The Experts below are selected from a list of 255 Experts worldwide ranked by ideXlab platform
Kazuo Motoyoshi - One of the best experts on this subject based on the ideXlab platform.
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Signal Transduction in Macrophages: Negative Regulation for Macrophage Colony-Stimulating Factor Receptor Signaling
International Journal of Hematology, 2002Co-Authors: Shinya Suzu, Kazuo MotoyoshiAbstract:The receptor for macrophage colony-stimulating factor (M-CSF) is expressed in monocytes/Macrophages and their progenitor cells and stimulates both the growth and development of the blood-cell lineage.Although the specific components positively regulating M-CSF receptor signaling have been relatively well defined, it is now clear that important mechanisms to control the signaling cascades also exist.This review discusses the most recent results concerning the negative regulatory molecules for M-CSF receptor signaling. In particular, we focus on negative molecules for both proliferation of monocytes/macro-phages and differentiation into mature cells.
Yrjo T Konttinen - One of the best experts on this subject based on the ideXlab platform.
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the response of Macrophages to titanium particles is determined by macrophage polarization
Acta Biomaterialia, 2013Co-Authors: Jukka Pajarinen, Vesapetteri Kouri, Eemeli Jamsen, Jami Mandelin, Yrjo T KonttinenAbstract:Aseptic loosening of total joint replacements is driven by the reaction of Macrophages to foreign body particles released from the implant. It was hypothesized that the Macrophages' response to these particles is dependent, in addition to particle characteristics and contaminating biomolecules, on the state of macrophage polarization as determined by the local cytokine microenvironment. To test this hypothesis we differentiated M1 and M2 Macrophages from human peripheral blood monocytes and compared their responses to titanium particles using genome-wide microarray analysis and a multiplex cytokine assay. In comparison to non-activated M0 Macrophages, the overall chemotactic and inflammatory responses to titanium particles were greatly enhanced in M1 Macrophages and effectively suppressed in M2 Macrophages. In addition, the genome-wide approach revealed several novel, potentially osteolytic, particle-induced mediators, and signaling pathway analysis suggested the involvement of toll-like and nod-like receptor signaling in particle recognition. It is concluded that the magnitude of foreign body reaction caused by titanium particles is dependent on the state of macrophage polarization. Thus, by limiting the action of M1 polarizing factors, e.g. bacterial biofilm formation, in peri-implant tissues and promoting M2 macrophage polarization by biomaterial solutions or pharmacologically, it might be possible to restrict wear-particle-induced inflammation and osteolysis.
Sailesh C. Harwani - One of the best experts on this subject based on the ideXlab platform.
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Macrophages Under Pressure: The Role of Macrophage Polarization in Hypertension
Translational Research, 2017Co-Authors: Sailesh C. HarwaniAbstract:Hypertension is a multifactorial disease involving the nervous, renal, and cardiovascular systems. Macrophages are the most abundant and ubiquitous immune cells, placing them in a unique position to serve as key mediators between these components. The polarization of Macrophages confers vast phenotypic and functional plasticity, allowing them to act as proinflammatory, homeostatic, and anti-inflammatory agents. Key differences between the M1 and M2 phenotypes, the 2 subsets at the extremes of this polarization spectrum, place Macrophages at a juncture to mediate many mechanisms involved in the pathogenesis of hypertension. Neuronal and non-neuronal regulation of the immune system, that is, the “neuroimmuno” axis, plays an integral role in the polarization of Macrophages. In hypertension, the neuroimmuno axis results in synchronization of macrophage mobilization from immune cell reservoirs and their chemotaxis, via increased expression of chemoattractants, to end organs critical in the development of hypertension. This complicated system is largely coordinated by the dichotomous actions of the autonomic neuronal and non-neuronal activation of cholinergic, adrenergic, and neurohormonal receptors on Macrophages, leading to their ability to “switch” between phenotypes at sites of active inflammation. Data from experimental models and human studies are in concordance with each other and support a central role for macrophage polarization in the pathogenesis of hypertension.
Antonio Celada - One of the best experts on this subject based on the ideXlab platform.
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Dexamethasone enhances macrophage colony stimulating factor- and granulocyte macrophage colony stimulating factor- stimulated proliferation of bone marrow- derived Macrophages
International immunology, 1998Co-Authors: Jorge Lloberas, Concepció Soler, Antonio CeladaAbstract:Glucocorticoids are effective repressors of the immune system. We have examined the effect of glucocorticoids on the proliferation of murine Macrophages. Dexamethasone by itself did not affect proliferation of differentiated or undifferentiated bone marrow-derived Macrophages (BMM) and elicited peritoneal Macrophages. However, dexamethasone enhanced the proliferation induced by macrophage colony stimulating factor (M-CSF) of these cells. The effect of dexamethasone was not restricted to M-CSF-dependent proliferation. Similarly, dexamethasone enhanced granulocyte macrophage colony stimulating factor (GM-CSF)-dependent proliferation of BMM. In agreement, Macrophages transfected with the glucocorticoid receptor showed an enhancement of M-CSF-dependent proliferation. The enhancement of proliferation by dexamethasone or the glucocorticoid receptor was abolished by RU 486, an antagonist of the glucocorticoid receptor. Moreover, the addition of antibodies against M-CSF inhibits the effect of dexamethasone, suggesting that dexamethasone increases the autocrine production of M-CSF. This only occurs when M-CSF or GM-CSF, which induce M-CSF, are present in the media. In tissues, dexamethasone may enhance macrophage proliferation and contribute to the resolution of the inflammatory states.
Gregory G Freund - One of the best experts on this subject based on the ideXlab platform.
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Macrophages make me sick how macrophage activation states influence sickness behavior
Psychoneuroendocrinology, 2011Co-Authors: Morgan L Moon, Leslie Klis Mcneil, Gregory G FreundAbstract:The macrophage (MΦ) is an essential cellular first responder in the innate immune system, sensing, alerting, removing and destroying intrinsic and extrinsic pathogens. While congenital aplasia of granulocytes, T or B lymphocytes leads to serious disease, lack of MΦs is incompatible with life. The MΦ, however, is not a monomorphic entity. These constructers, repairers and defenders of the body are diverse in form and function. What controls MΦ phenotype is beginning to be understood and involves a complex interplay of origination, location and microenvironment. Common to all MΦ developmental pathways are pro-inflammatory and anti-inflammatory cytokines. MΦs respond to these bioactives in distinct ways developing recently recognized activation phenotypes that canonically support bacterial clearance (classical activation), parasite defense/tissue repair (alternative activation) and anti-inflammation (deactivation). Critically, the same cytokines which orchestrate immune defense and homeostasis dramatically impact sense of well being and cognition by eliciting sickness symptoms. Such behaviors are the manifestation of pro/anti-inflammatory cytokine action in the brain and are a direct consequence of MΦ function. This review describes the "new" archetypal MΦ activation states, delineates microglia phenotypic plasticity and explores the importance of these macrophage activation states to sickness behavior.
