Relevant bibliographies by topics / Macrophage

Academic literature on the topic 'Macrophage'

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Published: 4 June 2021
Last updated: 7 July 2024

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Journal articles on the topic "Macrophage"

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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 (July 1, 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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Liu, Shuangqing, Huilei Zhang, Yanan Li, Yana Zhang, Yangyang Bian, Yanqiong Zeng, Xiaohan Yao, et al. "S100A4 enhances protumor macrophage polarization by control of PPAR-γ-dependent induction of fatty acid oxidation." Journal for ImmunoTherapy of Cancer 9, no. 6 (June 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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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 (August 24, 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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Pedicillo, Maria Carmela, Ilenia Sara De Stefano, Rosanna Zamparese, Raffaele Barile, Mario Meccariello, Alessio Agostinone, Giuliana Villani, et al. "The Role of Toll-like Receptor-4 in Macrophage Imbalance in Lethal COVID-19 Lung Disease, and Its Correlation with Galectin-3." International Journal of Molecular Sciences 24, no. 17 (August 26, 2023): 13259. http://dx.doi.org/10.3390/ijms241713259.

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To the current data, there have been 6,955,141 COVID-19-related deaths worldwide, reported to WHO. Toll-like receptors (TLRs) implicated in bacterial and virus sensing could be a crosstalk between activation of persistent innate-immune inflammation, and macrophage’s sub-population alterations, implicated in cytokine storm, macrophage over-activation syndrome, unresolved Acute Respiratory Disease Syndrome (ARDS), and death. The aim of this study is to demonstrate the association between Toll-like-receptor-4 (TLR-4)-induced inflammation and macrophage imbalance in the lung inflammatory infiltrate of lethal COVID-19 disease. Twenty-five cases of autopsy lung tissues were studied by digital pathology-based immunohistochemistry to evaluate expression levels of TLR-4 (CD 284), pan-macrophage marker CD68 (clone KP1), sub-population marker related to alveolar macrophage Galectin-3 (GAL-3) (clone 9C4), and myeloid derived CD163 (clone MRQ-26), respectively. SARS-CoV-2 viral persistence has been evaluated by in situ hybridation (ISH) method. This study showed TLR-4 up-regulation in a subgroup of patients, increased macrophage infiltration in both Spike-1(+) and Spike-1(−) lungs (p < 0.0001), and a macrophage shift with important down-regulation of GAL-3(+) alveolar macrophages associated with Spike-1 persistence (p < 0.05), in favor of CD163(+) myeloid derived monocyte-macrophages. Data show that TLR-4 expression induces a persistent activation of the inflammation, with inefficient resolution, and pathological macrophage shift, thus explaining one of the mechanisms of lethal COVID-19.
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Fahey, T. J., K. J. Tracey, P. Tekamp-Olson, L. S. Cousens, W. G. Jones, G. T. Shires, A. Cerami, and B. Sherry. "Macrophage inflammatory protein 1 modulates macrophage function." Journal of Immunology 148, no. 9 (May 1, 1992): 2764–69. http://dx.doi.org/10.4049/jimmunol.148.9.2764.

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Abstract Macrophage inflammatory protein 1 (MIP 1), initially purified from the conditioned medium of endotoxin-stimulated macrophages, is a low m.w. heparin-binding protein doublet comprising two peptides, MIP 1 alpha and MIP 1 beta. Although native doublet MIP 1 has previously been shown to exert pyrogenic, mitogenic, and proinflammatory effects on other cell types, its actions on its cell of origin, the macrophage, have not been well catalogued. Our study reports several aspects of macrophage function that are modulated by MIP 1. MIP 1 was not directly cytotoxic for WEHI tumor cells, but MIP 1-treated macrophage exhibited enhanced antibody-independent macrophage cytotoxicity for tumor targets. MIP 1 treatment stimulated proliferation of mature tissue macrophages, and this effect was enhanced upon costimulations with either CSF-1 or granulocyte-macrophage-CSF. Thioglycollate-elicited peritoneal exudate macrophages incubated with native doublet MIP 1-secreted bioactive TNF and IL-6, as well as immunoreactive IL-1 alpha, and these effects were enhanced significantly when the cells were costimulated with IFN-gamma. Purified preparations of the recombinantly derived MIP 1 alpha peptide alone stimulated the secretion of TNF, IL-1 alpha, and IL-6 by peritoneal macrophages, but MIP 1 beta did not. In fact, as little as eightfold excess MIP 1 beta blocked TNF-induction by MIP 1 alpha to a significant degree. By contrast to these apparent "macrophage activating" properties of MIP 1, the cytokine failed to trigger the macrophage oxidative burst, or to up-regulate the expression of Ia on the macrophage surface. Taken together, these data reveal that MIP 1 peptides act as autocrine modulators of their cells of origin, and raise the possibility that MIP 1 peptides may play a role in modulating macrophage responses to inflammatory stimuli in vivo.
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Xu, Jiawei, Lanya Fu, Junyao Deng, Jiaqi Zhang, Ying Zou, Liqiang Liao, Xinrui Ma, et al. "miR-301a Deficiency Attenuates the Macrophage Migration and Phagocytosis through YY1/CXCR4 Pathway." Cells 11, no. 24 (December 7, 2022): 3952. http://dx.doi.org/10.3390/cells11243952.

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(1) Background: the miR-301a is well known involving the proliferation and migration of tumor cells. However, the role of miR-301a in the migration and phagocytosis of macrophages is still unclear. (2) Methods: sciatic nerve injury, liver injury models, as well as primary macrophage cultures were prepared from the miR-301a knockout (KO) and wild type (WT) mice to assess the macrophage’s migration and phagocytosis capabilities. Targetscan database analysis, Western blotting, siRNA transfection, and CXCR4 inhibition or activation were performed to reveal miR301a’s potential mechanism. (3) Results: the macrophage’s migration and phagocytosis were significantly attenuated by the miR-301a KO both in vivo and in vitro. MiR-301a can target Yin-Yang 1 (YY1), and miR-301a KO resulted in YY1 up-regulation and CXCR4 (YY1′s down-stream molecule) down-regulation. siYY1 increased the expression of CXCR4 and enhanced migration and phagocytosis in KO macrophages. Meanwhile, a CXCR4 inhibitor or agonist could attenuate or accelerate, respectively, the macrophage migration and phagocytosis. (4) Conclusions: current findings indicated that miR-301a plays important roles in a macrophage’s capabilities of migration and phagocytosis through the YY1/CXCR4 pathway. Hence, miR-301a might be a promising therapeutic candidate for inflammatory diseases by adjusting macrophage bio-functions.
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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 (May 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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McKenzie, C. G. J., U. Koser, L. E. Lewis, J. M. Bain, H. M. Mora-Montes, R. N. Barker, N. A. R. Gow, and L. P. Erwig. "Contribution of Candida albicans Cell Wall Components to Recognition by and Escape from Murine Macrophages." Infection and Immunity 78, no. 4 (February 1, 2010): 1650–58. http://dx.doi.org/10.1128/iai.00001-10.

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ABSTRACT The pathogenicity of the opportunistic human fungal pathogen Candida albicans depends on its ability to escape destruction by the host immune system. Using mutant strains that are defective in cell surface glycosylation, cell wall protein synthesis, and yeast-hypha morphogenesis, we have investigated three important aspects of C. albicans innate immune interactions: phagocytosis by primary macrophages and macrophage cell lines, hyphal formation within macrophage phagosomes, and the ability to escape from and kill macrophages. We show that cell wall glycosylation is critically important for the recognition and ingestion of C. albicans by macrophages. Phagocytosis was significantly reduced for mutants deficient in phosphomannan biosynthesis (mmn4Δ, pmr1Δ, and mnt3 mnt5Δ), whereas O- and N-linked mannan defects (mnt1Δ mnt2Δ and mns1Δ) were associated with increased ingestion, compared to the parent wild-type strains and genetically complemented controls. In contrast, macrophage uptake of mutants deficient in cell wall proteins such as adhesins (ece1Δ, hwp1Δ, and als3Δ) and yeast-locked mutants (clb2Δ, hgc1Δ, cph1Δ, efg1Δ, and efg1Δ cph1Δ), was similar to that observed for wild-type C. albicans. Killing of macrophages was abrogated in hypha-deficient strains, significantly reduced in all glycosylation mutants, and comparable to wild type in cell wall protein mutants. The diminished ability of glycosylation mutants to kill macrophages was not a consequence of impaired hyphal formation within macrophage phagosomes. Therefore, cell wall composition and the ability to undergo yeast-hypha morphogenesis are critical determinants of the macrophage's ability to ingest and process C. albicans.
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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 (September 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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Dende, Chaitanya, Mihir Pendse, Daniel Propheter, Gabriella Quinn, and Lora V. Hooper. "Vitamin A regulates phagocytosis by resident macrophages of the small intestine." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 113.23. http://dx.doi.org/10.4049/jimmunol.208.supp.113.23.

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Abstract Intestinal Tim4+ CD4+ macrophages are a distinctive macrophage subset that express Tim4, a receptor for phosphatidylserine on dying apoptotic cells, Unlike other macrophage subsets, they do not depend on blood monocytes for their turnover, instead self-maintained in the small intestine. The signal(s) responsible for the self-maintenance and function of Tim4+ CD4+ macrophages is not known. We have discovered that maintenance of the gut resident Tim4+ CD4+ macrophage population depends on dietary vitamin A and its derivative retinoic acid (RA). Retinoic acid receptors, which direct RA-dependent transcription, were required for maintenance of Tim4+ CD4+ macrophages. Chemical blockade of retinoic acid receptor (RAR) signaling and macrophage-specific genetic inactivation of RARs in mice further revealed that macrophage-intrinsic RARα signaling was required for Timd4 expression and maintenance of Tim4+ CD4+ macrophages. Macrophage RARα signaling was furthermore essential for phagocytosis by Tim4+ CD4+ macrophages. Ongoing studies are examining the role of Tim4+ CD4+ macrophages and vitamin A in the clearance of apoptotic intestinal epithelial cells. Our findings reveal that vitamin A provides an essential dietary signal for the maintenance and function of a gut resident macrophage subset. Supported by Welch foundation grant I-1874
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Dissertations / Theses on the topic "Macrophage"

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Svensson, Ulf. "Macrophage activation by bacteria signalling to prostaglandin and cytokine responses /." Lund : Dept. of Medical & Physiological Chemistry, Lund University, 1994. http://books.google.com/books?id=sAhrAAAAMAAJ.

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Higuera, González Laura 1993. "Novel transcription regulators of tissue macrophages and alternative macrophage polarization." Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2021. http://hdl.handle.net/10803/672702.

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Macrophages play crucial roles in the defense of the organism against a wide range of pathogens. Macrophages can rapidly adapt to perturbations in the microenvironment due to the existence of a network of transcription factors that modulates their responses. While transcription factors that regulate macrophage identity have been widely described in the past decades, the role of transcription regulators that fine-tune tissue macrophage responses in homeostasis and infection is starting to be elucidated. Our group has previously identified transcription regulators of pro-inflammatory macrophage responses, and in the present work we have explored the function of novel transcription mechanisms that participate in the regulation of the homeostatic distribution of tissue macrophages and in anti-inflammatory macrophage responses. We have studied ontogenically different macrophage populations inhabiting different tissues and have characterized their transcription regulation. We have also compared the anti-inflammatory response of tissue macrophages and identified a specific transcriptional control of anti-inflammatory gene expression that depends on their ontogeny.
Los macrófagos juegan un papel muy importante en la defensa del organismo frente a una amplia variedad de patógenos. Los macrófagos se adaptan rápidamente a las perturbaciones en el microambiente gracias a que existe una compleja red de factores de transcripción que modulan sus respuestas. En los últimos años se han identificado factores de transcripción que regulan la identidad de los macrófagos, sin embargo, apenas se está comenzando a conocer la importancia de otros factores de transcripción que permiten adaptar la respuesta de los macrófagos, tanto en condiciones homeostáticas como frente a infecciones. Anteriormente nuestro grupo identificó reguladores transcripcionales de las respuestas pro-inflamatorias de los macrófagos, y en este trabajo hemos explorado la función de nuevos mecanismos reguladores que participan en la regulación de la distribución de los macrófagos en homeostasis, así como en las respuestas anti-inflamatorias de los macrófagos. Hemos estudiado poblaciones de macrófagos con diferentes ontogenias que habitan dentro de los tejidos y hemos caracterizado su regulación transcripcional. Además, hemos comparado la respuesta anti-inflamatoria de los diferentes macrófagos tisulares y así hemos identificado que existe un mecanismo transcripcional específico que controla la expresión de genes anti-inflamatorios según el origen del macrófago.
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Tabata, Yasuhiko. "Macrophage phagocytosis of polymer microspheres and antitumor activation of macrophages." Kyoto University, 1987. http://hdl.handle.net/2433/74704.

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Raborn, Erinn Shenee. "Cannabinoid Modulation of Chemotaxis of Macrophages and Macrophage-like Cells." VCU Scholars Compass, 2007. http://hdl.handle.net/10156/1333.

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Adler, Heiko. "Fetal bovine bone marrow-derived macrophages : a model for studying basic aspects of macrophage biology and pathogen-macrophage interaction in cattle /." [S.l.] : [s.n.], 1994. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Grand-Perret, Thierry A. R. "Induction d'une activité anti-tumorale chez les macrophages péritonéaux murins." Paris 11, 1986. http://www.theses.fr/1986PA112301.

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Di, Maggio Paula. "Dietary lipids and inflammation : chylomicron remnants suppress pro-inflammatory pathways and activate antioxidant defence mechanisms in human macrophages." Thesis, Royal Veterinary College (University of London), 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618287.

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Soe-Lin, Shan. "Macrophage iron recycling." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66717.

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In an absurd twist of nature, the physiological role of iron is paradoxical. Iron is the most abundant element found on Earth and yet is insoluble under physiological conditions. Furthermore, life is not possible without iron; iron is indispensible for life, as it is a vital co-factor for essential enzymes due to its unique redox abilities. And yet, high concentrations of iron lead to the formation of reactive oxygen species and are toxic. Consequently, living creatures have evolved ingenious strategies for acquiring and managing otherwise insoluble iron atoms, and for tightly regulating its levels within the organism. The majority of bodily iron in humans is contained within the red blood cell (RBC) mass, as a component of hemoglobin. RBCs become more damaged and less deformable as they age, and at the end of their 120 day lifespan, senescent RBCs are engulfed by macrophages of the reticuloendothelial system of the liver and spleen. These specialized macrophages ingest 2 million RBCs/sec, catabolize the hemoglobin, and release the iron contained within to plasma transferrin for reincorporation into new RBCs within the bone marrow. It is remarkable how reticuloendothelial macrophages safely manage the enormous quantities of iron which would otherwise prove toxic to other cells. In my studies, I have examined the specific aspects of iron metabolism within these iron-handling macrophages. Natural resistance-associated macrophage protein 1 (Nramp1) is a divalent metal transporter expressed only within the phagosomes of professional phagocytic cells such as macrophages and neutrophils. Nramp1 has since been found to be the gene responsible for conferring host resistance against intracellular pathogens. Mice deficient in Nramp1 have been found to be susceptible to infection with intracellular pathogens. Nramp1 is thought to confer protection by depleting the phagosome of divalent metals necessary for pathogen
La majorité du fer dans le corps humain est contenu dans la masse de globule rouge, en tant que composante de l'hémoglobine. Les GR deviennent plus endommagés et moins déformables en vieillissant, et à la fin de leurs durée de vie de 120 jours, les GR sénescents sont ingurgités par les macrophages du système réticuloendothélial du foie et de rate. Ces macrophages spécialisés ingèrent 2 millions de GR∕sec, catabolisent l'hémoglobine et relâche le fer qui y est contenu à la transferrine plasmatique pour permettre son réincorporation dans de nouveau GR dans la moelle épinière. C'est remarquable comment les macrophages réticuloendothéliaux gèrent de manière sécuritaire l'énorme quantité de fer qui serait sinon toxique pour les autres cellules. Dans mes recherches, j'ai examiné les aspects spécifiques du métabolisme du fer dans ces macrophages spécialisés dans sa manutention.La protéine associée à la résistance naturelle du macrophage (Nramp1) est un transporteur de métaux divalents exprimé seulement dans les phagosomes de cellules phagocytiques telle que les macrophages et les neutrophiles. Nramp1 a depuis été reconnu comme le gène responsable de conférer à l'hôte la résistance contre les pathogènes intracellulaires. Nramp 1 est présumé donner une protection en vidant le phagosome de métaux divalents nécessaires à la croissance de pathogènes.Au cours des recherches nous avons trouvé qu'en plus de jouer un rôle significatif dans la résistance de l'hôte, Nramp1 est aussi important pour la régularisation de l'homéostasie du fer. Nous avons remarqué que les macrophages sans Nramp1 sont incapables de recycler le fer (après l'erythrophagocytose in vitro) de manière aussi efficace que les macrophages qui ont le Nramp1 fonctionnel. On a ensuite observé les souris knockout et trouvé que les animaux sans Nramp1 ont une surdose progressive de fer en vieil
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Georges, George Tharwat. "Novel Characteristics of Murine Bone Marrow-Derived Macrophages and Human Macrophage-Like Cells." VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd/932.

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These studies provide evidence for novel properties of macrophages derived from bone marrow stem cells. In study 1, treatment of activated mouse bone marrow-derived macrophages (BMM) with either catecholamine synthesis inhibitors (α-methyl-para-tyrosine and fusaric acid) or the β2 adrenergic receptor antagonist ICI 118,551 demonstrated that BMM produce catecholamines. The catecholamines modulated macrophage cytokine production through autocrine actions on adrenergic receptors. In study II, undifferentiated human bone marrow cells were incubated in 30% mouse L929 fibroblast conditioned medium and generated adherent cells within three days. The cells were clearly identifiable as macrophages based on surface proteins and phagocytic activity but produced only low levels of the cytokines tumor necrosis factor-α and interleukin-lβ. Cytokine production did not increase in response to the bacterial endotoxin lipopolysaccharide (LPS). Generation of these macrophage-like cells was not repeatable with other samples of human bone marrow, but the cells continue to proliferate in cell culture and will be investigated further in future studies.
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Sobhani, Kimia. "Proteomic analysis of macrophage proinflammatory programmed cell death and macrophage activation /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8688.

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Books on the topic "Macrophage"

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Bernard, Burke, and Lewis Claire E, eds. The macrophage. 2nd ed. Oxford: Oxford University Press, 2002.

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E, Lewis Claire, and McGee J. O'D, eds. The Macrophage. Oxford: IRL Press at Oxford University Press, 1992.

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The human macrophage system: Activity and functional morphology. Basel: Karger, 1988.

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Röszer, Tamás. The M2 Macrophage. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50480-9.

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Clemens, Sorg, and Immunologische Tage. (1987 : Münster, West Germany), eds. The Alveolar macrophage. Münster: Regensberg & Biermann Wissenschaftliche Verlagsgellschaft, 1988.

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1943-, Zwilling Bruce S., and Eisenstein Toby K, eds. Macrophage-pathogen interactions. New York: M. Dekker, 1994.

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Gupta, Swati, and Yashwant V. Pathak, eds. Macrophage Targeted Delivery Systems. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-84164-5.

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Russell, Stephen W., and Siamon Gordon, eds. Macrophage Biology and Activation. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77377-8.

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Harris, James, and Eric F. Morand, eds. Macrophage Migration Inhibitory Factor. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-4939-9936-1.

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W, Russell Stephen, and Gordon Siamon, eds. Macrophage biology and activation. Berlin: Springer-Verlag, 1992.

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Book chapters on the topic "Macrophage"

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Kawauchi, Hideyuki. "Macrophage." In Nasal Physiology and Pathophysiology of Nasal Disorders, 77–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-37250-6_6.

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Chazaud, Bénédicte. "Macrophage." In Encyclopedia of Exercise Medicine in Health and Disease, 537–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_245.

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Gooch, Jan W. "Macrophage." In Encyclopedic Dictionary of Polymers, 906. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14168.

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Aribi, Mourad. "Macrophage Bactericidal Assays." In Macrophages, 135–49. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_14.

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Guidi-Rontani, C., and M. Mock. "Macrophage Interactions." In Current Topics in Microbiology and Immunology, 115–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-05767-4_6.

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Vignery, Agnès. "Macrophage Fusion." In Cell Fusion, 149–61. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-250-2_9.

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Verschoor, Chris P., Alicja Puchta, and Dawn M. E. Bowdish. "The Macrophage." In Methods in Molecular Biology, 139–56. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-527-5_10.

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Schomburg, Dietmar, and Dörte Stephan. "Macrophage elastase." In Enzyme Handbook 16, 473–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-58903-4_87.

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Lewis, J. G. "Macrophage Activation." In Encyclopedia of Immunotoxicology, 573–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_936.

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Hartwig, J. H., and T. P. Stossel. "Macrophage movements." In Mononuclear Phagocytes, 329–36. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5020-7_34.

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Conference papers on the topic "Macrophage"

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Mahgoub, Yasmine, Rida Arif, and Susu Zughaier. "Pyocyanin pigment from Pseudomonas aeruginosa modulates innate immune defenses in macrophages." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0137.

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Background: Pseudomonas aeruginosa is a well-known opportunistic pathogen. The gram-negative bacillus, commonly associated with hospital-acquired infections, utilizes the host’s impaired immune responses to establish infection. Of its many virulence factors, pyocyanin is essential for P. aeruginosa to establish its full infectivity. Macrophages act as sentinels of the innate immune system, as well as play other roles in homeostasis, tissue remodeling, and bridging between the innate and adaptive immune systems. Aim: This study aimed to investigate the effects of pyocyanin on macrophage innate immune defenses by assessing the function of macrophages treated with pyocyanin and TLR ligands. Phagocytosis of opsonized zymosan, LPS-induced nitric oxide release and cytokine release were used as measures of functional responses. Results: This study found that pyocyanin inhibited phagocytosis-induced ROS release in a dose-dependent manner and reduced nitric oxide release from macrophages induced with P. aeruginosa LPS. In addition, pyocyanin modulated cytokines and chemokines release from macrophages exposed to P. aeruginosa LPS in a dose-dependent manner. Pyocyanin significantly enhanced IL-1β release as well as several chemokines. Therefore, pyocyanin facilitates Pseudomonas aeruginosa to persevere in the immunocompromised host through modulating macrophage’s innate immune defenses. Conclusion: Pyocyanin inhibits macrophage functional defense responses to facilitate Pseudomonas aeruginosa infection.
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van Dam-Mieras, M. C. E., A. D. Muller, and G. Hornstra. "DIETARY LIPIDS, INFECTION AND MACROPHAGE PROCOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643398.

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It is generally accepted that the type of dietary fat influences arterial thrombosis and atherosclerosis. Although it is still largely unknown how the dietary lipid composition influences the process of atherogenesis, it is evident that several cell types are involved. Morphological evidence for the involvement of monocyte/macropages has been given.We described before that the dietary lipid composition has striking effects on the procoagulant activity of macrophages. When macrophages were isolated from the spleens of healthy rats the procoagulant activity slightly decreased during the first few hours after isolation, and reached a plateau value after 4 hours. When, however, macrophages were obtained from animals infected with a pneumona virus (PVM) different results were obtained:Experiments carried out with peripheral blood monocytes showed close resemblance to those described in the table.These results show that:- moncytes/macrophages isolated from PVM-infected animals increase their procoagulant activity during in vitro culture- the differences in macrophage procoagulant activity found in cells obtained from healthy animals fed diets containing different lipids no longer were found in PVM-infected animalsThis would implicate that the infection process has a more profound influence on macrophage procoagulant activity that the composition of the diet
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Reinhard, Björn M., Hongyun Wang, and Linxi Wu. "Monitoring Cellular Trafficking of Nanoparticle Cargo in Murine Macrophages Through Plasmon Coupling Microscopy." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93078.

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A detailed analysis of silver nanoparticle (NP) uptake and trafficking in the murine macrophage cell line J774A.1 through spectral analysis of the resonance wavelength of the metal NP cargo is presented. The NP spectra reveal a strong phenotypic variability in the NP uptake and processing on the single cell level. Cells containing non- or low-agglomerated NPs are found to coexist with cells containing NPs of varying degrees of NP agglomeration, clearly indicated by a spectral red-shift in the resonance wavelength. Pharmacological inhibition studies indicate that the observed differences in the intracellular NP organization result from coexisting actin- and clathrin-dependent endocytosis mechanisms. Correlation with fluorescence macrophage maturity markers shows that differentiated J774A.1 macrophages preferentially contain compact NP agglomerates, whereas monocyte-like macrophages contain non-agglomerated NPs.
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Gijsen, Frank, Anna Ten Have, Jolanda Wentzel, and Antonius Van Der Steen. "Temperature Measurement of Advanced Murine Atherosclerotic Plaques." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176307.

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Ischaemic heart disease is most frequently caused by coronary atherosclerosis, of which the vulnerable plaque is one of the developmental stages. Rupture of a vulnerable plaque with superimposed thrombosis frequently leads to acute coronary syndromes. The major components of a vulnerable plaque are a lipid-rich, atheromatous core, and a thin fibrous cap with macrophage and macrophage infiltration (Schaar et al., 2004). After the first paper suggesting the possibility of thermographic detection of vulnerable plaques (Casscells et al., 1996), intracoronary thermography as a vulnerable plaque detection technique has been investigated. Increased metabolic activity of macrophages is suggested as the main reasons for the increased temperatures (ten Have et al., 2005).
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McGee, Maria, and Henry Rothberger. "MECHANISMS OF PROCOAGULANT GENERATION BY ALVEOLAR MACROPHAGES DURING MATURATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643168.

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During maturation in vivo and in vitro alveolar macrophages generate procoagulant(s) capable of activating the extrinsic pathway. It is generally agreed that at least part of the activity is due to TF (tissue factor). However, whether or not macrophages also generate functional factor VII or X is controversial. To characterize procoagulant activity increases, we measured kinetic parameters defining interactions between components of the TF-VII complex on membranes of alveolar macrophages either freshly isolated or cultured in serum free medium. In incubation mixtures with fixed concentrations of macrophages and added factor VII, the rate of factor Xa formation (measured by S-2222 hydrolysis) approached a maximum as factor X concentration was increased. Estimated concentrations of factor X yielding 1/2 maximal activation rates, (apparent Km) were 127.1±26 nM and 99.7±34 nM for fresh and cultured cells, respectively. Vmax (maximal velocities) were 1.21±0.24 and 8.9±5 nM Xa/min/106 cells. When concentrations of added factor X were kept constant, the rate of factor X activation increased as the added factor VII concentration was increased. For fresh and cultured cells, the respective apparent Kd were 1.810.7 and 1.410.25 nM. Maximal rates observed with X concentration fixed at 108 nM were 0.46±10.06 and 5.7±1.6 nM Xa/min/106 cells. In the absence of either added factor X or added factor VII, no factor Xa generation was detected in fresh or cultured cells, during 10-20 min incubation periods used for kinetic studies. The observed increase in Vmax without changes in apparent Km and Kd indicate that gains in procoagulant activity during macrophage maturation are due to increases in the number of functional binding sites for factor VII, without significant generation of functional vitamin K dependent factors (VII and X) by the cells. The data also indicate that maturation does not alter the rate behaviour of the TF-VII enzymatic complex on macrophage membranes. Mechanisms of complex assembly that we observed on macrophage membranes are similar to those described for the TF-VII complex assembly on purified systems.
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DUBOR, F., A. M. DOSNE, and L. CHEDID. "Effect of dexamethasone and endothelial cell supernatant on u-PA produced by human promyelocyte cells treated with phorbol myristate acetate (PMA)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643191.

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After treatment with PMA the human promyelocytic HL60 cells were induced to differentiate into a monocyte-macrophage population and to produce a high amount of plasminogen activator in the supernatant. This response was detected from 0,5 ng/ml of PMA and culminated at 5 ng. The plasminogen activator appeared of urokinase-type as showed by fibrinenzymographic analysis : the enzymatic profile of cell supernatant showed 2 lysis band (Mr 33.000 and 55.000) corresponding to those of urokinase of low and high mol. weight. Dexamethasone (100 pM) suppressed the production of this macrophage u-PA without evidence of plasminogen activator inhibitor (PAI) generation in the supernatant : free PAI was not detected in urokinase inhibition assays ; complexes of u-PA-PAI were not observed in fibrinoenzymographic studies. Supernatant of human endothelial cells added to HL60 cell supernatant neutralized the two molecular species of macrophage u-PA and gave rise to complexes (Mr 110.000 and 84.000) detected by fibrinoenzymography. These results suggested different possible levels for controlling u-PA of inflammatory macrophages including interaction with endothelial cells secretion since endothelial PAI is increased by some inflammatory monokine and also by dexamethasone, it appears that endothelium could have a regulatory role on inflammatory fibrinolysis.
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Belchamber, K., and E. Sapey. "S51 Hungry hungry macrophages: how multiple prey affects macrophage phagocytosis." In British Thoracic Society Winter Meeting, Wednesday 17 to Friday 19 February 2021, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2021. http://dx.doi.org/10.1136/thorax-2020-btsabstracts.56.

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Adany, R., A. Kiss, J. Kappelmayer, R. J. Ablin, and L. Muszbek. "EXPRESSION OF FACTOR XIII SUBUNIT A IN DIFFERENT TYPES OF HUMAN MACROPHAGES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644651.

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In addition to plasma the presence of subunit a of blood coagulation Factor XIII (FXIIl) has been verified in platelets and megakariocytes. Most recently, we demonstrated that human peripheral blood monocytes also contain FXIII subunit a. The present study was designed 1/ to determine the stage in the maturation sequence of bone marrow monocytopoesis in which FXIII appears 2/ to establish if FXIII is retained during differentiation into macrophages 3/ to assess how general is the presence of FXIII subunit a in different types of macrophages. FXIII subunit a was immunomorphologically detected in bone marrow smears, in cytospin preparations of cells from serous cavities (pleural, peritoneal, pericardial and synovial spaces), and paraformaldehyde-fixed paraffin-embedded or frozen sections of different organs where classical types of macrophages have been described earlier (liver, lung, thymus, skin, connective tissue, prostate and developing bone) . Cells containing FXIII subunit a were intensively characterized by immunofluorescent and enzymecytochemical techniques in double and treble labeling systems. Its presence was clearly demonstrated in promonocytes of bone marrow, and in all probability, it is present in monoblasts, as well. FXIII was also found in macrophages from different serous cavities and in embryonic osteoclasts. Cells containing FXIII subunit a of connective tissue were found to be tissue histiocytes, and not fibroblasts as previously thought. Kupffer cells of the liver and Langerhans cells of the epidermis were negative supporting theories that these cells are not members of monocyte-derived macrophage cell population. Immunomorphological detection of FXIII subunit a seems to be a useful marker for labeling the continuum of monocyte/macrophage cell line from the earliest ftrais in the bone marrow to the mature forms of macrophages and might be a valuable tool in the cytological diagnosis of malignant disorders of this cell line.
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Muszbek, L., and R. Adány. "CELLULAR DISTIBUTION OF FACTOR XIII IN HUMAN UTERUS AND PLACENTA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644648.

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As spontaneous abortion is a frequent finding in females with Factor XIII (FXIIl) deficiency it has been presumed that the plasmatic or cellular form of this clotting factor is essential to normal fetus development. In this context it is of special interestthat FXIII subunit a has been demonstrated in the homoge-nate of human uterus and placenta by activity measurements and immunobiochemical methods. However, no information on its cellular distribution has beenpublished, so far. In the present study first FXIII subunit a was detected in paraformaldehyde-fixed, paraffin-embedded sections by immunoperoxidase technique. FXIII containing cells were localized in the connective tissue of uterus and in the mesenchyme of placental chorionic villi. Though in a single report FXIII containing connective tissue cells were interpreted as fibroblasts (Fear et al., J.Clin.Pathoi.,37,560, 1984) the mononuclear, multipolar, stellate morphological appearance of these cells suggested that they rather belong to the monocyte/macrophage cell line. To characterize them the immuno-fluorescent detection of FXIII subunit a was combined by the visualization of different marker antigens for tissue macrophages (RFDT, Leu M3, HLA-DR) and fibroblasts (IIG10) on frozen sections. The coexpression of FXIII subunit a with RFD7 and Leu M3 macrophage markers, butnot with fibroblast membrane antigen IIG10 clearly proves that FXIII containing cells both in the uterusand in the placenta are tissue macrophages. HLA-DR was strongly expressed in cells positive for FXIII subunit a. in the uterus, but not or only very weakly in the placental mesenchyme, which might be due to the relative absence of extrinsic antigens during fetal development. The morphological findings on the presence of FXIII subunit a in placental macrophages were further strengthened by immunobiochemical experiments. FXIII subunit a, but not b content of isolated placental macrophages was also verified by immunoblotting, while fibroblasts were shown to be exemptof this factor. The results well agree with our previous findings demonstrating FXIII subunit a in humanmonocytes and peritoneal macrophages (Muszbek et al., Thrombos. Res. ,37, 401,1985; Adány et al. , Eur.J.Cell Biol.,38,171,1985).
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Wang, Yijie, Noura Ismail, Duaa Dakhlallah, Valerie P. Wright, Clay B. Marsh, and Melissa G. Piper. "Macrophage Microvesicles Induce Macrophage Differentiation And Transfer Of MiR-223." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5054.

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Reports on the topic "Macrophage"

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Hanna, Philip C. Macrophage Responses to B. Anthracis. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada456287.

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Peterson, Scott N. Macrophage Responses to B. Anthracis. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada428855.

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Broaddus, V. C. Role of Macrophage-induced Inflammation in Mesothelioma. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada582550.

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Abrass, Itamar B., and Christine K. Abrass. Influence of Stress-Induced Catecholamines on Macrophage Phagocytosis. Fort Belvoir, VA: Defense Technical Information Center, April 1989. http://dx.doi.org/10.21236/ada206608.

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Blystone, Robert V. Image Analysis of Viral-Expressing Mouse Macrophage Cells. Fort Belvoir, VA: Defense Technical Information Center, May 1991. http://dx.doi.org/10.21236/ada238230.

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Groopman, Jerome E. Pathobiology of HTLV-III/LAV In Human Monocyte-Macrophage. Fort Belvoir, VA: Defense Technical Information Center, April 1990. http://dx.doi.org/10.21236/ada221724.

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Laouar, A., C. B. H. Chubb, F. Collart, and E. Huberman. Human macrophage differentiation involves an interaction between integrins and fibronectin. Office of Scientific and Technical Information (OSTI), November 1996. http://dx.doi.org/10.2172/495739.

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Laouar, A., C. B. H. Chubb, F. Collart, and E. Huberman. Human macrophage differentiation involves an interaction between integrins and fibronectin. Office of Scientific and Technical Information (OSTI), March 1997. http://dx.doi.org/10.2172/515532.

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Cioffi, William G., Burleson Jr, Jordan David G., Becker Bryan S., McManus William K., and William F. Effects of Granulocyte-Macrophage Colony-Stimulating Factor in Burn Patients. Fort Belvoir, VA: Defense Technical Information Center, January 1991. http://dx.doi.org/10.21236/ada245115.

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Ciraci, Ceren, Christopher K. Tuggle, Michael J. Wannemuehler, Daniel S. Nettleton, and Susan J. Lamont. Kinetic Profile of Chicken Macrophage Immune Response upon exposure to Salmonella-derived Endotoxin. Ames (Iowa): Iowa State University, January 2010. http://dx.doi.org/10.31274/ans_air-180814-134.

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