Academic literature on the topic 'Macrophages – Migration'
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Journal articles on the topic "Macrophages – Migration"
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Hargarten, Jessica C., Tyler C. Moore, Thomas M. Petro, Kenneth W. Nickerson, and Audrey L. Atkin. "Candida albicans Quorum Sensing Molecules Stimulate Mouse Macrophage Migration." Infection and Immunity 83, no. 10 (July 20, 2015): 3857–64. http://dx.doi.org/10.1128/iai.00886-15.
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The polymorphic commensal fungusCandida albicanscauses life-threatening disease via bloodstream and intra-abdominal infections in immunocompromised and transplant patients. Although host immune evasion is a common strategy used by successful human fungal pathogens,C. albicansprovokes recognition by host immune cells less capable of destroying it. To accomplish this,C. albicanswhite cells secrete a low-molecular-weight chemoattractive stimulant(s) of macrophages, a phagocyte that they are able to survive within and eventually escape from.C. albicansopaque cells do not secrete this chemoattractive stimulant(s). We report here a physiological mechanism that contributes to the differences in the interaction ofC. albicanswhite and opaque cells with macrophages.E,E-Farnesol, which is secreted by white cells only, is a potent stimulator of macrophage chemokinesis, whose activity is enhanced by yeast cell wall components and aromatic alcohols.E,E-farnesol results in up to an 8.5-fold increase in macrophage migrationin vitroand promotes a 3-fold increase in the peritoneal infiltration of macrophagesin vivo. Therefore, modulation of farnesol secretion to stimulate host immune recognition by macrophages may help explain why this commensal is such a successful pathogen.
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Shaw, Maureen A., Zhen Gao, and Eric S. Mullins. "Plasmin(ogen) Mediates Macrophage Migration in a Fibrin(ogen) Dependent Mechanism." Blood 128, no. 22 (December 2, 2016): 18. http://dx.doi.org/10.1182/blood.v128.22.18.18.
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Abstract Mounting evidence ties both fibrin(ogen) and plasmin(ogen) to inflammatory diseases. Indeed, both fibrin(ogen) and plasmin(ogen) have been linked to critical macrophage functions in multiple disease processes. Migration of macrophages to sites of sterile inflammation is, at least partially, dependent on plasmin(ogen). Mice lacking plasminogen, when challenged with sterile thioglycollate-induced peritonitis, have both diminished overall leukocyte migration and decreased macrophage migration. Additionally, macrophage migration defects have been identified in both mice lacking plasminogen and plasminogen receptors. Plasmin has many targets that may play a role in supporting macrophage migration. In addition to proteolysis of fibrin(ogen), plasmin activates matrix metalloprotease (MMP) 2 and MMP9 and cleaves collagen and laminin. Indeed, mice that lack MMP9 have a migration defect similar to mice that lack plasminogen, suggesting that MMP9 is a biologically relevant proteolytic target in this context. To further examine the targets of plasmin that regulate macrophage migration, we challenged animals that have individual and combined genetic deficiencies in fibrinogen and plasminogen with thioglycollate-induced peritonitis. We have found that mice that lack fibrinogen alone have a significantly increased migration of macrophages to the peritoneal cavity. Mice with lack of plasminogen alone demonstrated the expected diminution in macrophage migration to the peritoneal cavity. However, mice that were deficient in both plasminogen and fibrinogen demonstrated macrophage migration that was indistinguishable from wildtype. These data suggest that fibrin(ogen) impedes macrophage migration to the peritoneal cavity. To further confirm this mechanism, we examined macrophage migration in a transwell assay in vitro, in response to macrophage chemoattractant protein-1 (MCP-1). Here, a macrophage cell line (RAW 264.7) migration was examined in the absence and presence of fibrin matrices. Macrophages, in the absence of plasminogen, did demonstrate a modest, but statistically significant, increase in migration across the transwell membrane in the absence of fibrinogen. When a fibrin matrix was generated on the transwell membrane, macrophages were essentially unable to cross in the absence of plasminogen. These data further support the concept that macrophages require plasmin(ogen) to cross fibrin matrices. To further explore the plasmin(ogen)-fibrin(ogen) interaction in macrophage migration, we assessed the migration of macrophages to fibrin degradation products (FDPs). First, we examined macrophage transwell migration in response to MCP-1 in the presence of FDPs to assess if FDPs impede macrophage migration. Instead of impeding macrophage migration, FDPs significantly increased macrophage migration across the transwell membrane. Indeed FDPs initiated macrophage migration even in the absence of MCP-1. To confirm that this was FDP induced migration, and not direct plasmin signaling on macrophages, we examined macrophage migration to FDPs in the presence of an irreversible plasmin inhibitor. We again found that plasmin degradation of fibrin was needed for migration, however, further plasmin activity was not required. Taken together, these data suggest that macrophages require plasmin(ogen) to navigate fibrin matrices and that the by-product of this degradation (FDPs) is a signal for additional macrophage migration to sites of fibrin deposition. Disclosures Mullins: Baxalta (now part of Shire): Honoraria; US WorldMeds: Membership on an entity's Board of Directors or advisory committees.
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Mullins, Eric S., Maureen A. Shaw, Zhen Gao, and Matthew J. Flick. "Plasmin-Mediated Fibrinolysis Enables Macrophage Migration Via Liberation from Fibrin-αMβ2 Interactions." Blood 132, Supplement 1 (November 29, 2018): 136. http://dx.doi.org/10.1182/blood-2018-99-117018.
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Abstract Mounting evidence ties both fibrin(ogen) and plasmin(ogen) to inflammatory diseases. Indeed, both fibrin(ogen) and plasmin(ogen) have been linked to critical macrophage functions in multiple disease processes. Migration of macrophages to sites of sterile inflammation is, at least partially, dependent on plasmin(ogen). Mice lacking plasminogen, when challenged with sterile thioglycollate-induced peritonitis, have both diminished overall leukocyte migration and decreased macrophage migration. Additionally, macrophage migration defects have been identified in both mice lacking plasminogen and plasminogen receptors. Plasmin has many targets that may play a role in supporting macrophage migration. In addition to proteolysis of fibrin(ogen), plasmin activates matrix metalloprotease (MMP) 2 and MMP9 and cleaves collagen and laminin. Indeed, mice that lack MMP9 have a migration defect similar to mice that lack plasminogen, suggesting that MMP9 is a biologically relevant proteolytic target in this context. To further examine the targets of plasmin that regulate macrophage migration, we challenged animals that have individual and combined genetic deficiencies in fibrinogen and plasminogen with thioglycollate-induced peritonitis. We have found that mice that lack fibrinogen alone have a significantly increased migration of macrophages to the peritoneal cavity. Mice that lack plasminogen alone demonstrated the expected diminution in macrophage migration to the peritoneal cavity. However, mice that were deficient in both plasminogen and fibrinogen demonstrated macrophage migration that was indistinguishable from wildtype. These data suggest that fibrin(ogen) impedes macrophage migration to the peritoneal cavity. To further confirm this mechanism, we examined macrophage migration in a transwell assay in vitro. Here, a macrophage cell line (RAW 264.7 or BMDM) migration was examined in the absence and presence of fibrin matrices. Macrophages, in the presence of plasminogen, did demonstrate a modest, but statistically significant, increase in migration across the transwell membrane in the absence of fibrinogen. When a fibrin matrix was generated on the transwell membrane, macrophages were essentially unable to cross in the absence of plasminogen. These data further support the concept that macrophages require plasmin(ogen) to cross fibrin matrices. We further sought to determine if the fibrin-αMβ2 interaction was implicated in the macrophage migration phenotype. To do this, we first examined macrophage migration in vivo in mice expressing a form of fibrinogen that cannot interact with αMβ2, Fibγ390-396A mice. Similar to mice lacking fibrinogen, an increase in peritoneal macrophages was observed at 72 hours following a challenge with 4% thioglycollate. To confirm that this was related to the fibrin-αMβ2 interaction, and not due to abnormal factor XIII crosslinking, factor XIII deficient animals were also challenged with thioglycollate induced peritonitis. Mice lacking factor XIII exhibited no difference from wildtype in this model of peritonitis. We further confirmed in the in vitro transwell migration assay that macrophages were able to cross a fibrin barrier, derived from Fibγ390-396A mice, in the absence of plasminogen. Taken together, these data suggest that plasmin allows macrophage migration via liberation from the fibrin-αMβ2 interaction. Disclosures Mullins: Shire: Honoraria, Membership on an entity's Board of Directors or advisory committees.
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Munugalavadla, Veerendra, Jovencio Borneo, David A. Ingram, and Reuben Kapur. "p85α subunit of class IA PI-3 kinase is crucial for macrophage growth and migration." Blood 106, no. 1 (July 1, 2005): 103–9. http://dx.doi.org/10.1182/blood-2004-10-4041.
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Macrophages play an essential role in defending against invading pathogens by migrating to the sites of infection, removing apoptotic cells, and secreting inflammatory cytokines. The molecular mechanisms whereby macrophages regulate these processes are poorly understood. Using bone marrow–derived macrophages (BMMs) deficient in the expression of p85α-subunit of class IA phosphatidylinositol 3 (PI-3) kinase, we demonstrate 50% reduction in proliferation in response to macrophage–colony-stimulating factor (M-CSF) as well as granulocyte macrophage–colony-stimulating factor (GM-CSF) compared with wild-type controls. Furthermore, p85α–/– BMMs demonstrate a significant reduction in migration in a wound-healing assay compared with wild-type controls. The reduction in migration due to p85α deficiency in BMMs is associated with reduced adhesion and directed migration on fibronectin and vascular cell adhesion molecule-1. In addition, deficiency of p85α in BMMs also results in defective phagocytosis of sheep red blood cells. Biochemically, loss of p85α in BMMs results in reduced activation of Akt and Rac, but not Erk (extracellular signal-related kinase) mitogen-activated protein (MAP) kinase. Taken together, our results provide genetic evidence for the importance of p85α in regulating both actin- and growth-based functions in macrophages, and provide a potential therapeutic target for the treatment of diseases involving macrophages, including inflammation.
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Kobayakawa, Kazu, Yasuyuki Ohkawa, Shingo Yoshizaki, Tetsuya Tamaru, Takeyuki Saito, Ken Kijima, Kazuya Yokota, et al. "Macrophage centripetal migration drives spontaneous healing process after spinal cord injury." Science Advances 5, no. 5 (May 2019): eaav5086. http://dx.doi.org/10.1126/sciadv.aav5086.
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Traumatic spinal cord injury (SCI) brings numerous inflammatory cells, including macrophages, from the circulating blood to lesions, but pathophysiological impact resulting from spatiotemporal dynamics of macrophages is unknown. Here, we show that macrophages centripetally migrate toward the lesion epicenter after infiltrating into the wide range of spinal cord, depending on the gradient of chemoattractant C5a. However, macrophages lacking interferon regulatory factor 8 (IRF8) cannot migrate toward the epicenter and remain widely scattered in the injured cord with profound axonal loss and little remyelination, resulting in a poor functional outcome after SCI. Time-lapse imaging and P2X/YRs blockade revealed that macrophage migration via IRF8 was caused by purinergic receptors involved in the C5a-directed migration. Conversely, pharmacological promotion of IRF8 activation facilitated macrophage centripetal movement, thereby improving the SCI recovery. Our findings reveal the importance of macrophage centripetal migration via IRF8, providing a novel therapeutic target for central nervous system injury.
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Yakubenko, Valentin P., and Tatiana P. Ugarova. "The Role of Integrin αDβ2 in Macrophage Migration." Blood 106, no. 11 (November 16, 2005): 2215. http://dx.doi.org/10.1182/blood.v106.11.2215.2215.
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Abstract Integrin αDβ2 (CD11d/CD18), the most recently discovered member of the β2 sub-family of adhesion receptors, is strongly upregulated on macrophage foam cells which underscores its potential role in atherosclerosis. However, the contribution of αDβ2 to monocyte/macrophage adhesive reactions and the significance of its overexpression on these cells remain unknown. Recently we characterized αDβ2 as a multiligand receptor capable of binding many extracellular matrix proteins with the recognition specificity overlapping that of the major myeloid-specific integrin αMβ2 (Mac-1). We hypothesized that the αDβ2 ability to bind numerous ligands in the extracellular matrix and its capacity to be upregulated to high density on the surface of macrophages may modulate cell adhesiveness and, thus, affect migration. To evaluate the role of αDβ2 in migration, we generated model and natural cells expressing different densities of αDβ2 and tested their migration to different extracellular matrix proteins. In vitro studies demonstrated that αDβ2 expressed at low densities, either on the surface of HEK293 cells or the mouse macrophage cell line IC-21, supported migration which was partially inhibited by anti-αD function-blocking antibodies. Furthermore, β1 and β3 integrins expressed on HEK293 cells and IC-21 macrophages, respectively, contributed to migration because anti-β1 and anti-β3 antibodies inhibited migration. Increased expression of αDβ2 on the surface of HEK293 cells and its upregulation by PMA on IC-21 macrophages resulted in the inhibition of cell migration. Ligation of αDβ2 with anti-αD antibodies restored β1- and β3-driven cell migration by means of removing restraints imposed by the excess of the αDβ2-ligand adhesive bonds. To test the possibility that progressive upregulation of αDβ2 can block macrophage migration in vivo, we assessed the effect of anti-αD function blocking antibodies using the thioglycollate-induced peritonitis model. More than 4-fold upregulation of αDβ2 was detected on macrophages in 72 h after thioglycollate stimulation and, similar to in vitro studies, the numbers of migration macrophages increased in the presence of anti-αD antibodies. These results demonstrate that the density of αDβ2 can modulate cell migration and suggest that low levels of αDβ2 can contribute to monocyte migration while αDβ2 upregulation on differentiated macrophages might facilitate their retention at the site of inflammation.
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Rumianek, Agata N., and David R. Greaves. "How Have Leukocyte In Vitro Chemotaxis Assays Shaped Our Ideas about Macrophage Migration?" Biology 9, no. 12 (December 2, 2020): 439. http://dx.doi.org/10.3390/biology9120439.
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Macrophage chemotaxis is crucial during both onset and resolution of inflammation and unique among all leukocytes. Macrophages are able to switch between amoeboid and mesenchymal migration to optimise their migration through 3D environments. This subtle migration phenotype has been underappreciated in the literature, with macrophages often being grouped and discussed together with other leukocytes, possibly due to the limitations of current chemotaxis assays. Transwell assays were originally designed in the 1960s but despite their long-known limitations, they are still one of the most popular methods of studying macrophage migration. This review aims to critically evaluate transwell assays, and other popular chemotaxis assays, comparing their advantages and limitations in macrophage migration studies.
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Benyamini, Noam, Samah Waked, Lina Bisharat, Noam Bettman, and Tami Katz. "The Effect of Lenalidomide on Multiple Myeloma Associated Macrophages." Blood 128, no. 22 (December 2, 2016): 3689. http://dx.doi.org/10.1182/blood.v128.22.3689.3689.
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Abstract Introduction: In multiple myeloma (MM), accessory cells, such as monocytes and macrophages, located in the bone marrow (BM) tumor microenvironment play a crucial role in the fate of malignant cells. Under the influence of the surrounding milieu, monocytes can change their migratory capacity and differentiate into tumor-associated macrophages (TAMs). In the tumor site, TAMs can alter their profile from M1 macrophages with antitumor activities to M2-like macrophages that support tumor growth. Lenalidomide (Len), an immunomodulatory drug, used for MM treatment, is known to target different immune components inducing inflammatory responses; however, its direct influence on monocyte migration, macrophage differentiation and function in the tumor microenvironment is still unclear. The current study has aimed to explore the effect of Len on monocyte recruitment, macrophage polarization and pro-tumor functions. Methods: Monocytes were isolated from peripheral blood mononuclear cells of healthy donors, using anti-CD14 microbeads. To assess their migration capacity, monocytes were allowed to migrate through transwell insert towards the conditioned medium (CM) obtained from the BM of newly diagnosed MM patients or from MM cell lines (RPMI or U266) in the presence or absence of Len (10µM); the percentage of migrating monocytes was determined by FACS. For macrophage generation, monocytes were cultured with M-CSF followed by incubation with IL-4 to obtain M2 macrophages. To generate TAMs, CM obtained from the BM of MM patients was used. Len was added to the culture every 24 hours. The phenotype and functional properties of the generated macrophages were assessed. Endocytosis was evaluated by an antigen uptake assay. Macrophages were incubated with FITC-dextran at 37°C or 4°C, as a control, for 60 minutes, and analyzed by FACS. To test T cell proliferation, autologous lymphocytes labeled with CFSE, were stimulated with PHA and co-cultured with macrophages. T cell (CD3+) division was assessed by FACS. For IFN-γ secretion evaluation, lymphocytes co-cultured with macrophages were stimulated with PMA and ionomycin. The percentage of T cells expressing IFN-γ was quantified by FACS. Results: Monocyte migration towards CM obtained from MM cell lines (RPMI or U266) or from BM of MM patients (80.89%; n=4; p<0.01, 57.17%; n=4; p<0.01 and 42.9%; n=9; p<0.05, respectively) was significantly higher compared to migration towards normal BM CM (25.39%; n=2). Monocytes treated with Len demonstrated significantly decreased migration toward CM of MM cell lines (RPMI or U266) compared to untreated monocytes (45% vs. 80.8%; n=4 and 30.2% vs. 57.1%; n=4, respectively; p<0.01). The effect of Len on monocyte migration toward patient- derived CM was diverse. While 4 samples demonstrated decreased migration compared to untreated cells [51.1% vs. 59.6%; n=4; p<0.01], in 5 samples it increased [39.8% vs. 29.7%; n=5; n=5; p<0.01]. To evaluate the effect of Len on macrophage polarization we examined their phenotype and functions. Both M2 macrophages and TAMs treated with Len expressed higher levels of M2 markers CD206, CD163, and cytokine IL-10 compared to untreated macrophages. Functional assays showed that Len increased endocytosis of both M2 macrophages [50% vs. 20%; n=5; P<0.01] and TAMs [47.4% vs. 41.4%; n=6; NS]. Exposure to Len led to suppression of T cell proliferation, when T cells were co-cultured with either autologous M2 macrophages [31% vs. 16%; n=4; p<0.05] or TAMs [39.7% vs. 31.5%; n=3; p<0.01]. In addition, M2 macrophages treated with Len demonstrated a reduction in IFN-γ secretion from T cells compared to untreated M2 macrophages (10.6% vs. 7.1%; n=4; NS). Conclusions: This study has demonstrated that Len has a direct effect on monocyte/macrophage behavior in the microenvironment generated by MM cells. Len is found to reduce monocyte migration, support polarization of macrophages towards the M2 phenotype and promote macrophage immunosuppressive functions, such as endocytosis, reduction of T-cell proliferation and inhibition of IFN-γ production. These findings need to be further investigated in in vivo experiments and could support the benefit of using agents targeting specific pathways associated with TAM development in the treatment of MM patients. Disclosures No relevant conflicts of interest to declare.
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Cho, Sun Wook, Young A. Kim, Hyun Jin Sun, Ye An Kim, Byung-Chul Oh, Ka Hee Yi, Do Joon Park, and Young Joo Park. "CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma." Endocrine-Related Cancer 23, no. 2 (November 11, 2015): 113–24. http://dx.doi.org/10.1530/erc-15-0196.
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Macrophages in tumor microenvironment have pivotal roles in tumor growth, metastasis, and angiogenesis. We investigated the interacting mechanism of macrophage actions in human papillary thyroid cancer (PTC). Co-cultures of macrophage/PTC significantly increased the cancer cell migration potentials, compared with the PTC culture alone. Treatment of conditioned medium (CM) of macrophage/PTC co-cultures enhanced cell invasions in 3D invasion assay. Cytokine array analysis demonstrated that CM of macrophage/PTC co-cultures contained a high level of CXCL16, while it was not found in CM of PTC culture alone. Treatment with CXCL16 enhanced the cell migration potentials in PTC cells, and blocking CXCL16 signaling using anti-CXCL16 antibody or metalloproteinase inhibitor (TAPI2) attenuated macrophage-mediated enhancement of PTC cell migration potentials. In PTC cells, CXCL16 treatment or co-cultures with macrophages increased Akt phosphorylation, and these macrophage-dependent increases of Akt phosphorylation was inhibited by anti-CXCL16 antibody. Moreover, Akt inhibitor attenuated macrophage-mediated increases of PTC cell migration potential. In macrophages, treatment of macrophage/PTC co-cultured CMs up-regulated CD163, Il10, and CD206, which were attenuated by anti-CXCL16 antibody treatment. Finally, CXCR6 and CXCL16 expressions were evaluated by immunohistochemical staining with a thyroid tissue microarray including 136 PTC. CXCR6 expressions showed positive correlation with the density of CD163+ macrophages and associated with lymph node metastasis. In conclusion, CXCL16 signaling partly mediated macrophage actions on PTC tumor cell invasion and also changed the macrophage phenotypes into M2-macrophages in PTC tumor microenvironment. These data suggested that CXCL16 signaling, a bidirectional player in macrophage-associated tumor microenvironment, might be a potential therapeutic target of human PTC.
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Li, Xue, Deana Mikhalkova, Erhe Gao, Jin Zhang, Valerie Myers, Carmen Zincarelli, Yonghong Lei, et al. "Myocardial injury after ischemia-reperfusion in mice deficient in Akt2 is associated with increased cardiac macrophage density." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (November 2011): H1932—H1940. http://dx.doi.org/10.1152/ajpheart.00755.2010.
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Akt2 protein kinase has been shown to promote cell migration and actin polymerization in several cell types, including macrophages. Because migrating macrophages constitute an important inflammatory response after myocardial ischemia, we determined cardiac macrophage expression after ischemia-reperfusion (I/R) injury and cryo-injury in mice lacking Akt2 (Akt2-KO). At 7 days post-I/R, Akt2-KO cardiac tissues showed an increase in immunohistochemical staining for macrophage markers (Galectin 3 and F4/80) compared with wild-type (WT) mice, indicating macrophage density was increased in the injured Akt2-KO myocardium. This change was time dependent because macrophage density was similar between WT and Akt2-KO myocardium at 3 days post-I/R, but by 7 and 14 days post-I/R, macrophage density was significantly increased in Akt2-KO myocardium. Concomitantly, infarct size was larger and cardiac function was reduced in Akt2-KO mice subjected to I/R. However, when cryo-infarction produced similar infarct sizes in the anterior wall in both WT and Akt2-KO mice, macrophage density remained higher in Akt2-KO mouse myocardium, suggesting Akt2 regulates myocardial macrophage density independent of infarct size. Consistently, bone marrow from Akt2-KO mice enhanced myocardial macrophage density in both C57/B6 WT and Akt2-KO recipient mice. Finally, reciprocal ex-vivo coculturing of macrophages and cardiac myocytes showed that activated Akt2-KO peritoneal macrophages had reduced mobility and adhesion when compared with WT littermate controls. Thus, although Akt-2 KO mice did not affect the initial inflammation response after injury and Akt2 deficiency has been shown to impair cell migration or motility in macrophages, our data suggested a novel mechanism in which increasing retention of Akt2-KO macrophages resulted in increasing cardiac Akt2-KO macrophage density in the myocardial space.
Dissertations / Theses on the topic "Macrophages – Migration"
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Gui, Philippe. "Caractérisation de la migration trans-tissulaire des macrophages." Toulouse 3, 2014. http://thesesups.ups-tlse.fr/2612/.
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L'infiltration de macrophages dans les tumeurs est associée à un mauvais pronostic. Le contrôle de leur migration trans-tissulaire représente donc un enjeu thérapeutique important. Ma thèse a consisté à identifier les mécanismes impliqués dans cette migration. Grâce à des approches d'observation directe du comportement migratoire des cellules dans des tissus vivants (microscopie intravitale et explants tissulaires ex vivo), je montre que les macrophages in vivo adoptent un mode de migration distinct selon le tissu. Dans un fibrosarcome (tissu dense), ils ont une migration de type mésenchymateux (dépendante des protéases), tandis que dans le derme sain adjacent, ils ont une migration de type amiboïde (indépendante des protéases). De plus, j'ai identifié une protéine, p27kip1, impliquée dans la migration mésenchymateuse. Ainsi, en montrant que la migration mésenchymateuse des macrophages existe in vivo, notamment dans les tumeurs, elle pourra devenir une cible thérapeutique prometteuseThe infiltration of macrophages inside tumors is associated with a poor prognosis. Therefore, the specific control of their trans-tissular migration represents an important therapeutic challenge. My thesis has consisted in identifying the mechanisms involved in this migration. Using approaches allowing the observation of the migration behavior of cells directly inside living tissues (intravital microscopy and ex vivo tissue explants), I show that macrophages adopt a distinct migration mode in vivo depending on the tissue. In a fibrosarcoma (dense tissue), they use a mesenchymal-like migration (protease-dependent), whereas in the healthy surrounding derma, they use an amoeboid-like migration (protease-independent). Moreover, I identified a protein, p27kip1, involved in mesenchymal migration. In conclusion, by showing that the mesenchymal migration of macrophages exists in vivo, particularly in tumors, it could become a promising therapeutic target
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Van, Goethem Emeline. "Caractérisation de la migration trans-matricielle des phagocytes humains." Toulouse 3, 2010. http://thesesups.ups-tlse.fr/1061/.
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Le recrutement des macrophages et neutrophiles sur un site infecté ou enflammé est une étape clé de la réponse immunitaire innée. Cependant, dans certaines maladies (maladies inflammatoires chroniques, cancers. . . ), le recrutement chronique et massif des macrophages participe à la progression de la pathologie. In vivo, les phagocytes migrent essentiellement au sein d'un environnement tri-dimensionnel (3D). Si rien n'était connu sur la migration 3D des macrophages, celle des cellules tumorales, bien documentée, avait permis de montrer qu'elle fait appel à des mécanismes très différents de la migration 2D et de définir deux modes principaux de migration : le mode mésenchymal, dépendant de la dégradation de la matrice extra-cellulaire (MEC) par les protéases et le mode amiboide, indépendant de cette dégradation. L'objectif de ma thèse a été de caractériser le mode migratoire 3D des macrophages humains dans un modèle d'étude simple in vitro permettant de comparer la migration dans des matrices de compositions, d'architectures et de propriétés visco-élastiques différentes. J'ai ainsi pu montrer que 1) les macrophages humains sont capables d'adopter les deux modes migratoires décrits à ce jour, 2) le choix du mode migratoire est dicté par l'architecture de la matrice rencontrée, 3) les macrophages utilisent le mode mésenchymal pour traverser les MEC les moins poreuses notamment via la mise en place de structures dégradatives : les podosomes 3D. L'évaluation des modes migratoires des différentes sous populations de macrophages et des autres phagocytes humains (monocytes, neutrophiles et cellules dendritiques) a fait suite à ce travail et est encore en cours d'expérimentationRecruitment of macrophages and neutrophils to the inflamed or infected site is a critical step of innate immune response. However, in some diseases (chronic inflammatory disorders, cancers. . . ), the recruitment becomes chronic and massive, and participates in pathology progression. In vivo, phagocytes are mainly migrating within a three-dimensional (3D) environment. If nothing was known about 3D migration of macrophages, the one of tumor cells is well documented. It allowed to establish that 2D migration and 3D migration do not require the same mechanisms and to identify two main migration modes: the mesenchymal mode, dependent on extra-cellular matrix (ECM) degradation by proteases and the amoeboid mode, independent on that degradation. The aim of my PhD was to characterize the 3D migratory behaviour of human macrophages using a simple in vitro model that allowed us to compare migration within matrices of different composition, architecture and visco-elastic properties. I was thus able to show that 1) human macrophages are able to adopt the two migration modes described so far, 2) the choice of migratory mode is dictated by the architecture of the matrix encountered, 3) macrophages are using the mesenchymal mode to migrate within the least porous ECM, through the formation of degradative structures: the 3D podosomes. Following this work, 3D migration of different macrophage sub-populations and of other human leukocytes: monocytes, neutrophils and dendritic cells has been evaluated and this study is still on going
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Stamps, Stacy Leanne. "Determination of a catalytic mechanism for the enzymatic activity of macrophage migration inhibitory factor /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.
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Murray, Megan. "Metalloproteinase expression in bone marrow-derived macrophages : roles in cell migration." Thesis, University of East Anglia, 2010. https://ueaeprints.uea.ac.uk/20512/.
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Desvignes, Emma. "Dispositifs fluidiques 3D pour l'étude de la migration cellulaire des macrophages." Thesis, Toulouse, INSA, 2018. http://www.theses.fr/2018ISAT0046.
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Au cours des deux dernières décennies, des études ont été réalisée pour mesurer les forces mécaniques exercées par des cellules vivantes sur leur environnement. Cela a conduit au développement de diverses techniques ingénieuses qui ont principalement été réalisées pour comprendre la façon dont les cellules exercent des forces pendant leur migration sur des substrats bidimensionnels (2D). Cependant, in vivo, les cellules migrent à travers des environnements tridimensionnels (3D) et les mécanismes utilisés pour migrer en 3D diffèrent significativement de ceux de la migration 2D. A titre d'exemple, les cellules confinées en 3D rencontrant des constrictions ont besoin de déformer leur noyau, leur organelle le plus grand et le plus rigide. En 2D, les noyaux ne sont pas des facteurs limitants pour la migration. Il est donc nécessaire de développer des outils pour comprendre comment les cellules migrent en 3D. En particulier, des études doivent être menées pour déterminer comment les cellules appliquent des forces en fonction du niveau de confinement auquel elles se trouvent confrontées. Pour répondre à cette question difficile, nous avons développé deux types de micro-dispositifs. Tout d'abord, nous avons conçu et fabriqué un dispositif de microfluidique pour étudier les forces générées par les cellules pendant une migration confinée. Ce dispositif est constitué de microcanaux de dimensions contrôlées équipés de micropiliers, servant de capteurs de forces .Ces capteurs de forces présentent une sensibilité de l’ordre de 70 pN. Nous avons ensuite introduit dans le dispositif des macrophages humains, cellules du système immunitaire, à l'intérieur du dispositif et évalué la flexion des micropiliers engendrée par les forces cellulaires appliquées lors de leur migration. Grâce au développement d’un algorithme permettant l’analyse des images, nous avons pu évaluer les forces générées dans différentes zones cellulaires et révéler que les cellules redirigent les forces de pression de l'intérieur vers l'extérieur lorsque le degré de confinement augmente. Cette observation suggère un mode de migration très spécifique lié au confinement spatial qui est basé sur l’appui sans adhésion sur les obstacles de l’environnement. Dans un deuxième temps nous avons fabriqué des réseaux tri-dimensionnels obtenus par une méthode de lithographie bi-photonique 3D. Les motifs de ces réseaux possèdent des dimensions caractéristiques de l'échelle cellulaire (1-10 μm) et sont composés de poutres suspendues qui peuvent être courbés par les cellules vivantes qui migrent au sein du treillis tri-dimensionnel. En enregistrant une séquence vidéo des déformations de l'échafaudage, nous pouvons étudier l'activité mécanique de la cellule dans l'espace et le temps pendant sa migration 3D. Nos résultats montrent que les macrophages sont capables de pénétrer dans des réseaux de géométrie cubique lorsque la période du réseau est supérieure à 5 μm et que le support de migration lui-même peut être utilisé comme capteur pour mesurer les forces exercées par les cellules. Grâce à la mesure de la rigidité du matériau constituant le treillis 3D et des modélisations de la déformation élastique de la structure 3D, nous avons pu évaluer que la contrainte mécanique globale qu’exerce un macrophage sur son microenvironnement est de l’ordre de 500 kPa. Grâce à la combinaison de la microfabrication, l'imagerie cellulaire et l'analyse automatisée des images, nous sommes parvenus à quantifier les efforts mécaniques cellulaires mis en jeu lors de la migration de macrophages humains au sein d’environnements confinés et nous mettons ainsi en lumière la mécanique spécifique des cellules migrant en 3DOver the past two decades, studies have been conducted to measure the mechanical forces exerted by living cells on their environment. This has led to the development of a variety of ingenious techniques that have been primarily developed to understand how cells exert forces during their migration on 2D substrates. However, in vivo, cells migrate through three-dimensional (3D) environments and the mechanisms used to migrate in 3D differ significantly from those of 2D migration. For example, confined cells in 3D encountering constrictions need to deform their nucleus, their largest and most rigid organelle. In 2D, kernels are not limiting factors for migration. It is therefore necessary to develop tools to understand how cells migrate in 3D. In particular, studies need to be conducted to determine how cells apply forces based on the level of containment they encounter. To answer this difficult question, we have developed two types of micro-devices. First, we designed and manufactured a microfluidic device to study the forces generated by cells during a confined migration. This device consists of microchannels of controlled dimensions equipped with micropiliers, serving as force sensors. These force sensors have a sensitivity of the order of 70 pN. We then introduced into the device human macrophages, cells of the immune system, inside the device and evaluated the bending of micropiliers generated by the cellular forces applied during their migration. Through the development of an algorithm for image analysis, we have been able to evaluate the forces generated in different cell areas and reveal that cells are redirecting pressure forces from the inside to the outside as the degree of containment increases. This observation suggests a very specific mode of migration related to spatial confinement that is based on the support without adhesion on the obstacles of the environment. In a second time we made three-dimensional networks obtained by a 3D bi-photonic lithography method. Les motifs de ces réseaux possèdent des dimensions caractéristiques de l'échelle cellulaire (1-10 μm) et sont composés de poutres suspendues qui peuvent être courbés par les cellules vivantes qui migrent au sein du treillis tri-dimensionnel. En enregistrant une séquence vidéo des déformations de l'échafaudage, nous pouvons étudier l'activité mécanique de la cellule dans l'espace et le temps pendant sa migration 3D. Nos résultats montrent que les macrophages sont capables de pénétrer dans des réseaux de géométrie cubique lorsque la période du réseau est supérieure à 5 μm et que le support de migration lui-même peut être utilisé comme capteur pour mesurer les forces exercées par les cellules. Grâce à la mesure de la rigidité du matériau constituant le treillis 3D et des modélisations de la déformation élastique de la structure 3D, nous avons pu évaluer que la contrainte mécanique globale qu’exerce un macrophage sur son microenvironnement est de l’ordre de 500 kPa. Grâce à la combinaison de la microfabrication, l'imagerie cellulaire et l'analyse automatisée des images, nous sommes parvenus à quantifier les efforts mécaniques cellulaires mis en jeu lors de la migration de macrophages humains au sein d’environnements confinés et nous mettons ainsi en lumière la mécanique spécifique des cellules migrant en 3D
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Prieto-Lafuente, Lidia. "Macrophage-migration Inhibitory Factor (MIF) homologues in the host-parasite interaction." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/3458.
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The ability of filarial parasites to persist in an immunological competent host, has led to the suggestion that they have evolved specific measures to counter immune defences. Filarial nematodes produce and secrete excretory-secretory (ES) products, some of which have been described to have a potential role in immune evasion. As part of these ES products, two homologues of the mammalian cytokine macrophage-migration inhibitory factor (MIF) have been described from the filarial nematode Brugia malayi, Bm-MIF-1 and Bm-MIF-2. Mammalian MIF is a widely distributed protein constitutively expressed in many immune and non-immune cell types. Although firstly characterised by its ability to stop migration of peritoneal macrophages, it has now been shown to play an important role during different inflammation processes. The main aim of this study is to elucidate the role of Brugia MIF homologues and their relation with the mammalian cytokine. This thesis studies the effect of both filarial and host MIF homologues on two major immune cell types, macrophages and dendritic cells (DC). We found that both Brugia and mouse-MIF synergise with IL-4 to activate macrophages to an alternative phenotype, by enhancing expression of IL-4-induced alternative activation markers Arginase-1, Ym-1 and the macrophage Mannose Receptor. MIF also synergises with IL-4 to render macrophages suppressive, an important outcome during filarial infection. Additionally we found that MIF homologues induce IL-4Ra expression, suggesting a mechanism by which MIF enhances IL-4 activation. We showed that filarial and mouse MIF homologues differ in their capacity to activate bone marrow-derived immature dendritic cells. Mouse-MIF up-regulates MHC-II and CD40 expression and induces pro-inflammatory cytokine production after overnight treatment. On the other hand Bm-MIF-2 induces low levels of cytokine production but does not up-regulate activation markers, and Bm-MIF-1 failed to activate DC. Furthermore, we demonstrate that filarial MIF homologues impair DC differentiation from bone marrow precursors. While bone marrow cells cultured in the presence of GM-CSF, with or without mouse-MIF, differentiate into CD11c+ DC, addition of Bm-MIF-2 to the culture media impairs differentiation arresting the cells in an undifferentiated phenotype characterised by the expression of myeloid and granulocyte markers CD11b and GR1. Finally, using an in vivo model where we implant Brugia malayi parasites in the peritoneal cavity of mice, we observed that host MIF does not play an essential role in the activation of macrophages by adult parasites as macrophages form MIF deficient mice present the same phenotype as their wild type counterparts.
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Smolders, Sophie. "La migration des microglies et les molécules adhésives au cours du développement embryonnaire du cerveau." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066533/document.
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Les microglies sont des cellules hématogène mais prennent place dans le système nerveux central (SNC) au cours du développement embryonnaire pour constituer la population résidente des cellules immunitaires. Elles sont les médiateurs crucials du bon développement et de l'entretien des réseaux de neurones dans le SNC. De nombreux aspects de la physiologie microgliale et les mécanismes qui sous-tendent leurs fonctions au cours du développement embryonnaire du cerveau sont encore largement méconnues. Cette thèse de doctorat porte sur la migration des cellules microgliales au cours du développement embryonnaire du cortex et elle débouche sur trois grandes conclusions. (1) Les cellules microgliales embryonnaires in situ sont très dynamiques et adaptent leur phénotype à leur environnement local. (2) La vitesse de migration des microglies ex vivo dépend des intégrines beta1 qui exercent des fonctions à la fois inhibitrices et promotrices sur la migration selon l'âge embryonnaire. (3) Les microglies jouent probablement un rôle dans l'étiologie des troubles du développement neurologique, mais il faudrait que les futures recherches se concentrent sur le dysfonctionnement des microglies plutôt que sur leur activation immunitaire classiqueMicroglia are blood-borne cells but take up residence in the central nervous system (CNS) during embryonic development to constitute the resident pool of immune cells. They are crucial mediators of the healthy development and maintenance of neural networks in the CNS. Many aspects of the physiology of microglia and the mechanisms underpinning their tasks during embryonic brain development are still unresolved. This doctoral dissertation focuses on migration of microglial cells during embryonic cortical development. All together, this dissertation brings forwards three major conclusions. (1) In situ embryonic microglia are highly dynamic cells that adapt their phenotype to their local environment. (2) Microglial migration speed ex vivo is dependent on β1 integrins that exert both migration promoting and inhibiting functions which are age-specifically regulated. (3) Microglia likely play a role in the etiology of neurodevelopmental disorders, but further research should focus on microglia dysfunction rather than classical microglial immune activation
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Souriant, Shanti. "Rôle des macrophages au cours de l'infection par le VIH-1 et dans un contexte de co-infection avec Mycobacterium tuberculosis." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30209.
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Les macrophages sont une cible cellulaire du VIH-1, et jouent un rôle important dans la pathogenèse virale. Au cours de ma thèse, je me suis intéressée au rôle des macrophages dans la pathogenèse du VIH-1, mais aussi au cours de la co-infection avec Mycobacterium tuberculosis (Mtb), l'agent étiologique de la tuberculose. J'ai tout d'abord participé à une étude mettant en évidence que l'infection par le VIH-1 reprogramme la migration des macrophages, favorisant notamment le mode migratoire protéolytique. Cet effet est médié par l'interaction de la protéine virale Nef avec les protéines de l'hôte Hck et WASP, ce qui conduit à une modification de l'organisation et de la fonction des podosomes, structures impliquées dans la dégradation de la matrice extracellulaire et la migration dépendante des protéases. La meilleure capacité à migrer des macrophages infectés par le VIH-1 in vitro se traduit in vivo par une augmentation du recrutement des macrophages dans différents tissus de souris transgéniques qui expriment la protéine Nef. Ces travaux ont ainsi révélé un nouveau mécanisme par lequel le VIH-1 dissémine dans les tissus, via l'action de Nef dans les macrophages. L'association fréquente du VIH-1 avec Mtb complique le problème de santé publique posé par l'infection virale. En effet, Mtb aggrave la pathogenèse du VIH-1 chez les patients co-infectés. L'étude des mécanismes impliqués et le rôle des macrophages dans ce phénomène constituent les objectifs principaux de ma thèse. J'ai révélé que les macrophages infectés par Mtb génèrent un microenvironnement qui active les macrophages voisins vers un programme de polarisation anti-inflammatoire dit M(IL-10). J'ai mis en évidence que ces macrophages M(IL-10) sont particulièrement efficaces pour la production de VIH-1. J'ai démontré que le microenvironnement associé à la tuberculose entraîne la formation de nanotubes entre les macrophages, grâce à l'activation de la signalisation cellulaire médiée par l'axe IL-10/STAT3. Ces nanotubes, qui favorisent le transfert du virus d'un macrophage à un autre, sont à l'origine de la spectaculaire production de VIH-1 par les macrophages. Nous avons également constaté que ces cellules M(IL-10) s'accumulent dans la circulation sanguine des patients co-infectés ainsi que dans les poumons de primates non-humains co-infectés. Dans l'ensemble, mes travaux identifient les nanotubes comme des acteurs clés dans l'aggravation de la pathogenèse du VIH-1 lors de la co-infection avec Mtb. Ainsi, les nanotubes et la voie de signalisation IL-10/STAT3 pourraient représenter des cibles pour développer de nouvelles thérapies de lutte contre la comorbidité VIH/Mtb. Les résultats obtenus lors de ma thèse contribuent à une meilleure compréhension du rôle des macrophages dans la pathogenèse et la dissémination du VIH-1 dans un contexte de mono-infection, ou lors d'une co-infection avec MtbMacrophages are both crucial host effector cells for HIV-1 and important leukocytes involved in viral pathogenesis. For my doctoral thesis, I was interested in further characterizing the role of macrophages in HIV-1 pathogenesis, and during co-infection with Mycobacterium tuberculosis (Mtb), the etiological agent for tuberculosis (TB). I first participated in a study that provided evidence that HIV-1 infection reprograms the migration of macrophages, particularly by triggering the protease-dependent migration mode. This effect was mediated by the interaction of the viral protein Nef with the host proteins Hck and WASP, which leads to modification in the organization and proteolytic activity of podosomes, important structures for protease-dependent migration. The higher migration capacity of HIV-1-infected macrophages translated in vivo by an increase in the recruitment of macrophages in several tissues of Nef-transgenic mice. This work revealed a novel mechanistic understanding of how HIV-1 infection drives macrophages into tissues, contributing to viral dissemination and possibly creating a hidden cellular reservoir of virus. Worsening this public health issue posed by the HIV-1 epidemic is the frequent association of the virus with Mtb. Indeed, Mtb aggravates HIV-1 pathogenesis in co-infected individuals. Yet, the mechanisms involved in this process are still poorly understood, including the contribution of macrophages. To investigate how Mtb exacerbates the HIV-1 infection in human macrophages was the main focus of my thesis. First, I revealed that Mtb-infected macrophages generate a microenvironment that drives bystander macrophages towards phenotypic and functional features of the so-called M(IL-10) anti-inflammatory program. I found that these M(IL-10) macrophages are highly efficient for HIV-1 production. I demonstrated that the TB-associated microenvironment induces the formation of macrophage-to-macrophage connecting tunneling nanotubes (TNTs) through the IL- 10/STAT3 axis, a phenomenon that is responsible for the dramatic increase of HIV-1 production in M(IL-10) macrophages. Moreover, I provided evidence that M(IL-10) cells are expanded in the peripheral blood of co-infected patients and accumulate in the lungs of co-infected non-human primates. Altogether, this central part of my PhD thesis sheds light to TNTs as key players in the aggravation of HIV-1 pathogenesis in human macrophages during co-infection with Mtb. Thus, this cellular mechanism (together with the IL- 10/STAT3 axis) could represent an unexpected target to develop novel therapeutics against AIDS/TB co-morbidity. Collectively, the results obtained during my thesis contribute to a better understanding of the role of macrophages during HIV-1 pathogenesis and their ability to disseminate the virus in a mono-infection context, or during co-infection with Mtb
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Veillat, Véronique. "Régulation et mécanismes d'action du facteur inhibiteur de la migration des macrophages (MIF) dans l'endométriose." Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27082/27082.pdf.
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Barnes, Mark Aaron Jr. "MACROPHAGE MIGRATION INHIBITORY FACTOR AND LIVER DISEASE: THE ROLE OF MIF IN ALCOHOL-INDUCED LIVER INJURY AND CARBON TETRACHLORIDE (CCI4)-INDUCED LIVER FIBROSIS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1396429556.
Full textBooks on the topic "Macrophages – Migration"
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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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Paladi, Magdalena. A genetic analysis of Drosophila embryonic macrophage migration. Ottawa: National Library of Canada, 2003.
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Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.
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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.
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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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Richard, Bucala, ed. MIF: Most interesting factor. Singapore: World Scientific, 2007.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
Book chapters on the topic "Macrophages – Migration"
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Taylor, Lewis, Carlota Recio, David R. Greaves, and Asif J. Iqbal. "In Vitro Migration Assays." In Macrophages, 197–214. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7837-3_19.
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Flynn, Jacqueline K., Nadia S. Deen, and James Harris. "Flow Cytometry Phenotyping of Bone Marrow-Derived Macrophages from Wild-Type and Mif−/− Mice." In Macrophage Migration Inhibitory Factor, 57–66. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_6.
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Humphrey, J. H. "Macrophages and the Differential Migration of Lymphocytes." In Ciba Foundation Symposium 71 - Blood Cells and Vessel Walls, 287–98. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720547.ch15.
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Shaw, L. M., and A. M. Mercurio. "Regulation of α6β1 Integrin-Mediated Migration in Macrophages." In Inflammation: Mechanisms and Therapeutics, 101–6. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7343-7_8.
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van Furth, R. "Production and migration of monocytes and kinetics of macrophages." In Mononuclear Phagocytes, 3–12. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-015-8070-0_1.
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Sorg, C., E. Michels, U. Malorny, and J. Knop. "Induction of phenotypic alterations in macrophages by migration inhibitory factors." In Mononuclear Phagocytes, 583–90. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5020-7_61.
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de Souza, G. E. P., F. Q. Cunha, and S. H. Ferreira. "Resident Macrophages Control Initial Neutrophil Migration in the Acute Inflammatory Response." In Inflammatory Mediators, 149–56. London: Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07834-9_13.
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Buzney, Sheldon M., and Salim A. Bishara. "Stimulation of Retinal Pigment Epithelium (RPE) Proliferation and Migration of Macrophages." In Proliferative Vitreoretinopathy (PVR), 124–29. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3910-9_16.
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Springeii, Timothy A., and Donald C. Anderson. "The Importance of the Mac-1, LFA-1 Glycoprotein Family in Monocyte and Granulocyte Adherence, Chemotaxis, and Migration into Inflammatory Sites: Insights from an Experiment of Nature." In Ciba Foundation Symposium 118 - Biochemistry of Macrophages, 102–26. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720998.ch8.
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Rüder, Marike, Benedikt M. Nagel, and Sven Bogdan. "Analysis of Cell Shape and Cell Migration of Drosophila Macrophages In Vivo." In Methods in Molecular Biology, 227–38. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7701-7_17.
Full textConference papers on the topic "Macrophages – Migration"
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Rakovich, T., C. Cunningham, S. Ansboro, T. McGarry, DJ Veale, and U. Fearon. "P169 Effect of macrophage migration inhibitory factor on human macrophages from arthritis patients." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.151.
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Green, Teresa D., Joungjoa Park, Samuel L. Jones, Kenneth B. Adler, and Troy Ghashghaei. "MARCKS Protein Is Involved In Migration Of Murine Macrophages." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1276.
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Green, TD, J. Park, SL Jones, and KB Adler. "A MARCKS-Related Peptide Inhibits Migration of Murine Macrophages." 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.a1346.
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Green, Teresa D., and Kenneth B. Adler. "The Role Of Marcks-Related Peptide In Migration Of Primary Murine Macrophages." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4542.
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Rego, Stephen, Rachel Helms, Alexander De Piante, Amritha Kidiyoor, Amanda Lance, Pinku Mukherjee, and Didier Dréau. "Abstract 1540: TNFRs shed by tumor cells inhibit the migration of macrophages." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1540.
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Zhang, Zhihong. "Dynamical optical imaging monocytes/macrophages migration and activation in contact hypersensitivity (Conference Presentation)." In Biophotonics and Immune Responses XII, edited by Wei R. Chen. SPIE, 2017. http://dx.doi.org/10.1117/12.2251088.
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Ramasamy, Kumaraguruparan, Gagan Deep, Alpna Tyagi, Chapla Agarwal, and Rajesh Agarwal. "Abstract 2579: Silibinin inhibits tumor associated macrophages-induced lung cancer cell growth and invasiveness by down-regulating macrophage migration inhibitory factor ." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2579.
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Madden, Julie, Steve Allen, Yu-Chi Shen, Chelsea Fournier, ZhiFen Wu, Liwei Bao, and Sofia Merajver. "Abstract 3236: Macrophages increase the expression of RhoC in inflammatory breast cancer leading to increased migration." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3236.
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Wu, Caren Yu-Ju, Chia-Hua Chen, Chun-Yen Lin, Li-Ying Feng, Yung-Chang Lin, Kuo-Chen Wei, Chiung-Yin Huang, Jia-You Fang, and Pin-Yuan Chen. "Abstract 3794: CCL5 from tumor-associated macrophages/microglia (TAMs) regulates glioma migration and invasion via calcium-dependent matrix metalloproteinase-2." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3794.
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Kato, Sumie, Lorena Abarzua-Catalan, Isidora Solar-Costabal, Karen García, Jorge Branes, Gareth I. Owen, and Mauricio A. Cuello. "Abstract 2395: Leptin induces an IL-6 mediated interaction between macrophages and ovarian cancer cells that prompted invasiveness and migration." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2395.
Full textReports on the topic "Macrophages – Migration"
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Guess, Jennifer C., and Dennis J. McCance. Decreased Migration of Langerhans Precursor-Like Cells in Response to Human Keratinocytes Expressing HPV-16 E6/E7 is Related to Reduced Macrophage Inflammatory Protein-3Alpha Production. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada435872.
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