Relevant bibliographies by topics / Macrophage activation

Academic literature on the topic 'Macrophage activation'

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Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Macrophage activation"

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Sharma, Preeti, Shailza Shreshtha, Pradeep Kumar, Rachna Sharma, and T. K. Mahapatra. "A Review on Macrophage Activation Syndrome." Journal of Pure and Applied Microbiology 13, no. 1 (March 31, 2019): 183–91. http://dx.doi.org/10.22207/jpam.13.1.19.

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Van Epps, Heather L. "Macrophage activation unveiled." Journal of Experimental Medicine 202, no. 7 (October 3, 2005): 884. http://dx.doi.org/10.1084/jem.2027fta.

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In the early 1960s, George Mackaness showed that macrophages from mice infected with intracellular bacteria could launch an indiscriminate attack against unrelated bacteria. Thus began an explosion of research on the biology of what Mackaness first termed “macrophage activation.”
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Gilbreath, M. J., C. A. Nacy, D. L. Hoover, C. R. Alving, G. M. Swartz, and M. S. Meltzer. "Macrophage activation for microbicidal activity against Leishmania major: inhibition of lymphokine activation by phosphatidylcholine-phosphatidylserine liposomes." Journal of Immunology 134, no. 5 (May 1, 1985): 3420–25. http://dx.doi.org/10.4049/jimmunol.134.5.3420.

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Abstract Resident peritoneal macrophages from untreated mice develop microbicidal activity against amastigotes of the protozoan parasite Leishmania tropica (current nomenclature = Leishmania major) after in vitro exposure to LK from antigen-stimulated leukocyte culture fluids. This LK-induced macrophage microbicidal activity was completely abrogated by addition of 7:3 phosphatidylcholine: phosphatidylserine liposomes. Liposome inhibition was not due to direct toxic effects against the parasite or macrophage effector cell; factors in LK that induce macrophage microbicidal activity were not adsorbed or destroyed by liposome treatment. Other phagocytic particles, such as latex beads, had no effect on microbicidal activity. Moreover, liposome inhibition of activated macrophage effector function was relatively selective: LK-induced macrophage tumoricidal activity was not affected by liposome treatment. Liposome inhibition was dependent upon liposome dose (5 nmoles/culture) and time of addition of leishmania-infected, LK-treated macrophage cultures. Addition of liposomes through the initial 8 hr of culture completely inhibited LK-induced macrophage microbicidal activity; liposomes added after 16 hr had no effect. Similarly, microbicidal activity by macrophages activated in vivo by BCG or Corynebacterium parvum was not affected by liposome treatment. Liposome treatment also did not affect the increased resistance to infection induced in macrophages by LK. These data suggest that liposomes interfere with one or more early events in the induction of activated macrophages (macrophage-LK interaction) and not with the cytotoxic mechanism itself (parasite-macrophage interaction). These studies add to the growing body of data that implicate cell lipid in regulatory events controlling macrophage effector function.
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ONOZAKI, Kikuo. "Macrophage activation by macrophage activation factor, macrophage migration inhibitory factor." Nippon Saikingaku Zasshi 40, no. 5 (1985): 811–17. http://dx.doi.org/10.3412/jsb.40.811.

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Serraj Andaloussi, Meriem, Hayat Midyani, Chadia Khalloufi, Amine Lamrissi, Karima Fichtali, Said Bouhya, Salah Hayar, Ihsane Moussaid, Smaïl El Youssoufi, and Said Salmi. "Macrophage Activation Syndrome Discovered During Pregnancy: Case Report." Obstetrics Gynecology and Reproductive Sciences 5, no. 7 (September 25, 2021): 01–04. http://dx.doi.org/10.31579/2578-8965/081.

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Macrophage activation syndrome (MAS) or Haemophagocytic syndrome (HPS) results from an inappropriate stimulation of macrophages in bone marrow and lymphoid organs, leading to haemophagocytosis and hypercytokinemia. HPS may be primitive, essentially in pediatric population, or secondary to malignancy, infection or autoimmune disease. This disease is rare and prognosis is poor. The diagnosis of hemophagocytic syndrome remains a challenge especially during pregnancy. We report a case collected at the Elharouchimaternity service, taken in charge jointly with its intensive care unit, of a 26-year-old patient with no pathological history leading to an unsuccessful pregnancy presumed at 5 months in whom the MAS syndrome was retained due to pancytopenia. , hyperferitinemia, hypertriglyceridemia with the presence of a few hemophagocytes in the myelogram with a good evolution under bolus of solumedrol and symptomatic treatment. We discuss through this case the diagnostic difficulties, the obstetric complications as well as the options therapeutic.
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Heidenreich, S., M. Weyers, J. H. Gong, H. Sprenger, M. Nain, and D. Gemsa. "Potentiation of lymphokine-induced macrophage activation by tumor necrosis factor-alpha." Journal of Immunology 140, no. 5 (March 1, 1988): 1511–18. http://dx.doi.org/10.4049/jimmunol.140.5.1511.

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Abstract In this study, we examined the possible role of TNF-alpha and lymphotoxin (TNF-beta) as cofactors of macrophage activation. The results demonstrate that both TNF were capable of enhancing the cytostatic and cytolytic activity of murine peritoneal macrophages against Eb lymphoma cells. The potentiation of tumor cytotoxicity became apparent when macrophages from DBA/2 mice were suboptimally activated by either a T cell clone-derived macrophage-activating factor or by IFN-gamma plus LPS. Neither TNF-alpha nor TNF-beta could induce tumor cytotoxicity in IFN-gamma-primed macrophages, indicating that TNF cannot replace LPS as a triggering signal of activation. In LPS-resistant C3H/HeJ macrophages, which were unresponsive to IFN-gamma plus LPS, a supplementation with TNF fully restored activation to tumor cytotoxicity. Furthermore, TNF-alpha potentiated a variety of other functions in low-level activated macrophages such as a lactate production and release of cytotoxic factors. At the same time, TNF-alpha produced a further down-regulation of pinocytosis, tumor cell binding and RNA synthesis observed in activated macrophages. These data demonstrate new activities for both TNF-alpha and TNF-beta as helper factors that facilitate macrophage activation. In particular, the macrophage product TNF-alpha may serve as an autocrine signal to potentiate those macrophage functions that were insufficiently activated by lymphokines.
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Seljelid, R. "Macrophage Activation." Scandinavian Journal of Rheumatology 17, sup76 (January 1988): 67–72. http://dx.doi.org/10.3109/03009748809102954.

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Petit, J. F., and G. Lemaire. "Macrophage activation." Annales de l'Institut Pasteur / Immunologie 137 (January 1986): 191–92. http://dx.doi.org/10.1016/s0771-050x(86)80024-9.

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Pinder, M. "Macrophage activation." Veterinary Immunology and Immunopathology 14, no. 2 (February 1987): 205–6. http://dx.doi.org/10.1016/0165-2427(87)90055-9.

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Rios, Francisco J., Marianna M. Koga, Mateus Pecenin, Matheus Ferracini, Magnus Gidlund, and S. Jancar. "Oxidized LDL Induces Alternative Macrophage Phenotype through Activation of CD36 and PAFR." Mediators of Inflammation 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/198193.

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OxLDL is recognized by macrophage scavenger receptors, including CD36; we have recently found that Platelet-Activating Factor Receptor (PAFR) is also involved. Since PAFR in macrophages is associated with suppressor function, we examined the effect of oxLDL on macrophage phenotype. It was found that the presence of oxLDL during macrophage differentiation induced high mRNA levels to IL-10, mannose receptor, PPARγand arginase-1 and low levels of IL-12 and iNOS. When human THP-1 macrophages were pre-treated with oxLDL then stimulated with LPS, the production of IL-10 and TGF-βsignificantly increased, whereas that of IL-6 and IL-8 decreased. In murine TG-elicited macrophages, this protocol significantly reduced NO, iNOS and COX2 expression. Thus, oxLDL induced macrophage differentiation and activation towards the alternatively activated M2-phenotype. In murine macrophages, oxLDL induced TGF-β, arginase-1 and IL-10 mRNA expression, which were significantly reduced by pre-treatment with PAFR antagonists (WEB and CV) or with antibodies to CD36. The mRNA expression of IL-12, RANTES and CXCL2 were not affected. We showed that this profile of macrophage activation is dependent on the engagement of both CD36 and PAFR. We conclude that oxLDL induces alternative macrophage activation by mechanisms involving CD36 and PAFR.
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Dissertations / Theses on the topic "Macrophage activation"

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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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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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Pound, J. D. "Parameters of human macrophage activation." Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381442.

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Cano, Antonella. "Characterization of Acanthamoeba macrophage activation." Thesis, University of Strathclyde, 2015. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=25992.

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Hunter, Catriona Mhairi. "MicroRNA regulation of macrophage activation." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/31027.

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Macrophages are mononuclear phagocytic cells that have diverse roles within the body. Tissue specific macrophages, e.g. Kupffer cells, microglia and osteoclasts, have roles in tissue homeostasis, while circulating macrophages play an important role in the innate immune system. Macrophages detect the presence of pathogen associated molecular patterns (PAMPs) via a range of receptors known collectively as pathogen recognition receptors (PRRs). Detection of pathogens causes the macrophages to become ‘activated,’ during which the macrophages undergo extreme morphological and translational changes that enable the pathogen to be neutralised and other immune system components to be recruited. Macrophage activation must be carefully regulated and promptly resolved, as chronic inflammation is damaging to the host. MicroRNAs have emerged as one mechanism by which activation is regulated. MicroRNAs are small, non-coding pieces of RNA that function as a post-transcriptional regulatory mechanism. Their action is exerted through binding with a complementary region in the 3’ untranslated region (3’UTR) of the target mRNA. This binding, facilitated by the ribonuclear protein complex RISC, prevents successful translation of the mRNA into its protein product. MicroRNAs have been shown to function across species, throughout development and during the adult life-span. In the immune system, microRNAs are known to be required for correct formation of germinal centres and normal development of B- and T-cells. MicroRNAs have also been shown to be differentially regulated during macrophage activation with different stimuli. In particular, miR-155, miR-146a and miR-21 are associated with macrophage activation by lipopolysaccharide (LPS). The objective of this work was to further understand the role of microRNAs during macrophage activation with LPS. Two approaches were adopted. Firstly, the regulation of individual microRNAs in LPS-activated bone marrow derived macrophages (BMDMs) was characterised by the use of illumina small RNA sequencing. Secondly, the requirement of the global microRNA population during macrophage biology was investigated through the use of DGCR8 and Dicer knockout systems. In keeping with the large number of changes reported in mRNA translation upon activation, expression of >400 microRNAs were found to be differentially regulated by exposure to LPS. Twelve of these microRNAs were chosen for further study (miR- 142-3p, -146a, -15b, -155, -16, -191, -21, -27b, -30b, -322-5p, -378 and -7a). Individual knock-down of these microRNAs in the RAW264.7 macrophage-like cell line mostly demonstrated subtle, rather than dramatic changes to the activation marker genes studied by RT-QPCR analysis. However, knock-down of miR-146a, -15b, - 155 and -191 were able to significantly alter the expression of the activation marker genes (Tnf-a, Cox2, Cxcl2, Il-6 and Saa3). Interestingly, knock-down of miR-142-3p, miR-146a and miR-155 appeared to show cross-regulation of these microRNAs. The cell index (CI) data suggested that miR-191 and miR-21 influence adhesion in activated macrophages. Studies with the DGCR8 and Dicer knockout systems showed that the global microRNA population was required for successful differentiation of macrophages from embryonic stem cells, and for normal expression of differentiation and activation markers in bone marrow derived macrophages. Overall, these results show that dynamic expression of microRNAs is an integral part of the macrophage response to LPS.
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Ghanipour, Ali. "IL-10 regulates macrophage activation through activation of SHIP." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/30873.

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IL-10 is a potent anti-inflammatory and immunosuppressive cytokine, which regulates macrophages by activation of the STAT3 pathway. However, several lines of evidence suggest that IL-10 can inhibit macrophage activation independent of STAT3 through currently unknown mechanisms and pathways. Here for the first time, we show that in murine macrophages, IL-10 activates Src Homology 2 Domain-containing Inositol 5'-Phosphatase (SHIP), a molecule with reported anti-inflammatory effects. Activation of SHIP by IL-10 is required for inhibition of Tumor necrosis factor alpha (TNFα) in macrophages. Additional experiments revealed that IL-10 activation of SHIP acted at the post-transcriptional level and inhibited translation of TNFα . Using a novel small molecule activator of SHIP, AQX-016A, we further confirmed that activation of SHIP alone could inhibit TNFα translation. IL-10 activation of SHIP results in the inhibition of the LPS induced increase in the PI3K product, PIP3, at the membrane. However, conflicting data as to the role of PI3K in regulation of TNFα have been presented. Our studies show that PI3K inhibition downregulates TNFα production in peritoneal and several other macrophage lines, and upregulates it bone marrow derived macrophages (BMDM). Interestingly, this difference is due to the increased amount of autocrine negative regulators produced in BMDM, removal of which exposes the positive role PI3K plays in regulation of TNFα. Therefore, our studies confirm that PI3K activity positively regulates TNFα production in macrophages and that inhibition of TNFα by IL-10 or AQX-016A through activation of SHIP is likely due to SHIP'S ability to antagonize this pathway. The importance of this pathway is further highlighted as IL-10 inhibition of LPS-induced septic shock in mice lacking one allele of SHIP is significantly attenuated. Furthermore, activation of SHIP by AQX-016A inhibits TNFα production in septic mice. We also found that IL-10 inhibited LPS induced p38 activity in a cell-dependent manner. However in all cells tested, IL-10 activated p38 rapidly. We identified several IL-10 induced genes including CRIM1, a transmembrane protein with no previous report of involvement in the immune system. We found that IL-10 induction of CRIM1 was partly dependent on the activity of p38. However, expression of CRIM1 does not seem to be involved in the anti-inflammatory effects of IL-10.
Medicine, Faculty of
Biochemistry and Molecular Biology, Department of
Graduate
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Wu, Wei-Kang. "Modulating angiogenesis via altering macrophage activation." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539772.

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DUARTE, Madalena Bento. "Macrophage direct activation by Leishmania Spp." Master's thesis, Instituto de Higiene e Medicina Tropical, 2019. http://hdl.handle.net/10362/97877.

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Leishmanioses é um grupo de doenças causadas por parasitas do género Leishmania que apresenta elevada morbidade e de mortalidade. As manifestações clínicas dependem de interações complexas que se estabelecem entre Leishmania spp. e a resposta imunitária do hospedeiro. A doença pode manifestrar-se de maneiras diferentes, desde uma simples úlcera cutânea até ao envolvimento dos órgãos profundos que pode originar doença visceral fatal ou kala-azar. A resistência a drogas terapêuticas é um problema muito evidente em países endémicos, existindo uma crescente procura por alternativas eficazes. A pesquisa de vacina(s) capaz de deter a propagação da doença tem sido exaustiva. Um dos aspectos mais importante de Leishmania spp. é a capacidade destes parasitas conseguirem, por um lado, evitar e, por outro, alterar a resposta imunitária do hospedeito, que permita a sobrevivência do parasita e do hospedeiro, originando infeção crónica. O objectivo desta dissertação é investigar a capacidade de Leishmania spp. (L.shawi, L.amazonensis, L.guyanensis e L.infantum) modular a activação de MØ humanos, avaliando o fenótipo de MØ infetados através da expressão de dois biomarcadores de superfície, o CD68 e o CD163, associados à fagocitose e á actividade oxidativa. Os resultados mostraram que promastigotas de Leishmania induziram a mudança no fenótipo dos MØ que aponta para a existência de fagocitose intensa e inibação da actividade oxidativa. O incremento da fagocitose associado á diminuição da actividade oxidativa dos MØ infetados facilita o estabelecimento da infeção no hospedeito humano, garante a sobrevivência do parasita e assegura a conclusão do seu ciclo de vida, sobretudo nos parasitas causadores de leishmaniose cutânea
Leishmanias is a group of diseases with different clinical manifestations and is the leading cause of high morbidity and mortality worldwide. The clinical manifestations of Leishmanias in humans depend on complex interactions between the virulence characteristics of infecting Leishmania spp. and the immune responses of its hosts. The disease can manifest in a number of forms, ranging from simple cutaneous ulcers to the involvement of visceral organs, causing highly fatal visceral disease or kala-azar. Drug resistance is a very evident problem in some of endemic countries within the increasing demand for effective alternatives. The urgent demand for a vaccine capable of halting the spread of the disease has been exhausting. One of the most important aspects of Leishmania spp. infection is the ability of these parasites to evade and sabotage the host immune responses, which allow the parasite to persist and established chronic infection. The aim of the present dissertation is to investigate Leishmania spp. (L. shawi, L. amazonensis, L. guyanensis, and L. infantum) ability in modulating MØ activation, by accessing cell phenotype through the expression of two surface biomarkers, CD68 and CD163that are associated with phagocytosis and oxidative burst. Results showed that Leishmania promastigotes induced a change in MØ phenotype that point towards active phagocytosis and inhibition of the oxidative burst. Modulating the MØ activity to increase phagocytosis and decrease oxidative burst allows the parasite to establish host infection and ensures their own survival and the accomplishment of the life cycle, at least by the parasites that cause cutaneous leishmaniasis.
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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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Graham, Susan. "Studies on the activation of rainbow trout (Salmo gairdneri) macrophages and the characterization of a macrophage activating factor." Thesis, University of Aberdeen, 1989. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU498113.

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Rainbow trout macrophages were stimulated with PMA to produce 02- and H2O2 as detected by the reduction of nitroblue tetrazolium (NBT) and the oxidation of phenol red respectively. Addition of DDC or nitroprusside, inhibitors of superoxide dismutase (SOD) increased O2-levels and decreased H2O2 levels, whereas addition of exogenous SOD had the reverse effect. Such data are indicative of a respiratory burst pathway in teleost macrophages comparable with that of mammals. Respiratory burst activity, acid phosphatase activity and RNA synthesis in rainbow trout macrophages which have been stimulated in vitro with the mitogen Concanavalin A (Con A) or in vivo by injection of formalin-fixed Aeromonas salmonicida in Freund's incomplete adjuvant (FIA) was analysed. With Con A, in vitro stimulated head kidney (HK) or elicited macrophages had increased O2-production and RNA synthesis but no significant increases in H2O2 or acid phosphatase activity after 72h post-stimulation with Con A. In contrast, all functions were increased in in vivo stimulated macrophages compared with FIA-elicited peritoneal macrophages. In a bactericidal assay, Con A stimulated macrophages did not show an increase in killing of an avirulent strain of A. salmonicida (004) above control levels whereas in vivo stimulated macrophages not only displayed increased killing of the avirulent strain of bacteria but also acquired the ability to kill a virulent strain (048). Thus, Con A stimulated macrophages only possessed some of the features of activation whereas in vivo stimulated macrophages were activated as defined by the increased bactericidal activity. Peritoneal washes obtained in the collection of activated macrophages were able to increase NBT reduction in normal HK macrophages suggesting the presence of a soluble activating factor. Lymphokine (LK)-containing supernatants produced using either HK or blood derived leucocytes, by pulsing with 10ug/ml Con and 5ng/ml PMA, were able to increase O2- and H2O2 production, to enhance the killing of an avirulent strain of A. Salmonicida and conferred the ability to kill a virulent strain of A. salmonicida. The LK present in these supernatants was therefore designated a macrophage activating factor (MAF). The use of potential second signals to enhance the killing of bacteria by LK-treated macrophages, met with limited success. Only A. salmonicida (strain 004) LPS was able to produce a small increase in killing above LK-treatment. The MAF produced in this study was tested for antiviral/interferon (IFN) activity. The results showed that the supernatants did contain IFN activity. Attempts to semi-purify the MAF from antiviral activity showed the two activities to co-purify, indicating that both activities may be due to the same molecular species. The retention time of the MAF/IFN, coupled with the results of SDS-PAGE analysis showed the molecular weight of the moiety to be approximately 19K daltons. Both activities were sensitive to low pH (pH 2), high temperature (60oC) and trypsin, providing further evidence that the MAF and IFN activity produced in these studies may be due to the same molecular species, possibly akin to IFN- of higher vertebrates.
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Books on the topic "Macrophage activation"

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

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The human macrophage system: Activity and functional morphology. Basel: Karger, 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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1955-, Suttles Jill, ed. T-cell signaling of macrophage activation: Cell contact-dependent and cytokine signals. Austin: R.G. Landes, 1995.

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Kucey, Daryl Stanton. Modulation of macrophage procoagulant activity by platelet activating factor. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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Adams, Dolph O. Macrophage Activation. Springer, 2013.

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Adams, Dolph O. Macrophage Activation. Springer, 2013.

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Grom, Alexei A., and Athimalaipet V. Ramanan. Macrophage activation syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0168.

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Macrophage activation syndrome (MAS) is a life-threatening condition caused by excessive activation and proliferation of T lymphocytes and haemophagocytic macrophages. Although MAS has been reported in association with almost any rheumatic disease, it is by far most common in systemic juvenile idiopathic arthritis. Flares of the underlying disease or infection are most common triggers of MAS. The pathognomonic feature of MAS is typically found in bone marrow: numerous, well-differentiated macrophagic histiocytes phagocytosing normal haematopoietic elements. The expansion of these histiocytes leads to a massive systemic inflammatory reaction associated with three cardinal clinical features: severe cytopenias, liver dysfunction, and coagulopathy consistent with disseminated intravascular coagulation. Clinically, MAS is strikingly similar to the autosomal recessive disorders collectively known as familial haemophagocytic lymphohistiocytosis (FHLH). FHLH has been associated with various genetic defects affecting the cytolytic pathway. Cytolytic function is profoundly depressed in MAS patients as well, and this abnormality is caused by both genetic and acquired factors. Studies in animals suggest that uncontrolled expansion of activated CD8+ T lymphocytes secreting cytokines that activate macrophages is central to the pathophysiology of haemophagocytic syndromes. Consistent with this view, the combination of steroids and ciclosporin, an immunosuppressant that preferentially inhibits T lymphocytes, is an effective treatment for the majority of MAS patients. Patients in whom MAS remains active despite this treatment present a serious challenge and require more aggressive immunosuppression. However, in MAS triggered by infection, the optimal level of immunosuppression is difficult to determine. As a result, reported mortality rates reach 20%.
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Gordon, Siamon, and Stephen W. Russell. Macrophage Biology and Activation. Springer London, Limited, 2012.

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Book chapters on the topic "Macrophage activation"

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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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Iweala, Onyinye, and Eveline Y. Wu. "Macrophage Activation Syndrome." In Rare Rheumatic Diseases of Immunologic Dysregulation, 1–25. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99139-9_1.

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Davì, Sergio, Francesca Minoia, Randy Q. Cron, and Angelo Ravelli. "Macrophage Activation Syndrome." In Pediatric Rheumatology, 275–92. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-1750-6_22.

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Eloseily, Esraa M., and Randy Q. Cron. "Macrophage Activation Syndrome." In The Microbiome in Rheumatic Diseases and Infection, 151–82. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-79026-8_14.

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Vinh, Donald C., and Steven M. Holland. "Macrophage Classical Activation." In Phagocyte-Pathogen Interactions, 301–23. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816650.ch19.

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Comalada, Mònica, Andree Yeramian, Manuel Modolell, Jorge Lloberas, and Antonio Celada. "Arginine and Macrophage Activation." In Methods in Molecular Biology, 223–35. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-527-5_16.

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Mehta, Bella, and Petros Efthimiou. "Macrophage Activation Syndrome (MAS)." In Auto-Inflammatory Syndromes, 193–201. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-96929-9_14.

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Classen, Andrea, Jorge Lloberas, and Antonio Celada. "Macrophage Activation: Classical Vs. Alternative." In Macrophages and Dendritic Cells, 29–43. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-396-7_3.

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Coates, Anthony R. M., Ana Cehovin, and Yanmin Hu. "Chaperonin 60 and Macrophage Activation." In Novartis Foundation Symposia, 160–72. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470754030.ch12.

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Langermans, J. A. M., P. H. Nibbering, M. E. B. Van Der Hulst, and R. Van Furth. "Macrophage activation by recombinant cytokines." In Mononuclear Phagocytes, 602–17. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-015-8070-0_80.

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Conference papers on the topic "Macrophage activation"

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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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"02 Macrophage activation syndrome in SLE." In 8th ANNUAL MEETING OF THE LUPUS ACADEMY, Warsaw, Poland, September 6–8, 2019. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-la.5.

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Kumar, Ashna. "657 Macrophage activation syndrome and sepsis." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference–Online, 15 June 2021–17 June 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-rcpch.124.

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Kuis, W., NM Wulffraat, and GT Rijkers. "SP0075 Macrophage activation syndrome and systemic jia." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.26.

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Jain, D., Y. Tomer, A. Malur, MJ Thomassen, and MF Beers. "SP-D Modulates Alveolar Macrophage Polarization and Activation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6270.

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Song, Sheng, Feifan Zhou, Wei R. Chen, and Da Xing. "Direct imaging of macrophage activation during PDT treatment." In Photonics and Optoelectronics Meetings 2011. SPIE, 2012. http://dx.doi.org/10.1117/12.919005.

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Oliveira, Renato Lucindo Bolelli de, Maria Clara de Castro e. Caetano, Natalia Lamas Rosario, Alonzo Armani Prata, Ana Luíza dos Santos Machado Costa, Bethânia Silva Meireles, Ketty Lysie Libardi Lira Machado, et al. "ADULT-ONSET STILL’S DISEASE WITH MACROPHAGE ACTIVATION SYNDROME." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.1992.

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Chang, Haocai. "Photobiomodulation enhances macrophage phagocytic capacity via Rac1 activation." In Twelfth International Conference on Information Optics and Photonics, edited by Yue Yang. SPIE, 2021. http://dx.doi.org/10.1117/12.2604421.

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Huang, J., and J. Chao. "ZC3H4-Mediated Macrophage Activation in Silica-Induced Pulmonary Fibrosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2641.

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Squizatto Leite, Douglas, Matheus Zanata Brufatto, Sean Hideo Shirata Lanças, Andrea de Almeida Peduti Batista, Laura Maria Silva de Siqueira, Henrique Pereira Sampaio, Luiz Eduardo Valente, Daniela Esteves Temporim, João Flávio Gomes Faria, and Sula Glaucia Lage Drumond Pacheco. "Macrophage activation syndrome(MAS) treated with tocilizumab: Case Report." In SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.1988.

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Reports on the topic "Macrophage activation"

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Schwartz, Bertha, Vaclav Vetvicka, Ofer Danai, and Yitzhak Hadar. Increasing the value of mushrooms as functional foods: induction of alpha and beta glucan content via novel cultivation methods. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600033.bard.

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During the granting period, we performed the following projects: Firstly, we differentially measured glucan content in several pleurotus mushroom strains. Mushroom polysaccharides are edible polymers that have numerous reported biological functions; the most common effects are attributed to β-glucans. In recent years, it became apparent that the less abundant α-glucans also possess potent effects in various health conditions. In our first study, we explored several Pleurotus species for their total, β and α-glucan content. Pleurotuseryngii was found to have the highest total glucan concentrations and the highest α-glucans proportion. We also found that the stalks (stipe) of the fruit body contained higher glucan content then the caps (pileus). Since mushrooms respond markedly to changes in environmental and growth conditions, we developed cultivation methods aiming to increase the levels of α and β-glucans. Using olive mill solid waste (OMSW) from three-phase olive mills in the cultivation substrate. We were able to enrich the levels mainly of α-glucans. Maximal total glucan concentrations were enhanced up to twice when the growth substrate contained 80% of OMSW compared to no OMSW. Taking together this study demonstrate that Pleurotuseryngii can serve as a potential rich source of glucans for nutritional and medicinal applications and that glucan content in mushroom fruiting bodies can be further enriched by applying OMSW into the cultivation substrate. We then compared the immune-modulating activity of glucans extracted from P. ostreatus and P. eryngii on phagocytosis of peripheral blood neutrophils, and superoxide release from HL-60 cells. The results suggest that the anti-inflammatory properties of these glucans are partially mediated through modulation of neutrophileffector functions (P. eryngiiwas more effective). Additionally, both glucans dose-dependently competed for the anti-Dectin-1 and anti-CR3 antibody binding. We then tested the putative anti-inflammatory effects of the extracted glucans in inflammatory bowel disease (IBD) using the dextran sulfate sodium (DSS)–induced model in mice. The clinical symptoms of IBD were efficiently relieved by the treatment with two different doses of the glucan from both fungi. Glucan fractions, from either P. ostreatus or P. eryngii, markedly prevented TNF-α mediated inflammation in the DSS–induced inflamed intestine. These results suggest that there are variations in glucan preparations from different fungi in their anti-inflammatory ability. In our next study, we tested the effect of glucans on lipopolysaccharide (LPS)-induced production of TNF-α. We demonstrated that glucan extracts are more effective than mill mushroom preparations. Additionally, the effectiveness of stalk-derived glucans were slightly more pronounced than of caps. Cap and stalk glucans from mill or isolated glucan competed dose-dependently with anti-Dectin-and anti-CR-3 antibodies, indicating that they contain β-glucans recognized by these receptors. Using the dextran sulfate sodium (DSS)-inflammatory bowel disease mice model, intestinal inflammatory response to the mill preparations was measured and compared to extracted glucan fractions from caps and stalks. We found that mill and glucan extracts were very effective in downregulatingIFN-γ and MIP-2 levels and that stalk-derived preparations were more effective than from caps. The tested glucans were equally effective in regulating the number of CD14/CD16 monocytes and upregulating the levels of fecal-released IgA to almost normal levels. In conclusion, the most effective glucans in ameliorating some IBD-inflammatory associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii. These spatial distinctions may be helpful in selecting more effective specific anti-inflammatory mushrooms-derived glucans. We additionally tested the effect of glucans on lipopolysaccharide-induced production of TNF-α, which demonstrated stalk-derived glucans were more effective than of caps-derived glucans. Isolated glucans competed with anti-Dectin-1 and anti-CR3 antibodies, indicating that they contain β-glucans recognized by these receptors. In conclusion, the most effective glucans in ameliorating IBD-associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii grown at higher concentrations of OMSW. We conclude that these stress-induced growing conditions may be helpful in selecting more effective glucans derived from edible mushrooms. Based on the findings that we could enhance glucan content in Pleurotuseryngii following cultivation of the mushrooms on a substrate containing different concentrations of olive mill solid waste (OMSW) and that these changes are directly related to the content of OMSW in the growing substrate we tested the extracted glucans in several models. Using dextran sulfate sodium (DSS)–inflammatory bowel disease (IBD) mice model, we measured the colonic inflammatory response to the different glucan preparations. We found that the histology damaging score (HDS) resulting from DSS treatment reach a value of 11.8 ± 2.3 were efficiently downregulated by treatment with the fungal extracted glucans, glucans extracted from stalks cultivated at 20% OMSWdownregulated to a HDS value of 6.4 ± 0.5 and at 80% OMSW showed the strongest effects (5.5 ± 0.6). Similar downregulatory effects were obtained for expression of various intestinal cytokines. All tested glucans were equally effective in regulating the number of CD14/CD16 monocytes from 18.2 ± 2.7 % for DSS to 6.4 ± 2.0 for DSS +glucans extracted from stalks cultivated at 50% OMSW. We finally tested glucans extracted from Pleurotuseryngii grown on a substrate containing increasing concentrations of olive mill solid waste (OMSW) contain greater glucan concentrations as a function of OMSW content. Treatment of rat Intestinal epithelial cells (IEC-6) transiently transfected with Nf-κB fused to luciferase demonstrated that glucans extracted from P. eryngii stalks grown on 80% OMSWdownregulatedTNF-α activation. Glucans from mushrooms grown on 80% OMSW exerted the most significant reducing activity of nitric oxide production in lipopolysaccharide (LPS) treated J774A.1 murine macrophages. The isolated glucans were tested in vivo using the Dextran Sodium Sulfate (DSS) induced colitis in C57Bl/6 mice and found to reduce the histology damaging score resulting from DSS treatment. Expression of various intestinal cytokines were efficiently downregulated by treatment with the fungal extracted glucans. We conclude that the stress-induced growing conditions exerted by OMSW induces production of more effective anti-inflammatory glucans in P. eryngii stalks.
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