline. A low dose, that is, 200 mg/kg, of CPA still produced bladder pain symptoms in unstressed but not RC-stressed mice. Lipopolysaccharide-induced cytokine production in peritoneal macrophages from RC-stressed mice was less than that from unstressed mice. Thus, RC stress appears to reduce CPA-induced bladder pain in mice, which may be associated with the decreased macrophage activity.
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Singh, Gyanesh, U. C. Pachouri, Chirag Chopra, Preeti Bajaj, and Pushplata Singh. "Macrophage Gene Therapy: opening novel therapeutic avenues for immune disorders." F1000Research 4 (August 6, 2015): 495. http://dx.doi.org/10.12688/f1000research.6817.1.
Full textAbstract:
Macrophages are probably the most important cells of the mammalian immune system, and compromised macrophage function is known to cause several diseases. Their involvement in arthritis, cancer, infections, atherosclerosis, diabetes, and autoimmune disorders is well known. There has been a constantly growing need to transfer therapeutic genes into macrophages. Like most non-macrophage gene therapies,in vitrogene transfer has been attempted much more frequently in case of macrophages. However, primary macrophages are still somewhat recalcitrant to transfection. Macrophage-specific synthetic promoters, which were recently used successfully, can have up to 100-fold higher activity than that of native promoters. Adenovirus, lentivirus, and adeno-associated virus are commonly used for macrophage gene therapy. A number of non-viral methods are also popular for the transfer of exogenous DNA into macrophages. Gene transfer to macrophages using naked DNA has also been successful in a few cases. Macrophages have specific mechanisms to recognize and respond to bacterial DNA because of the presence of unmethylated CpG dinucleotides, which are rare in eukaryotic DNA. With interesting developments in this area, macrophage gene therapy appears to have great potential for immune therapies.
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Martins, Flávia, Rosa Oliveira, Bruno Cavadas, et al. "Hypoxia and Macrophages Act in Concert Towards a Beneficial Outcome in Colon Cancer." Cancers 12, no. 4 (2020): 818. http://dx.doi.org/10.3390/cancers12040818.
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In colon cancer, the prognostic value of macrophages is controversial, and it is still unknown how hypoxia modulates macrophage–cancer cell crosstalk. To unravel this, co-cultures of human primary macrophages and colon cancer cells were performed at 20% and 1% O2, followed by characterization of both cellular components. Different colon cancer patient cohorts were analyzed for hypoxia and immune markers, and their association with patient overall survival was established. A positive correlation between HIF1A and CD68 in colon cancer patients was identified but, unexpectedly, in cases with higher macrophage infiltration, HIF1A expression was associated with a better prognosis, in contrast to breast, gastric, and lung cancers. Under hypoxia, co-cultures’ secretome indicated a shift towards a pro-inflammatory phenotype. These alterations occurred along with increased macrophage phagocytic activity and decreased SIRPα expression. Cancer cells were more invasive and exhibited higher CD47 expression. We hypothesize that the better prognosis associated with HIF1AHighCD68High tumors could occur due to macrophagic pro-inflammatory pressure. Indeed, we found that tumors HIF1AHighCD68High expressed increased levels of CD8A, which is positively correlated with HIF1A. In conclusion, we show that in colon cancer, hypoxia drives macrophages into a pro-inflammatory phenotype, concomitant with increased infiltration of anti-tumor immune cells, favoring better disease outcome.
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Reddy, Raju C. "Immunomodulatory Role of PPAR-γ in Alveolar Macrophages". Journal of Investigative Medicine 56, № 2 (2008): 522–27. http://dx.doi.org/10.2310/jim.0b013e3181659972.
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The lung is constantly exposed to inhaled pathogens and toxins yet totally dependent on the integrity of a delicate alveolar-capillary interface for its function. Much of the balance between protection and collateral damage rests on the alveolar macrophage, which not only phagocytoses inhaled particles but also modulates the activity of both innate and acquired immune systems to limit unnecessary or exuberant inflammation. In its resting state, the alveolar macrophage secretes anti-inflammatory mediators while limiting antigen presentation to the adaptive immune system. The alveolar macrophage's state of activation is regulated by a variety of factors, including the activity of the nuclear receptor peroxisome proliferator-activated receptor γ (PPAR-γ). Peroxisome proliferator-activated receptor γ agonists reduce the ability of inflammatory stimuli to activate the alveolar macrophage while simultaneously stimulating phagocytosis of both opsonized and unopsonized particles, via the Fcγ and CD36 receptors, respectively. All known endogenous PPAR-γ ligands are fatty acid derivatives, and macrophage-specific knockout of the enzyme that converts esterified fatty acids to free fatty acids results in severe lung inflammation. Peroxisome proliferator-activated receptor γ expression is reduced in alveolar macrophages from patients with pulmonary sarcoidosis and alveolar proteinosis, suggesting that the deficiency may play a role in pathogenesis of these diseases. In summary, these observations point to PPAR-γ in the context of the alveolar macrophage as a crucial factor in limiting excessive and possibly injurious inflammation in the lung.
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Wahdaningsih, Sri, Subagus Wahyuono, Sugeng Riyanto, and Retno Murwanti. "In vitro Test of Macrophage Phagocytic Activity of Extracts and Fractions of Red Dragon Fruit Peel [Hylocereus polyrhizus (F.A.C.Weber) Britton and Rose]." Dhaka University Journal of Pharmaceutical Sciences 17, no. 2 (2018): 161–65. http://dx.doi.org/10.3329/dujps.v17i2.39171.
Full textAbstract:
The peel of red dragon fruit [Hylocereus polyrhizus (F.A.C.Weber) Britton and Rose] can be used to treat various diseases and to improve immune system of body. This study was aimed to investigate the in vitro macrophage phagocytic activity of extracts and fractions of red dragon fruit peel (Hylocereus polyrhizus). The in vitro test was conducted based on the method of Leijh et al. The parameters of phagocytic activity were based on the macrophages capacity to phagocytose latex beads using the calculation of phagocytic capacity and phagocytic index. The test results indicated significant difference (p < 0.05). The petroleum benzene extract showed higher phagocytic activity of macrophages than methanol extract of the fruit peel, sediment, and media control (-). The LSD test showed that macrophage phagocytic activity using fractions (500 and 100 μg/ml) was significantly different from macrophage phagocytic activity using fractions (20 μg/ml), sediment (500, 100 and 20 μg/ml), extracts (500, 100 and 20 μg/ml), and media control.
 Dhaka Univ. J. Pharm. Sci. 17(2): 161-165, 2018 (December)
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Muschter, Dominique, Anna-Sophie Beiderbeck, Tanja Späth, Christian Kirschneck, Agnes Schröder, and Susanne Grässel. "Sensory Neuropeptides and their Receptors Participate in Mechano-Regulation of Murine Macrophages." International Journal of Molecular Sciences 20, no. 3 (2019): 503. http://dx.doi.org/10.3390/ijms20030503.
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This study aimed to analyze if the sensory neuropeptide SP (SP) and the neurokinin receptor 1 (NK1R) are involved in macrophage mechano-transduction, similar to chondrocytes, and if alpha-calcitonin gene-related peptide (αCGRP) and the CGRP receptor (CRLR/Ramp1) show comparable activity. Murine RAW264.7 macrophages were subjected to a cyclic stretch for 1–3 days and 4 h/day. Loading and neuropeptide effects were analyzed for gene and protein expression of neuropeptides and their receptors, adhesion, apoptosis, proliferation and ROS activity. Murine bone marrow-derived macrophages (BMM) were isolated after surgical osteoarthritis (OA) induction and proliferation, apoptosis and osteoclastogenesis were analyzed in response to loading. Loading induced NK1R and CRLR/Ramp1 gene expression and altered protein expression in RAW264.7 macrophages. SP protein and mRNA level decreased after loading whereas αCGRP mRNA expression was stabilized. SP reduced adhesion in loaded RAW264.7 macrophages and both neuropeptides initially increased the ROS activity followed by a time-dependent suppression. OA induction sensitized BMM to caspase 3/7 mediated apoptosis after loading. Both sensory neuropeptides, SP and αCGRP, and their receptors are involved in murine macrophage mechano-transduction affecting neuropeptide impact on adhesion and ROS activity. OA induction altered BMM apoptosis in response to loading indicate that OA-associated biomechanical alterations might affect the macrophage population.