Academic literature on the topic 'Immunoglobulins; Adhesion molecules; Macrophages'
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Journal articles on the topic "Immunoglobulins; Adhesion molecules; Macrophages"
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Lin, Qiu-Yue, Ping-Ping Lang, Yun-Long Zhang, Xiao-Lei Yang, Yun-Long Xia, Jie Bai, and Hui-Hua Li. "Pharmacological blockage of ICAM-1 improves angiotensin II-induced cardiac remodeling by inhibiting adhesion of LFA-1+ monocytes." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 6 (December 1, 2019): H1301—H1311. http://dx.doi.org/10.1152/ajpheart.00566.2019.
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Intercellular adhesion molecule-1 (ICAM-1) is a member of an immunoglobulin-like superfamily of adhesion molecules that mediate leukocyte adhesion to vascular endothelium and are involved in several cardiovascular diseases, including ischemia-reperfusion injury, myocardial infarction, and atherosclerosis. However, the role of ICAM-1 in angiotensin II (ANG II)-induced cardiac remodeling in mice remains unclear. Wild-type mice were administered an IgG control or ICAM-1 neutralizing antibody (1 and 2 mg/mouse, respectively) and ANG II (1,000 ng·kg−1·min−1) for up to 14 days. Cardiac contractile function and structure were detected by echocardiography. Hypertrophy, fibrosis, and inflammation were assessed by histological examination. The infiltration of lymphocyte function-associated antigen-1 (LFA-1+) monocytes/macrophages was assessed by immunostaining. The mRNA expression of genes was evaluated by quantitative RT-PCR analysis. Protein levels were tested by immunoblotting. We found that ICAM-1 expression in ANG II-infused hearts and ICAM-1 levels in serum from human patients with heart failure were significantly increased. Moreover, ANG II infusion markedly enhanced ANG II-induced hypertension, caused cardiac contractile dysfunction, and promoted cardiac hypertrophy, fibrosis, and LFA-1+ macrophage infiltration. Conversely, blockage of ICAM-1 with a neutralizing antibody dose-dependently attenuated these effects. Moreover, our in vitro data further demonstrated that blocking ICAM-1 inhibited ANG II-induced LFA-1+ macrophage adhesion to endothelial cells and migration. In conclusion, these results provide novel evidence that blocking ICAM-1 exerts a protective effect in ANG II-induced cardiac remodeling at least in part through the modulation of adhesion and infiltration of LFA-1+ macrophages in the heart. Inhibition of ICAM-1 may represent a new therapeutic approach for hypertrophic heart diseases. NEW & NOTEWORTHY Leukocyte adhesion to vascular endothelium is a critical step in cardiovascular diseases. ICAM-1 is a member of immunoglobulin-like superfamily of adhesion molecules that binds LFA-1 to mediate leukocytes adhesion and migration. However, the significance of ICAM-1 in ANG II-induced cardiac remodeling remains unclear. This study reveals that blocking of ICAM-1 prevents ANG II-induced cardiac remodeling via modulating adhesion and migration of LFA-1+ monocytes, may serve as a novel therapeutic target for hypertensive cardiac diseases.
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Lee, Gloria, Annie Lo, Sarah Short, Tosti Mankelow, Stephen Parsons, Frances Spring, Narla Mohandas, David Anstee, and Joel Anne Chasis. "Targeted Gene Deletion Demonstrates That Adhesion Molecule ICAM-4 Is Critical for Erythroblastic Island Formation." Blood 106, no. 11 (November 16, 2005): 1661. http://dx.doi.org/10.1182/blood.v106.11.1661.1661.
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Abstract Erythroid progenitors proliferate, differentiate and enucleate within specialized bone marrow subcompartments, termed erythroblastic islands, which are comprised of developing erythroblasts surrounding a central macrophage. Growing evidence suggests that within erythroblastic islands adhesion events, in concert with cytokines, play critical roles in regulating erythropoiesis and apoptosis. We are exploring the potential function of erythroid ICAM-4, a recently characterized member of the immunoglobulin superfamily, in erythroblastic island formation. We earlier identified α4β1 and αV integrins as ICAM-4 binding partners. Since erythroblasts express α4β1 and ICAM-4 and macrophages exhibit αV, ICAM-4 is an attractive candidate for mediating erythroblast-erythroblast and erythroblast-macrophage attachments. Indeed, two synthetic peptides that block ICAM-4/αV adhesion caused a marked decrease in the percentage of islands formed. To more definitively test whether ICAM-4 attachments are active in erythroblastic islands we generated ICAM-4 knockout mice and compared the capacity of single cell suspensions from freshly harvested ICAM-4 null and wild type bone marrow to form erythroblastic islands in vitro, using a reproducible live cell island reconstitution assay that we have established. Islands and their cellular components were identified and quantitated by three-color immunofluorescent microscopy employing fluoresceinated erythroid-specific TER119 antibody, macrophage-specific F4/80 antibody and a DNA probe. Strikingly, we observed a 47% decrease in the percentage of islands formed from bone marrow of ICAM-4 null mice compared to wild type littermates (n=10 and n=10, respectively). We also studied the ability of ICAM-4 null erythroblasts to form islands in vivo by analyzing intact islands freshly harvested from mouse bone marrow. Similar to the in vitro data we found a marked decrease in the percentage of islands formed in the bone marrow of ICAM-4 null mice compared to wild type littermates. The null mice had 44% fewer islands than wild type mice. Taken together, the results of this phenotypic analysis provide convincing evidence that ICAM-4 is one of the adhesion molecules critical for erythroblastic island formation. We postulate that this newly identified erythroblast receptor may be important not only for adhesive integrity of the island structure but also for initiating intracellular signaling essential for normal erythroid terminal differentiation.
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Zhang, XG, JP Gaillard, N. Robillard, ZY Lu, ZJ Gu, M. Jourdan, JM Boiron, R. Bataille, and B. Klein. "Reproducible obtaining of human myeloma cell lines as a model for tumor stem cell study in human multiple myeloma." Blood 83, no. 12 (June 15, 1994): 3654–63. http://dx.doi.org/10.1182/blood.v83.12.3654.bloodjournal83123654.
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We report a novel, reproducible methodology which enabled 10 human myeloma cell lines (HMCL) to be obtained from each of 10 tumor samples harvested from 9 patients with extramedullary proliferation. Fresh samples were cultured with interleukin 6 (IL-6) and granulocyte macrophage-colony stimulating factor (GM-CSF) at a high cell density and resulting HMCL growth became progressively dependent on IL-6 alone, no longer requiring GM-CSF. These HMCL, which had the same immunoglobulin gene rearrangements as the patients' original myeloma cells, were designated XG-1 to XG-9. XG HMCL had a plasma cell morphology, expressed plasma cell antigen (Ag), namely cytoplasmic immunoglobulins, CD38, B-B4 Ag, and CD77, and lacked the usual B-cell Ag. They also expressed activation antigens such as CD28 with coexpression of CD28 and its ligand, B7 Ag, in four HMCL. Six HMCL expressed CD40, 4 CD23, and 5 its ligand, CD21. The XG HMCL bore adhesion molecules VLA-4 and CD44 (all 10 HMCL), VLA-5 (7 HMCL), and CD56 (4 HMCL). Finally, cytogenetic study of 8 HMCL indicated a 14q+ chromosome, and t(11,14) translocation was found in 6 of 8 and 5 of 8 HMCL, respectively. The possibility of obtaining malignant plasma cell lines reproducibly from each patient with extramedullary proliferation offers a unique tool for studying the phenotype and abnormalities of the still unidentified tumor stem cell in this disease.
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Kim, Hyunsoo, Noriko Takegahara, Matthew C. Walsh, and Yongwon Choi. "CD44 Can Compensate for IgSF11 Deficiency by Associating with the Scaffold Protein PSD-95 during Osteoclast Differentiation." International Journal of Molecular Sciences 21, no. 7 (April 10, 2020): 2646. http://dx.doi.org/10.3390/ijms21072646.
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Differentiation of osteoclasts, which are specialized multinucleated macrophages capable of bone resorption, is driven primarily by receptor activator of NF-κB ligand (RANKL). Additional signaling from cell surface receptors, such as cell adhesion molecules (CAMs), is also required for osteoclast maturation. Previously, we have demonstrated that immunoglobulin superfamily 11 (IgSF11), a member of the immunoglobulin-CAM (IgCAM) family, plays an important role in osteoclast differentiation through association with the scaffold protein postsynaptic density protein 95 (PSD-95). Here, we demonstrate that the osteoclast-expressed CAM CD44 can compensate for IgSF11 deficiency when cell–cell interaction conditions are suboptimal by associating with PSD-95. Impaired osteoclast differentiation in IgSF11-deficient (IgSF11−/−) cultures was rescued by antibody-mediated stimulation of CD44 or by treatment with low-molecular-weight hyaluronan (LMW-HA), a CD44 ligand. Biochemical analysis revealed that PSD-95, which is required for osteoclast differentiation, associates with CD44 in osteoclasts regardless of the presence or absence of IgSF11. RNAi-mediated knockdown of PSD-95 abrogated the effects of either CD44 stimulation or LMW-HA treatment on osteoclast differentiation, suggesting that CD44, similar to IgSF11, is functionally associated with PSD-95 during osteoclast differentiation. Taken together, these results reveal that CD44 can compensate for IgSF11 deficiency in osteoclasts through association with PSD-95.
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Zhang, XG, JP Gaillard, N. Robillard, ZY Lu, ZJ Gu, M. Jourdan, JM Boiron, R. Bataille, and B. Klein. "Reproducible obtaining of human myeloma cell lines as a model for tumor stem cell study in human multiple myeloma." Blood 83, no. 12 (June 15, 1994): 3654–63. http://dx.doi.org/10.1182/blood.v83.12.3654.3654.
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Abstract We report a novel, reproducible methodology which enabled 10 human myeloma cell lines (HMCL) to be obtained from each of 10 tumor samples harvested from 9 patients with extramedullary proliferation. Fresh samples were cultured with interleukin 6 (IL-6) and granulocyte macrophage-colony stimulating factor (GM-CSF) at a high cell density and resulting HMCL growth became progressively dependent on IL-6 alone, no longer requiring GM-CSF. These HMCL, which had the same immunoglobulin gene rearrangements as the patients' original myeloma cells, were designated XG-1 to XG-9. XG HMCL had a plasma cell morphology, expressed plasma cell antigen (Ag), namely cytoplasmic immunoglobulins, CD38, B-B4 Ag, and CD77, and lacked the usual B-cell Ag. They also expressed activation antigens such as CD28 with coexpression of CD28 and its ligand, B7 Ag, in four HMCL. Six HMCL expressed CD40, 4 CD23, and 5 its ligand, CD21. The XG HMCL bore adhesion molecules VLA-4 and CD44 (all 10 HMCL), VLA-5 (7 HMCL), and CD56 (4 HMCL). Finally, cytogenetic study of 8 HMCL indicated a 14q+ chromosome, and t(11,14) translocation was found in 6 of 8 and 5 of 8 HMCL, respectively. The possibility of obtaining malignant plasma cell lines reproducibly from each patient with extramedullary proliferation offers a unique tool for studying the phenotype and abnormalities of the still unidentified tumor stem cell in this disease.
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May, Andreas, Franz-Josef Neumann, and Klaus Preissner. "The Relevance of Blood Cell-Vessel Wall Adhesive Interactions for Vascular Thrombotic Disease." Thrombosis and Haemostasis 82, no. 08 (1999): 962–70. http://dx.doi.org/10.1055/s-0037-1615939.
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IntroductionFollowing an inflammatory or infectious stimulus, the body’s defense mechanism initiates recruitment of circulating leukocytes toward the inflammatory stimulus. The emigration of leukocytes into extravascular tissues occurs in a highly coordinated fashion in multiple steps, including rolling and tethering of blood cells along the vascular endothelium and their firm attachment and subsequent transmigration and invasion toward the inflammatory site.1 During these sequential steps, transcellular recognition of different adhesion receptor/counterligand pairs, such as selectins/sialyl LewisX-carbohydrates,2 integrins/ immunoglobulin superfamily cell adhesion molecules (ICAMs),3 or binding to (provisional) extracellular matrix components, such as fibrinogen/fibrin, vitronectin, or fibronectin, control the strength and duration of interactions between leukocytes (neutrophils [polymorphonucleocytes (PMN)], eosinophils, monocytes and macrophages, mast cells, lymphocytes) and the vessel wall.4 The importance of these cellular interactions is evident from patients with the rare congenital disorders of “leukocyte-adhesion-deficiency,” which are either caused by a lack or dysfunction of ß2-integrins (LAD I) or a deficiency in the expression of sialyl-LewisX carbohydrates (LAD II).5 The interdependent adhesion processes are regulated by vascular cell-derived chemokines and chemoattractants that may directly influence the expression profile and activation state of adhesion molecules, such as ß2- and ß1-integrins, the shedding of selectins, and the nonthrombogenic properties of endothelial cells.6 Prior to transmigration, leukocyte adhesion may induce the disruption of vascular endothelial (VE)-cadherin mediated endothelial cell-to-cell junctions7 involving the proteasome machinery.8 The spatio-temporal cellular expression of juxtacrine adhesion and signaling receptors–particularly on PMN, endothelial cells, and platelets–contribute to the coordination of adhesion and inflammatory mechanisms required for vascular homeostasis9 and prothrombotic outcome under imbalanced conditions. Not only do monocytes express tissue factor (a receptor for the protease factor VII/VIIa) on their surface after stimulation with endotoxin or cytokines, but PMN contain cell surface receptors, such as the factor X/Xa-binding ß2-integrin Mac-1 or effector cell protease receptor (EPR)-1, that link cellular activation and inflammation with the induction of the blood clotting cascade and serve as an alternate pathway for thrombin formation.10,11 Moreover, defects in natural anticoagulant mechanisms, such as the thrombomodulin/protein C pathway, are potential risk factors for vascular thrombotic complications, as in myocardial infarction.12 Pathophysiological stimuli, such as dysregulated direct (i.e., adhesive contact) or indirect (i.e., release of soluble factors) activation of leukocytes, serious infectious agonists, or autoantibodies, may result in endothelial cell dysfunction or injury with the amplification of inflammatory and prothrombotic responses. In the following, some of the principal juxtacrine interactions between leukocytes, platelets, and endothelium, together with their direct or indirect influence on hemostasis and consequences for vascular thrombotic disease, will be discussed. Further understanding of the bidirectional cross-talk of adhesion receptors and the contribution of connecting points, such as protease receptors, may lead to promising therapeutic strategies that aim to protect or regain the endothelial defense mechanisms.
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Lee, Gloria, Annie Lo, Sarah A. Short, Tosti J. Mankelow, Frances Spring, Stephen F. Parsons, Karina Yazdanbakhsh, Narla Mohandas, David J. Anstee, and Joel Anne Chasis. "Targeted gene deletion demonstrates that the cell adhesion molecule ICAM-4 is critical for erythroblastic island formation." Blood 108, no. 6 (September 15, 2006): 2064–71. http://dx.doi.org/10.1182/blood-2006-03-006759.
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AbstractErythroid progenitors differentiate in erythroblastic islands, bone marrow niches composed of erythroblasts surrounding a central macrophage. Evidence suggests that within islands adhesive interactions regulate erythropoiesis and apoptosis. We are exploring whether erythroid intercellular adhesion molecule 4 (ICAM-4), an immunoglobulin superfamily member, participates in island formation. Earlier, we identified αV integrins as ICAM-4 counterreceptors. Because macrophages express αV, ICAM-4 potentially mediates island attachments. To test this, we generated ICAM-4 knock-out mice and developed quantitative, live cell techniques for harvesting intact islands and for re-forming islands in vitro. We observed a 47% decrease in islands reconstituted from ICAM-4 null marrow compared to wild-type marrow. We also found a striking decrease in islands formed in vivo in knock-out mice. Further, peptides that block ICAM-4/αV adhesion produced a 53% to 57% decrease in reconstituted islands, strongly suggesting that ICAM-4 binding to macrophage αV functions in island integrity. Importantly, we documented that αV integrin is expressed in macrophages isolated from erythroblastic islands. Collectively, these data provide convincing evidence that ICAM-4 is critical in erythroblastic island formation via ICAM-4/αV adhesion and also demonstrate that the novel experimental strategies we developed will be valuable in exploring molecular mechanisms of erythroblastic island formation and their functional role in regulating erythropoiesis.
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Nishikawa, K., Y. J. Guo, M. Miyasaka, T. Tamatani, A. B. Collins, M. S. Sy, R. T. McCluskey, and G. Andres. "Antibodies to intercellular adhesion molecule 1/lymphocyte function-associated antigen 1 prevent crescent formation in rat autoimmune glomerulonephritis." Journal of Experimental Medicine 177, no. 3 (March 1, 1993): 667–77. http://dx.doi.org/10.1084/jem.177.3.667.
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In patients with glomerulonephritis widespread crescents are associated with a poor prognosis. Crescent formation appears to depend on the migration of mononuclear cells into Bowman's space, and therefore the interaction between leukocytes and glomerular endothelium may be a critical event in the genesis of crescents. We performed the present study to determine the effects of mouse monoclonal antibodies to the adhesion molecules intercellular adhesion molecule 1 (ICAM-1) and lymphocyte function-associated antigen 1 (LFA-1) in a model of crescentic glomerulonephritis in Wistar-Kyoto rats, induced by immunization with bovine glomerular basement membrane (GBM). By 10-14 d after immunization, the rats had developed circulating anti-GBM antibodies, reactive with the alpha 3 chain of type IV collagen (the Goodpasture antigen), accompanied by proteinuria, accumulation of rat immunoglobulin (Ig)G in the GBM, increased expression of ICAM-1 by glomerular endothelial cells, infiltration of glomerular tufts with LFA-1+ T cells and monocyte/macrophages, and early crescents. At 5 wk all rats had diffuse fibrocellular crescents, glomerular sclerosis, and tubulointerstitial damage. All rats developed severe renal insufficiency and died by 5 or 6 wk. The administration of monoclonal antibodies to rat ICAM-1 and LFA-1 markedly decreased the severity of the renal disease. In a group of rats injected three times a week with the monoclonal antibodies, from 2 d before immunization with GBM to day 14, glomerular abnormalities and proteinuria were virtually absent at day 14; even at 5 wk glomerular disease was quite mild, with only slight crescent formation and with only a mild decrease in renal function. When treatment was continued until 5 wk, the beneficial effects were even more marked, with virtual absence of crescents and with preservation of normal renal function. In a group of rats in which treatment was initiated on day 14, shortly after the appearance of glomerular abnormalities, progression of the disease was appreciably retarded, and the decrease in renal function was inhibited. The kidneys of rats treated from days -2 to 14 with antibodies to ICAM-1 and LFA-1 showed bright linear staining for rat IgG along the GBM, which did not differ in intensity from that seen in untreated rats. Furthermore, the titers of anti-GBM antibodies at 2 wk in treated rats were not lower than that seen in most of the untreated rats. There was, however, moderate reduction of anti-GBM antibodies at 5 wk in the treated rats.(ABSTRACT TRUNCATED AT 400 WORDS)
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Lee, Gloria, Annie Lo, Sarah Short, Tosti Mankelow, Stephen Parsons, Frances Spring, Mohandas Narla, David Anstee, and Joel Anne Chasis. "Adhesion Molecule ICAM-4 Participates in Erythroblastic Island Formation." Blood 104, no. 11 (November 16, 2004): 580. http://dx.doi.org/10.1182/blood.v104.11.580.580.
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Abstract Erythroblasts proliferate, differentiate and enucleate within erythroblastic islands, three dimensional structures comprised of developing erythroblasts surrounding a central macrophage. Collective evidence suggests that erythroblastic islands are highly specialized bone marrow subcompartments where adhesion events, in concert with cytokines, play critical roles in regulating erythropoiesis and apoptosis. ICAM-4, a recently characterized member of the immunoglobulin superfamily, is expressed early in erythroid differentiation. This adhesion molecule interacts with multiple integrin binding partners, including alpha4beta1 and alphaV integrins (alphaVbeta1, alphaVbeta3 and alphaVbeta5). Since erythroblasts express alpha4beta1 and ICAM-4 and macrophages exhibit alphaV, ICAM-4 is an attractive candidate for mediating erythroblast-erythroblast and erythroblast-macrophage attachments. A molecular model of ICAM-4 derived from the crystal structure of closely related ICAM-2 presents the extracellular region of ICAM-4 as two Ig-like domains comprised of A,B,C,D,E,F, and G strands. Employing targeted mutagenesis of surface-exposed amino acid residues, we earlier identified a patch or footprint that mediates adhesion to alphaV integrins comprised of three A strand residues and five G strand residues on N-terminal domain 1. To explore whether ICAM-4 attachments are active in erythroblastic islands we first developed a quantitative live cell assay for reforming islands from single cell suspensions of freshly harvested mouse bone marrow. Islands and their cellular components were identified and quantitated by three-color immunofluorescent microscopy employing fluoresceinated erythroid-specific TER119 antibody, macrophage-specific F4/80 antibody and a DNA probe. To determine the amount of variation in number of islands reformed from a single cell suspension of 1 x 105 cells, we counted islands at the beginning and conclusion of experiments on five different mice. The island numbers were very reproducible and equaled 1000 +/− 158. We then tested the effects of two synthetic peptides that we have previously shown block ICAM-4/alphaV adhesion: peptides FWV and ATSR, corresponding to sequences of the A and G strands of ICAM-4 domain 1, respectively. Both peptides caused a marked, concentration dependent decrease in the percentage of islands formed. 2mM ATSR inhibited island formation by 75% while 2mM FWV inhibited island formation by 70%. In marked contrast, a strand D control peptide had minimal to no effect on island formation. Our data strongly suggest that erythroblast ICAM-4 binding to macrophage alphaV is critical for erythroblastic island formation. We postulate that this newly identified receptor-counterreceptor interaction may be important not only for adhesive integrity of the island structure but also for initiating intracellular signaling essential for normal erythroid terminal differentiation.
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Sukarjati, Sukarjati, and Susie Amilah. "ROLE OF IMMUNOGLOBULIN G (IgG) FROM THE INDUCTION OF Escherichia coli PILI ADHESION PROTEIN ISOLATED FROM INFERTILE MALE SEMEN WITH 32.2 KDA MOLECULAR WEIGHT AS OPSONIN AND ANTI-ADHESION AN IN VITRO Escherichia coli INFECTION." Folia Medica Indonesiana 53, no. 2 (November 3, 2017): 94. http://dx.doi.org/10.20473/fmi.v53i2.6343.
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Escherichia coli (E. coli), a major cause of male genital tract infections, is asymptomatic and may result in male infertility. We have succeeded in isolating and characterizing proteins of E. Pili coli isolates from semen of infertile men who function as adhesin with a molecular weight (MW) 32.2 kDa. This study aims to prove the ability of IgG results adhesion proteins induced pili of E. MW coli 32.2 kDa as opsonin to determine the value of the activity and phagocytic capacity and as an anti- adhesion by calculating the average number of E. coli that attached to human spermatozoa. E. coli infertile men's semen were cultured using standard bacteriology. Peritoneal macrophages were isolated from mice. Spermatozoa from donors were prepared using Sil with Select Plus. IgG was obtained from mice immunized with (1) PBS (control), (2) E. coli pili adhesion protein isolated from infertile men semen with MW of 32.2 kDa and (3) weakened E. coli isolated from infertile men's semen. Phagocytic activity value was determined by counting the number of cells activated macrophage phagocytosis process in 100 cells. Phagocytic capacity value was determined by counting the number of bacteria ingested by 25 macrophages. Anti-adhesion test was done by counting the number of bacteria attached to 100 spermatozoa. The results of this study showed difference (p=0.000) in phagocytic activity and phagocytic capacity (p=0.000) between treatment (1) and (2), and between treatment (1) to (3). However, treatment (2) and (3) did not differ neither in phagocytic activity (p=0.693) nor in phagocytosis capacity (p=0.125). Anti-adhesion test produces difference (p=0.000) in the number of E. coli that attached to human spermatozoa between treatments (1) and treatment (2), and between treatments (1) and (3). The number of E. coli that attached to human spermatozoa between treatment (2) and treatment (3) was not significantly different (p=0.371). In conclusion, IgG from the induction of E. coli pili adhesion protein of infertile men semen isolates with MW of 32.2 kDa can increase phagocytic activity and capacity as well as serve as an anti- adhesion. Thus, IgG from the induction of E. coli pili adhesion protein of infertile men semen isolates with MW of 32.2 kDa is protective against in vitro E. coli infection, so that it can be used as material to prevent male reproductive tract infections due to E. coli.
Dissertations / Theses on the topic "Immunoglobulins; Adhesion molecules; Macrophages"
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Mucklow, Stuart. "Characterization and mapping of the murine sialoadhesin gene, Sn." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337593.
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Hughes, Derralynn A. "Murine macrophage adhesion molecules : characterisation and function." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670274.
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Morris, L. "Expression of surface molecules on mouse foetal macrophages." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235069.
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Collie, Angela M. B. "The macrophage response to biomaterial topography : gene expression, integrin signaling, and surface adhesions /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8115.
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Carvalhal, Djalma Gomes Ferrão. "Um ensaio de adesão otimizado para o estudo de interações entre macrófagos e tecido conjuntivo baseado no ensaio de Stamper-Woodruff." reponame:Repositório Institucional da FIOCRUZ, 2001. https://www.arca.fiocruz.br/handle/icict/5886.
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Submitted by Ana Maria Fiscina Sampaio (fiscina@bahia.fiocruz.br) on 2012-11-27T18:25:19Z
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Djalma Gomes Ferrão Carvalhal Um ensaio de adesao... 2001.pdf: 31649822 bytes, checksum: cea5fde124b280c0b60a4b69bc0b6cb3 (MD5)Made available in DSpace on 2012-11-27T18:25:19Z (GMT). No. of bitstreams: 1 Djalma Gomes Ferrão Carvalhal Um ensaio de adesao... 2001.pdf: 31649822 bytes, checksum: cea5fde124b280c0b60a4b69bc0b6cb3 (MD5) Previous issue date: 2001
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, Bahia, Brasil
O objetivo deste trabalho é desenvolver um ensaio de adesão, baseado no ensaio de Stamper- Woodruff, para o estudo das interações entre macrófagos e matriz conjuntiva. Foram induzidos bolsões inflamatórios em camundongos da linhagem BALB/c para obtenção de secções de pele inflamada, e células macrofágicas da linhagem J774G.8 foram utilizadas na padronização do ensaio. Secções de 7 i^m de espessura foram colocadas em lâminas de vidro, fixadas com acetona e bloqueadas com BSA. Foi estabelecida a concentração de 10® células/100 fil como a mais apropriada para a realização do ensaio, através de diluições seriadas. Células J774G.8 sem tratamento prévio ou tratadas com: ácido tetraacético diamino etileno, Mn++, lipopolissacarídeo, forbol miristato acetato, zimosan, os peptídios CS-1 e RGD, os anticorpos anti-CD49d ou contra a cadeia (32 de integrinas, foram adicionadas ás secções e incubadas por 30 minutos á temperatura ambiente. Como resultado, as células macrofágicas aderem preferencialmente ás áreas de inflamação. A adesão das células é dependente de cátions divalentes e pode ser modulada por substâncias que promovam a ativação celular. Além disso, a adesão mediada por integrinas pode ser inibida por peptídios RGD e CS-1 ou com anticorpos contra integrinas da família (31 e (32. A adesão das células macrofágicas é inibida mais intensivamente pela infecção com Leishmania mas não com a infecção por Mycobacterium ou por fagocitose de partículas de látex. Desta forma, o ensaio desenvolvido foi capaz de demonstrar a especificidade da adesão de células macrofágicas pela matriz conjuntiva bem como de sugerir a existência de mecanismos específicos de regulação das interações entre macrófagos e a matriz conjuntiva durante a infecção por Leishmania.
The aim of this work was to develop an adhesion assay, based on the Stamper-Woodruff’s assay to study the interactions between macrophages and the connective matrix. Inflammatory pouches were produced in BALB/c mice to obtain inflammed skin sections, and J774G.8 macrophage cell line was applied to standardize the assay. Sections of 7|im thick were placed onto glass slides, fixed with acetone and blocked with bovine serum albumin. The cell concentration of 10®/100 |xl was proved to be most appropriate for the assay, through serial dilutions. J774G.8 cells, with or without ethylene diamine tetraacetic acid, Mn'"'", Lipopolysaccharide, phorbol myristate acetate, zymosan, CS- 1, RGD peptide, antibodies anti-CD49d or against (32 chain integrin treatment, were added onto the sections and incubated for 30 minutes at room temperature. Macrophage cells adhered preferentially to inflammed areas. The adhesion of cells was dependent on divalent ions and could be modulated by substances that promote cell activation. Moreover, the adhesion mediated by integrin can be inhibited either by RGD or CS-1 peptides or by antibodies against integrins of the |31 or |32 sub-family. Adhesion of macrophage cells was intensively inhibited by infection with Leishmania and was not affected by infection with Mycobacterium or by endocytosis of latex beads. Thus, the developed assay was able to show the specific adhesion of macrophages to connective matrix, as well to illustrate a specific downregulation of macrophage adhesion to inflammed skin in Leishmania infection.
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Bologna, Sheyla Batista. "Melanoma primário da mucosa oral: estudo dos aspectos clínico-patológicos e da expressão das imunoglobulinas e integrinas em 35 casos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5133/tde-05022014-110422/.
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Melanoma primário da mucosa oral (MPMO) é um tumor raro e agressivo. Estudos recentes demonstraram uma correlação entre o aumento da invasão tumoral e o fenótipo metastático com uma alteração no padrão de expressão das moléculas de adesão. Neste estudo analisamos a expressão de integrinas e imunoglobulinas nos melanomas primários da mucosa oral e relacionamos os resultados com os parâmetros clínicos. As análises imunoistoquímicas dos padrões de expressão destas moléculas foram realizadas em 35 casos de melanomas primários da mucosa oral, e os resultados foram correlacionados com características clínicas e histológicas. Observou-se que a subunidade beta-4 de integrina foi negativa em casos com invasão vascular. A presença de integrina beta-3 e de CD166 (ALCAM) estavam estatisticamente associadas à extensa invasão vascular (p < 0,05). A menor expressão de CD54 (ICAM) foi marginalmente relacionada a casos com necrose extensa, enquanto a maioria dos casos com doença metastática foi negativa para CD66 (CEACAM). Conclusão: padrões alterados de expressão de moléculas de adesão, principalmente integrinas e imunoglobulinas, podem participar da patogênese e do desenvolvimento dos melanomas primários da mucosa oralPrimary oral mucosal melanoma is a rare and an aggressive tumor. Recent studies have demonstrated the correlation among increased tumor invasion, the metastatic phenotype and altered adhesion molecule expression profiles. The present study analyzed the expression of integrins and immunoglobulin-like adhesion molecules in oral mucosal melanomas and correlated results with clinical parameters. Immunohistochemical analyses of their expression patterns were performed on thirty-five cases of primary oral mucosal melanomas. The results were correlated with clinical and histological features of the cohort. The beta-4 subunit of integrin was negative and this was related with vascular invasion. Positivity of integrin beta-3 and CD166 (ALCAM) was statistically associated with extensive vascular invasion (p < 0.05). Lower expression of CD54 (ICAM) was associated with cases with extensive necrosis. Most cases with metastatic disease were negative for CD66 (CEACAM). Conclusion: Altered patterns of adhesion molecule expression, mainly integrins and immunoglobulin-like proteins, may participate in the pathogenesis and outcome of primary oral mucosal melanomas
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Kellokoski, E. (Eija). "Ghrelin and atherosclerosis:human, experimental animal and cell culture studies." Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514292590.
Full textAbstract:
Abstract Atherosclerosis is the major cause of cardiovascular diseases and the leading cause of death globally. Atherosclerosis is a complex, chronic disease characterized by lipid accumulation and inflammation within the intima layer of vessel wall. Novel biomarkers and therapeutics are still being sought to provide both better diagnosis and treatment. Ghrelin represents an attractive target for studies into atherosclerosis. Ghrelin is a gastric peptide hormone, which has multiple functions, including regulation of appetite and energy metabolism. Emerging evidence suggests that it may also have a role in the cardiovascular and immune systems. The aim of the present study was to explore the role of ghrelin in atherosclerosis. The specific aims were 1) to investigate the association between the plasma ghrelin level and early atherosclerosis as determined by carotid artery intima media thickness (IMT) in a large (n = 1024) cross-sectional population-based study of middle-aged subjects, 2) to measure the associations between plasma ghrelin levels and already established risk factors of atherosclerosis in human subjects, 3) to assess the effects of ghrelin on atherogenesis in vitro by analyzing monocyte adhesion to endothelial cells, oxidized low density lipoprotein (LDL) binding and acetylated LDL uptake using macrophages, and 4) to study the influence of ghrelin on atherosclerosis using ghrelin vaccination in a mouse model of atherosclerosis. Plasma total ghrelin levels were positively associated with carotid IMT in male subjects. Association studies demonstrated plasma ghrelin levels to be negatively associated with total and LDL cholesterol, and triglyceride concentrations as well as with body mass index (BMI), and positively assocated with high density lipoprotein (HDL) cholesterol concentration in postmenopausal women and in a population-based study. In addition, estrogen increased plasma acylated ghrelin levels in postmenopausal women. Cell culture studies demonstrated that ghrelin could increase the binding of oxidized LDL and monocytes to endothelial cells. Interestingly, when endothelial cells were stimulated with tumor necrosis factor α (TNFα), then ghrelin prevented monocyte adhesion. The study with LDL receptor knockout mice, revealed that ghrelin vaccination could increase plasma ghrelin levels but had no effects on the development of atherosclerosis. However, the plasma MCP-1 level decreased in mice immunized with ghrelin vaccine. In conclusion, these studies suggest that ghrelin has modulatory functions in the vascular system and atherogenesis though the effect may not be as dominant as that of the known traditional risk factors. Whether this effect of ghrelin is positive or negative in atherogenesis will be clarified in further studiesTiivistelmä Sydän- ja verisuonitaudit ovat suurin kuolinsyy niin Suomessa kuin useimmissa länsimaissakin. Näiden sairauksien taustalla on yleensä valtimonkovettumatauti eli ateroskleroosi, joka voi kliinisesti ilmentyä mm. sepelvaltimotautina, aivoveritulppana ja laskimotautina. Ateroskleroosissa tulehdussoluja ja kolesterolia kertyy verisuonen seinämään muodostaen ahtauman eli ateroomaplakin valtimoon. Valtimonkovettumataudin riskitekijäitä tunnetaan jo hyvin, mutta uusia tautia ennustavia merkkiaineita sekä hoitomuotoja tarvitaan yhä. Greliini on mahalaukusta eritettävä peptidihormoni, joka osallistuu elimistössä mm. ruokahalun, energiametabolian, tulehdustekijöiden sekä sydän- ja verenkiertoelimistön toiminnan säätelyyn. Tämän työn tavoitteena oli tutkia greliinin yhteyttä ihmisen valtimonkovettumatautiin. Tutkimus toteutettiin käyttämällä kahta eri potilasaineistoa, soluviljelykokeita sekä valtimonkovettumataudin hiirimallia. Laajassa väestöpohjaisessa potilasaineistossa tutkittiin veren greliinipitoisuuden yhteyttä kaulavaltimon seinämän paksuuteen, jota pidetään valtimonkovettumista kuvaavana tekijänä. Veren greliinipitoisuuden yhteyttä valtimonkovettumataudin tunnettuihin riskitekijöihin tutkittiin myös laajassa potilasaineistossa sekä vaihdevuosi-ikäisillä naisilla, joille annettiin estrogeenikorvaushoitoa. Solukokeilla selvitettiin greliinin vaikutusta tärkeisiin valtimonkovettumataudin syntyvaiheisiin käyttäen monosyytti-, endoteelisolu- sekä makrofaagi-soluviljelmiä. Greliinin vaikutusta ateroskleroosiin in vivo selvitettiin rokottamalla LDL-reseptoripuutteiset hiiret greliini-rokotteella. Tutkimuksessa havaittiin yhteys veren korkean greliinipitoisuuden ja kaulavaltimon seinämän paksuuden välillä miehillä laajassa potilasaineistossa (n = 1024). Tulosta tukivat soluilla tehdyt kokeet, joissa greliini lisäsi hapettuneen LDL:n sitoutumista makrofaageihin sekä monosyyttien tarttumista endoteelisolujen pinnalle. Greliinin vaikutukset monosyyttien tarttumiseen endoteelisolujen pinnalle olivat päinvastaiset silloin, kun endoteelisolut käsiteltiin tulehdusta stimuloivalla tekijällä. Matalat veren greliinipitoisuudet olivat myös yhteydessä korkeisiin LDL-kolesteroli- ja triglyseriditasoihin sekä painoindeksiin ja matalaan HDL-kolesterolitasoon potilasaineistoissa. Estrogeeni nosti veren greliinipitoisuutta vaihdevuosi-ikäisillä naisilla. Greliinirokote ei vaikuttanut ateroskleroosin kehittymiseen hiirimallissa. Tutkimustulosten perusteella greliinillä näyttäisi osallistuvan valtimonkovettumataudin kehitykseen, vaikkakin sen vaikutus on pienempi kuin aiemmin tunnetuilla taudin riskitekijöillä
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健吾, 川﨑, 川崎 健吾, and Kengo Kawasaki. "ウコン熱水エキスの抗炎症作用に関する研究." Thesis, https://doors.doshisha.ac.jp/opac/opac_link/bibid/BB13106341/?lang=0, 2019. https://doors.doshisha.ac.jp/opac/opac_link/bibid/BB13106341/?lang=0.
Full textAbstract:
ウコン利用の一形態であるウコン熱水エキスの抗炎症作用について検証することを目的として本研究を行った。内皮細胞もしくはマクロファージを使用した細胞試験を実施し、ウコン熱水エキスの抗炎症作用を実証した。また、その作用機序を一部明らかにし、その作用に寄与する成分を一部明らかにした。さらに、臨床試験を実施し、ウコン熱水エキスが健常者の気分状態に対する作用を評価し、その摂取が疲労を改善する可能性があることが示唆された。博士(理学)
Doctor of Philosophy in Science
同志社大学
Doshisha University
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Hoff, Uwe. "Bedeutung der Alloantigen-unabhängigen Faktoren in der Frühphase nach tierexperimenteller Nierentransplantation." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2005. http://dx.doi.org/10.18452/15249.
Full textAbstract:
Die Schädigung des Organs durch Ischämie-Reperfusion (IR) im Rahmen der kadaverischen Organtransplantation hat bedeutenden Anteil an der Pathogenese verzögert einsetzender Organfunktion und Auswirkungen auf das Langzeitüberleben des Transplantats. In der vorliegenden Studie sollte der Einfluss unspezifischer Schädigung durch IR verglichen mit spezifischen Alloantigen-abhängigen Mechanismen während der Frühphase nach der Transplantation sowie die Auswirkungen prolongierter Aufbewahrung auf Schädigung und Immunogenität des Organs ermittelt werden. Nach vorausgegangener vierstündiger kalter Ischämiezeit wurden Organe aus syngen (Lew/Lew) und allogen (F344/Lew) transplantierten Ratten an 8 aufeinander folgenden Zeitpunkten innerhalb der ersten 10 Tage zu funktionellen, immunhistochemischen und morphologischen Veränderungen untersucht. In weiteren Gruppen wurden syngen transplantierte Organe 24 Stunden nach der Transplantation untersucht, die zuvor ansteigenden kalten Ischämiezeiten zwischen 2 und 48 Stunden ausgesetzt wurden. Im zeitlichen Verlauf zeigten sich bis 7 Tage nach der Transplantation keine wesentlichen Unterschiede zu Nierenfunktion, Morphologie, Zellinfiltration und Expression von Adhesionsmolekülen zwischen allogenen und isogenen Gruppen. Die zunächst eintretende Verschlechterung der Nierenfunktion war begleitet von einem Einstrom neutrophiler und monozytärer Zellen und morphologischen Veränderungen im Sinne von akuter Tubulusnekrose (ATN). Unter zunehmender Infiltration von Monozyten/Makrophagen kam es funktionell und morphologisch zur Regeneration. Neutrophile traten vornehmlich über Interaktion von ICAM-1/LFA-1 und Monozyten/Makrophagen über VCAM-1/VLA-4 aus dem Gefäßsystem aus. Gabe von Cyclosporin A führte zu signifikanter Reduktion ED-1-positiver Makrophagen nach 10 Tagen, ohne jedoch den Anteil des aktivierten Makrophagensubtyps ED-2 zu beeinflussen. Ansteigende kalte Aufbewahrung des Organs führte zu größerer vaskulärer Schädigung, die sich durch abnehmende Intensität und lückenhaftere Verteilung von PECAM-1 auf dem Endothel äußerte. Die Zunahme der Intensität von Tissue Factor auf Endothel und infiltrierenden Leukozyten deutete neben gesteigerter Thrombogenese auf alternative Adhäsionsmechanismen hin. Diese Ergebnisse zeigen, dass innerhalb der ersten 10 Tage nach der Transplantation wichtige Phasen der Gewebeschädigung und Regeneration ausgelöst durch die Schädigung nach IR und weitestgehend ohne Beteiligung Alloantigen-abhängiger Faktoren ablaufen. Eine bedeutende Rolle als Mediatoren während dieser Phasen kommt dabei den Monozyten/Makrophagen zu.Organ damage due to long cold preservation is associated with delayed graft function and has important effects on graft survival. Aim of this study was to determine the impact of ischemia-reperfusion (IR) injury compared to antigen-specific mechanisms and the effect of prolonged cold ischemia on intragraft injury and antigenicity during the early phase post transplantation. Rat renal grafts were four-hours cold-preserved, transplanted to syngeneic (Lew/Lew) or allogeneic recipients (F344/Lew) and harvested at 8 different time points after transplantation for further investigation of functional, immunhistochemical and histologic changes. In five additional syngen groups organs were cold preserved from 2 hours to 48 hours and harvested after 24 hours post transplantation. No significant differences in renal function, morphologic changes, cellular infiltration and expression of adhesion molecules occurred between syngeneic and allogeneic groups within the first 7 days. Initial functional impairment was accompanied by the influx of neutrophils and monocytes/macrophages together with morphologic changes reflecting acute tubular necrosis (ATN). Increasing infiltration of monocytes/macrophages paralleled functional and morphologic regeneration. Extravasation of neutrophils was mediated mainly by interaction of ICAM-1/LFA-1 and infiltration of monocytes/macrophages by VCAM-1/VLA-4. Treatment with the standard dose of Cyclosporin A (CsA) lead to a significant decrease of ED1-positive macrophage infiltration 10 days post NTx but the portion of ED2-positive macrophage subtype was not affected. Prolonged cold organ preservation lead to more severe vascular damage indicated by decreased color intensity and continuity of PECAM-1 staining on endothelial cells. Higher staining intensity for Tissue Factor (TF) on endothelium and infiltrating leukocytes implicated enhanced intragraft procoagulant capacity and alternative adhesion mechanisms. These results show that within the first 10 days post transplantation phases of tissue injury and repair after ischemia-reperfusion are largely independent of the immunologic background and monocytes/macrophages play an important role as mediators during these processes.
Books on the topic "Immunoglobulins; Adhesion molecules; Macrophages"
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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.
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 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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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.
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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.
Full textAbstract:
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.
Book chapters on the topic "Immunoglobulins; Adhesion molecules; Macrophages"
1
Calabrese, A., G. Malizia, M. Raimondo, L. K. Trejdosiewicz, C. J. Smart, L. Olivia, L. Pagliaro, and M. Cottone. "Leucocyte adhesion molecules in inflammatory bowel disease: expression by colonic macrophages." In Advances in Mucosal Immunology, 699–700. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_216.
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Bullock, Ward E., and Samuel D. Wright. "Recognition and Binding of Pathogenic Yeasts by Adhesion Molecules of Human Macrophages." In Host Defenses and Immunomodulation to Intracellular Pathogens, 45–52. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-5421-6_5.
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"INTEGRIN SIGNALING IN MONOCYTES/MACROPHAGES." In Adhesion Molecules, 166–68. CRC Press, 2016. http://dx.doi.org/10.1201/9780429196393-30.
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Badimon, Lina, and Gemma Vilahur. "Atherosclerosis and thrombosis." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 447–62. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0037.
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 extracellular vesicles (mainly microvesicles) a role in all stages of atherosclerosis development 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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Collier, Jane. "Investigation and management of jaundice." In Oxford Textbook of Medicine, edited by Jack Satsangi, 3049–57. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0317.
Full textAbstract:
Haem molecules are degraded in macrophages to biliverdin and then to bilirubin, which is selectively removed by hepatocytes from sinusoidal blood and conjugated, chiefly with two glucuronic acid moieties. Conjugated bilirubin is excreted into the bile, but in many liver diseases it refluxes back into blood from which some is filtered into and darkens the urine (choluria). In the distal intestine, conjugated bilirubin is deconjugated and reduced to a series of uro- and stercobilinogens that give the normal colour to faeces. Jaundice is the clinical sign of hyperbilirubinaemia and usually indicates disease of the liver or biliary tree. Dark urine and pale stools indicate cholestasis. Stigmata of chronic liver disease do not define the cause of jaundice. Unconjugated hyperbilirubinaemia—presents with raised serum bilirubin levels and normal other liver-related blood tests. Causes include haemolysis and benign inherited unconjugated hyperbilirubinaemia (i.e. Gilbert’s syndrome). Conjugated hyperbilirubinaemia—routine liver-related blood tests cannot alone differentiate between intra- and extrahepatic causes of jaundice although high levels of transferases suggests hepatitis (e.g. viral, autoimmune) or hepatic necrosis (e.g. paracetamol). Alcohol and drug histories are needed in those with both elevated alkaline phosphatase and transferases. Extrahepatic cholestasis should be sought by abdominal ultrasonography to detect a dilated intra- and/or extrahepatic biliary tree (and often also to reveal its cause, e.g. gallstones, tumour). Further investigation depends on the clinical context: (1) likely large bile duct disease—endoscopic retrograde cholangiopancreatography, magnetic resonance cholangiography, and endoscopic ultrasonography; (2) likely intrahepatic cholestasis—autoantibodies, immunoglobulins, and liver biopsy.