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1
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.
3
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.
Full textAbstract:
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.
6
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.
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Beardsley, Diana S., Bing-guan Chen, and Oleg Kruglov. "Inhibition of FcγRIIA Mediated Platelet Phagocytosis with Syk-Specific siRNA Affects PECAM-1 Mediated Signal Transduction and Cell-Cell Detachment in Human Macrophages." Blood 104, no. 11 (November 16, 2004): 517. http://dx.doi.org/10.1182/blood.v104.11.517.517.
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Abstract We have previously shown that Syk-specific siRNA inhibits FcγRIIA mediated platelet phagocytosis in the human macrophage cell line, THP-1. Surprisingly, we observed that THP-1 cell-cell interactions were affected by Syk-specific siRNA suggesting that Syk may be important in the signaling pathway for physiological cell spreading. As reported by Brown et al. (Nature418:200, 2002), homophilic ligation of PECAM-1 on macrophages triggers cell-cell detachment, prompting us to speculate that Syk may be involved in PECAM-1 mediated signaling. PECAM-1 is a member of the immunoglobulin superfamily that contains an immunoreceptor tyrosine inhibitory motif (ITIM) required for inhibitory signaling and cell spreading via binding protein tyrosine phosphatase. The structure of Syk reveals considerable flexibility in the relative orientation of its tandem SH2 domains providing a molecular basis for the potential involvement of Syk in a variety of signal transduction pathways. Thus, the five tyrosine residues present in the cytoplasmic domain of human PECAM-1 could serve as docking sites for recruitment of other intracellular signaling molecules such as the protein tyrosine kinase, Syk. The present studies test the hypothesis that Syk may mediate an activation influence on intercellular interaction upon PECAM-1 ligation. METHODS: Association of Syk with PECAM-1 was studied in THP-1 cells by immunoprecipitation and immunoblotting with anti-PECAM-1 monoclonal antibody with or without Syk-specific siRNA. The effect of Syk-specific siRNA on THP-1 cells was evaluated by morphology, cell growth kinetics, Trypan Blue exclusion, annexin V staining, and DNA fragmentation analysis. A series of synthetic peptides including sequences within the ITIM region of PECAM-1 were evaluated for their ability to bind Syk directly in THP-1 lysates and to phosphorylate Syk intracellularly. RESULTS: First, Syk protein was co-immunoprecipitated from THP-1 cell lysates by anti-PECAM-1 monoclonal antibody, and Syk-specific siRNA knocked down PECAM-1 associated Syk in THP-1 cells. Second, knock down of Syk by siRNA resulted in decreased cell spreading and cell proliferation. Trypan Blue exclusion, annexin V staining, and DNA fragmentation were identical in THP-1 cells transfected with control dsRNA and Syk-specific siRNA. Third, the synthetic peptide of residues 658-691 within the ITIM region of PECAM-1 that contains two phosphotyrosines (N-S-D-V-Q-pY-T-E-V-Q-V-S-S-A-E-S-H-K-D-L-G-K-K- D-T-E-T-V-pY-S-E-V-R-K) bound directly to Syk. Fourth, ligation of PECAM-1 on THP-1 cells by anti-PECAM-1 monoclonal antibody resulted in Syk phosphorylation. Fifth, the dual phosphotyrosine 658-691 PECAM-1 peptide triggered direct phosphorylation of Syk in permeabilized THP-1 cells. CONCLUSIONS: Our novel observations suggest that signal transduction after PECAM-1 ligation may trigger an activation pathway through the tyrosine kinase, Syk, and facilitate intercellular adhesion. The decreased proliferation observed in THP-1 cells transfected with Syk-specific siRNA is not a result of cell death or apoptosis. Based on our findings, we propose that PECAM-1 may exhibit both ITIM (inhibitory) and ITAM (activation) properties and that the balance of phosphatase and Syk activity triggered by PECAM-1 homophilic binding may affect the fate of intercellular interaction. These processes are expected to influence the net degree of phagocytosis of opsonized platelets by the reticuloendothelial system in patients with immune thrombocytopenia.
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Peters, C., T. Aebischer, Y. D. Stierhof, M. Fuchs, and P. Overath. "The role of macrophage receptors in adhesion and uptake of Leishmania mexicana amastigotes." Journal of Cell Science 108, no. 12 (December 1, 1995): 3715–24. http://dx.doi.org/10.1242/jcs.108.12.3715.
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Amastigotes of the protozoan parasite Leishmania proliferate in phagolysosomes of mammalian macrophages. Propagation of the infection is considered to occur by host-cell rupture and uptake of released parasites by uninfected macrophages. In this study, the kinetics of binding of L mexicana mexicana amastigotes to COS cells and to COS cells transfected with three different macrophage receptors (FcRII-B2, receptor for the Fc-domain of immunoglobulins; CR3, complement type 3 receptor and the mannose receptor) is compared to the rate of adhesion to peritoneal macrophages. Amastigotes isolated from macrophages cultivated in vitro bind with slow, sigmoid kinetics to COS cells expressing either of the three receptors, or to peritoneal macrophages. In contrast, amastigotes isolated from mouse lesions bind with rapid, hyperbolic kinetics to COS cells expressing the Fc receptor or to peritoneal macrophages but with slow, sigmoid kinetics to COS cells expressing the CR3 or the mannose receptor. As shown by immunofluorescence experiments, lesion-derived amastigotes contain host-derived immunoglobulins (Ig) but no complement component 3 at their surface. It is concluded that amastigotes contain no intrinsic ligand at their surface, which enables high-affinity interactions with macrophages. Opsonization by specific Ig may be of relevance in vivo because firstly, in cryosections of mouse lesions extracellular amastigotes containing surface Ig can be detected and, secondly, B cell-deficient mice reconstituted with parasite-specific Ig show a modest increase in the rate of lesion development. In addition, it is shown that amastigotes are internalized by COS cells and grow in large parasitophorous vacuoles similar to those observed in macrophages.
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Rastaldi, M. P., F. Ferrario, L. Yang, S. Tunesi, A. Indaco, H. Zou, and G. D'Amico. "Adhesion molecules expression in noncrescentic acute post-streptococcal glomerulonephritis." Journal of the American Society of Nephrology 7, no. 11 (November 1996): 2419–27. http://dx.doi.org/10.1681/asn.v7112419.
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Clinicomorphological features of 11 cases of non-crescentic acute post-streptococcal glomerulonephritis (APSGN) were reviewed. Intraglomerular and interstitial leukocytes and their possible correlation with the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial-leukocyte adhesion molecule-1 (ELAM-1/E-selectin) were investigated by an immunohistochemical method. Intraglomerular leukocytes were primarily granulocytes (11.4 +/- 10 cells/glomerular cross-section) and monocytes-macrophages (13.4 +/- 19.4 cells/glomerular cross-section). The granulocytes outnumbered monocytes-macrophages in 7 of 11 specimens. The number of intraglomerular leukocytes correlated with proteinuria at the time of renal biopsy. Intraglomerular ICAM-1 staining was strongly positive in all biopsies, especially when intraglomerular monocytes-macrophages prevailed. Expression of intraglomerular VCAM-1 and E-selectin in diseased kidneys did not differ from that in normal kidneys. Interstitial leukocytes were primarily monocytes-macrophages (158.9 +/- 96.8 cells/mm2) and T lymphocytes (102.2 +/- 63.9 cells/mm2). The number of interstitial leukocytes, especially monocytes-macrophages, correlated with serum creatinine level at the time of biopsy. Interstitial ICAM-1 staining was strongly positive on tubules, peritubular capillaries, and small vessels. The tubular positivity for ICAM-1 correlated with the number of interstitial monocytes-macrophages. Interstitial VCAM-1 and E-selectin were expressed as in normal kidney tissues. The data from this study demonstrate that APSGN is characterized by the presence of both intraglomerular and interstitial leukocyte infiltration, correlating respectively with proteinuria and serum creatinine at the time of renal biopsy. Among the adhesion molecules studied, ICAM-1 seems the most involved in leukocyte recruitment, especially in that of monocytes-macrophages.
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Ihanus, Eveliina, Liisa M. Uotila, Anne Toivanen, Minna Varis, and Carl G. Gahmberg. "Red-cell ICAM-4 is a ligand for the monocyte/macrophage integrin CD11c/CD18: characterization of the binding sites on ICAM-4." Blood 109, no. 2 (September 19, 2006): 802–10. http://dx.doi.org/10.1182/blood-2006-04-014878.
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Abstract Intercellular adhesion molecule 4 (ICAM-4) is a unique member of the ICAM family because of its specific expression on erythroid cells and ability to interact with several types of integrins expressed on blood and endothelial cells. The first reported receptors for ICAM-4 were CD11a/CD18 and CD11b/CD18. In contrast to these 2, the cellular ligands and the functional role of the third β2 integrin, CD11c/CD18, have not been well defined. Here, we show that ICAM-4 functions as a ligand for the monocyte/macrophage-specific CD11c/CD18. Deletion of the individual immunoglobulin domains of ICAM-4 demonstrated that both its domains contain binding sites for CD11c/CD18. Analysis of a panel of ICAM-4 point mutants identified residues that affected binding to the integrin. By molecular modeling the important residues were predicted to cluster in 2 distinct but spatially close regions of the first domain with an extension to the second domain spatially distant from the other residues. We also identified 2 peptides derived from sequences of ICAM-4 that are capable of modulating the binding to CD11c/CD18. CD11c/CD18 is expressed on macrophages in spleen and bone marrow. Inhibition of erythrophagocytosis by anti–ICAM-4 and anti-integrin antibodies suggests a role for these interactions in removal of senescent red cells.
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MacPhail, Laurie A., Nusi P. Dekker, and Joseph A. Regezi. "Macrophages and vascular adhesion molecules in oral Kaposi's sarcoma." Journal of Cutaneous Pathology 23, no. 5 (October 1996): 464–72. http://dx.doi.org/10.1111/j.1600-0560.1996.tb01436.x.
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Schneider, Dunja, Hendrik Veelken, and Hassan Jumaa. "The Functional Role of Acquired N-Linked Glycosylation Sites On Follicular Lymphoma B Cell Antigen Receptors." Blood 120, no. 21 (November 16, 2012): 2704. http://dx.doi.org/10.1182/blood.v120.21.2704.2704.
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Abstract Abstract 2704 Follicular lymphoma (FL) is an indolent B-cell lymphoma characterized by apoptosis resistance due to overexpression of Bcl-2 as a consequence of the t(14;18) translocation, ongoing somatic hypermutation (SHM), and expression of B-cell receptors (BCR) with glycosylation of the antigen binding sites. Translocation and concomitant Bcl-2 overexpression can be found in healthy human blood B cells and is insufficient to drive lymphoma outgrowth in mouse models. Since most FL cells still express a surface B cell receptor (BCR) despite the disruption of one immunoglobulin heavy chain allele by the t(14;18) translocation, expression of an antigen receptor seems to be indispensable for FL development. Around 80% of FLs possess asparagine (N)-linked glycosylation sites (amino acid sequence: N-X-S/T) in their BCR variable regions that are not encoded in germ-line but are acquired through SHM. In contrast to germ-line-encoded glycosylation sites in the constant BCR region, where normal processing of the glycans results in termination on branched sugars like sialic acid, the variable region glycosylation sites carry mannose-terminating sugars. Recently, it has been shown that C-type lectins bind to and stimulate FL cells. Such lectins are normally expressed on cells of the innate immune system, e.g. dendritic cells (DCs), which also reside in close interaction with the transformed B cells in germinal centers. Importantly, previous studies point to an outstanding role of the tumor microenvironment in survival and proliferation of the FL cells. In this study, we demonstrate that the variable region glycosylation in FL BCRs contribute to stimulation of the cells as well as adhesion to cells of the innate immune system. The BCR from six FL and the appropriate glycosylation-defective controls in which the N-linked glycosylation sequons are removed by replacing the asparagine (N) residues with glutamine (Q) residues were expressed in the tko cellular reconstitution system. In tko cells, the BCR signaling cascade can be rendered functional at will through a tamoxifen-dependent mutant of the signal transducer SLP-65 (Meixlsperger et al., Immunity 2007; Dühren von Minden et al., Nature 2012). Tko cells expressing FL BCRs and their glycosylation-defective controls were tested for binding of a recombinant DC-SIGN/Fc fusion protein by flow cytometry. The mannosylated FL-derived BCR but not glycosylation-mutated receptors bound DC-SIGN. Stepwise mutation of individual glycosylation sites demonstrated variable contribution to the strength of lectin binding. Despite this specific binding to mannosylated FL BCRs, DC-SIGN/Fc failed to induce significant calcium mobilization of transduced tko cells. Crosslinking with anti-IgM, in contrast, led to a readily detectable BCR-mediated signal, thereby demonstrating functionality of the transduced BCR. To study the role of mannosylated FL receptors in interaction with their environment, we co-cultured cells expressing FL receptors containing or lacking N-linked glycans in the variable regions together with macrophages. Western blot analyses with a pan-phosphotyrosine antibody demonstrated higher global tyrosine phosphorylation in the lysates of cells expressing glycosylated receptors, thereby indicating a specific role for mannosylated V-regions in FL stimulation. Glycan-mediated interactions fulfill multiple important functions in the mammalian immune system including pathogen recognition and cell adhesion or trafficking. DC-SIGN serves as receptor for the uptake of mannosylated pathogens and contributes to cell-cell interaction by binding to the heavily glycosylated ICAM-2/3 (intracellular adhesion molecules-2/3). In the case of FL, it is therefore conceivable that DC-SIGN expressed on follicular DCs binds to the heavily mannosylated FL BCRs and serves thereby as adhesion molecule to keep the FL B cells within the follicular structure. We tested this hypothesis using live cell imaging on a DC sublayer and detected slightly slower movement and shorter tracks of cells expressing glycosylated FL BCRs as compared to control cells. Together, our results ascribe a role of the acquired glycosylation sites in FL BCRs for B-cell/DC interaction, thereby keeping the cells in the appropriate environment in a process that involves active signal transduction rather than triggering a classical antigen-induced BCR stimulation. Disclosures: No relevant conflicts of interest to declare.
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Shrivastava, Anju, Shishir Shishodia, and Ajit Sodhi. "Expression of LFA-1 adhesion molecules on cisplatin-treated macrophages." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1402, no. 3 (April 1998): 269–76. http://dx.doi.org/10.1016/s0167-4889(98)00025-1.
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Eidukaite, Audrone, and Vytas Tamosiunas. "Endometrial and Peritoneal Macrophages: Expression of Activation and Adhesion Molecules." American Journal of Reproductive Immunology 52, no. 2 (July 26, 2004): 113–17. http://dx.doi.org/10.1111/j.1600-0897.2004.00201.x.
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Lan, Hui Y., Michael Bacher, Niansheng Yang, Wei Mu, David J. Nikolic-Paterson, Christine Metz, Andreas Meinhardt, Richard Bucala, and Robert C. Atkins. "The Pathogenic Role of Macrophage Migration Inhibitory Factor in Immunologically Induced Kidney Disease in the Rat." Journal of Experimental Medicine 185, no. 8 (April 21, 1997): 1455–66. http://dx.doi.org/10.1084/jem.185.8.1455.
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Macrophage migration inhibitory factor (MIF) plays a pivotal role in the inflammatory response in endotoxemia and in the delayed-type hypersensitivity response, but its potential as a regulator of immunologically induced disease is unknown. We have addressed this issue by administering a neutralizing anti-MIF antibody in a rat model of immunologically induced crescentic anti-glomerular basement membrane (GBM) glomerulonephritis. Six individual experiments using paired inbred littermates were performed. Rats were primed with rabbit immunoglobulin on day −5 and then injection with rabbit anti–rat GBM serum on day 0. Pairs of animals were treated with anti-MIF or a control monoclonal antibody from the time of anti-GBM serum administration until being killed 14 d later. Control antibody-treated animals developed severe proteinuria and renal function impairment with severe histological damage due to marked leukocytic infiltration and activation within the kidney. In contrast, anti-MIF treatment substantially reduced proteinuria, prevented the loss of renal function, significantly reduced histological damage including glomerular crescent formation, and substantially inhibited renal leukocytic infiltration and activation (all P <0.001 compared with control treatment). Inhibition of renal disease by anti-MIF treatment was attributed to preventing the marked upregulation of interleukin-1β, leukocyte adhesion molecules including intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, and inducible nitric oxide synthase expression seen in the control antibody-treated animals. This inhibition of progressive renal injury was mirrored by the complete suppression of the skin delayed-type hypersensitivity response to the challenge antigen (rabbit IgG). Interestingly, anti-MIF treatment did not effect the secondary antibody response or immune deposition within the kidney, indicating that MIF participates in cellular-based immunity in this primed macrophage-dependent anti-GBM glomerulonephritis. In conclusion, this study has demonstrated a key regulatory role for MIF in the pathogenesis of immunologically induced kidney disease. These results argue that blocking MIF activity may be of benefit in the treatment of human rapidly progressive glomerulonephritis, and suggest that MIF may be important in immune-mediated disease generally.
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Janiszewska, Michalina, Marina Candido Primi, and Tina Izard. "Cell adhesion in cancer: Beyond the migration of single cells." Journal of Biological Chemistry 295, no. 8 (January 14, 2020): 2495–505. http://dx.doi.org/10.1074/jbc.rev119.007759.
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Homeostasis in healthy tissues strongly relies on cell-to-cell adhesion and cell-to-extracellular matrix interactions. For instance, normal epithelial cells maintain tissue structure by adhering to each other and to the extracellular matrix. The proteins that mediate these distinct interactions are collectively called cell adhesion molecules and are divided into four major groups: cadherins, integrins, selectins, and immunoglobulins. They not only physically anchor cells, but also critically integrate signaling between the extracellular microenvironment and cells. These signals include biochemical cues, as adhesion proteins can both act as ligand-activated receptors and activate mechanotransduction triggered by changes in the physical environment. Molecular mechanisms related to cell adhesion signaling have been extensively studied, especially because mutations and changes in expression of these proteins, particularly cadherins and integrins, are frequently associated with diseases ranging from developmental intellectual disability to cancer. In fact, two major hallmarks of cancer, loss of cell-to-cell adhesion and anchorage-independent growth, are both dependent on cell adhesion molecules. Despite many studies elucidating the relationships between malignant transformation and metastasis and cellular adhesion processes, several areas still await exploration. Here, we highlight recently discovered roles of adhesion molecules in collective cancer cell migration and discuss the utility of three-dimensional models in studying cell-cell adhesion. We also describe recent therapeutic approaches targeting adhesion molecules.
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Bachert, Claus, Martin Wagenmann, and Gabriele Holtappels. "Cytokines and Adhesion Molecules in Allergic Rhinitis." American Journal of Rhinology 12, no. 1 (January 1998): 3–8. http://dx.doi.org/10.2500/105065898782103007.
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This review summarizes our current knowledge of nasal allergic inflammation based on studies of cytokines, chemokines, and adhesion molecules in allergic rhinitis. The article also includes some aspects of viral rhinitis. Due to artificial or natural allergen exposure, an increase in the number of eosinophils and basophils, mast cells, IgE-positive cells, macrophages, monocyte-like cells, Langerhans cells, and activated T-cells can be observed within the mucosa and on the mucosal surface. Mediators are known to be released in response to allergens, but do not seem to be adequate to initiate the cell recruitment. After antigen challenge, the release of proinflammatory and regulatory cytokines could be demonstrated, and TH2-type cytokine mRNA upregulation in allergic mucosa has been shown. Proinflammatory cytokines initiate an adhesion cascade and activate T-cells that create an “atopic” cytokine environment within the tissue, which also may be linked to the long-term selective recruitment of eosinophils. However, the acute selective migration of eosinophils after allergen challenge is not fully understood, nor is the role of chemokines in allergic and viral rhinitis. Allergic rhinitis clearly represents an inflammatory reaction.
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Viebig, Nicola K., Ulrich Wulbrand, Reinhold Förster, Katherine T. Andrews, Michael Lanzer, and Percy A. Knolle. "Direct Activation of Human Endothelial Cells by Plasmodium falciparum-Infected Erythrocytes." Infection and Immunity 73, no. 6 (June 2005): 3271–77. http://dx.doi.org/10.1128/iai.73.6.3271-3277.2005.
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ABSTRACT Cytoadherence of Plasmodium falciparum-infected erythrocytes (PRBC) to endothelial cells causes severe clinical disease, presumably as a of result perfusion failure and tissue hypoxia. Cytoadherence to endothelial cells is increased by endothelial cell activation, which is believed to occur in a paracrine fashion by mediators such as tumor necrosis factor alpha (TNF-α) released from macrophages that initially recognize PRBC. Here we provide evidence that PRBC directly stimulate human endothelial cells in the absence of macrophages, leading to increased expression of adhesion-promoting molecules, such as intercellular adhesion molecule 1. Endothelial cell stimulation by PRBC required direct physical contact for a short time (30 to 60 min) and was correlated with parasitemia. Gene expression profiling of endothelial cells stimulated by PRBC revealed increased expression levels of chemokine and adhesion molecule genes. PRBC-stimulated endothelial cells especially showed increased expression of molecules involved in parasite adhesion but failed to express molecules promoting leukocyte adhesion, such as E-selectin and vascular cell adhesion molecule 1, even after challenge with TNF-α. Collectively, our data suggest that stimulation of endothelial cells by PRBC may have two effects: prevention of parasite clearance through increased cytoadherence and attenuation of leukocyte binding to endothelial cells, thereby preventing deleterious immune reactivity.
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Hughes, R. A. C., C. M. Gabriel, N. A. Gregson, and K. J. Smith. "Treatment of inflammatory neuropathy." Multiple Sclerosis Journal 3, no. 2 (April 1997): 88–92. http://dx.doi.org/10.1177/135245859700300206.
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Experimental autoimmune neuritis (EAN) provides an accurate model for understanding the mechanism of acute and chronic inflammatory demyelinating polyradiculoneuropathy (AIDP and CIDP). Treatments aimed at every stage of the immune process in EAN have been effective in inhibiting or treating the disease, including antibodies directed against cell adhesion molecules on the endothelium, inhibition of T cells, removal or blockade of antibodies, depletion of complement and interference with the release or action of macrophage effector molecules. In human disease the only proven treatments are plasma exchange and intravenous immunoglobulin (IVIg) in AIDP, and either of these regimens and also corticosteroids in CIDP. However the outcome from AIDP and CIDP remains unsatisfactory with existing immunosuppressive regimens. This problem arises from the fact that while demyelination appears to be effectively and promptly repaired by remyelination, it may be accompanied by axonal degeneration which can cause severe persistent disability. In addition to limiting demyelination, it will also be important to develop strategies to protect axons from degeneration and to enhance regeneration.
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Reza, Julie Naima, and Mary A. Ritter. "Differential Expression Of Adhesion Molecules Within The Human Thymus." Developmental Immunology 4, no. 1 (1994): 55–64. http://dx.doi.org/10.1155/1994/49301.
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Development of a diverse, MHC-restricted yet self-tolerant T-cell repertoire occurs within the thymus, and requires contact between developing T cells and their stromal microenvironment. Such interactions are likely to depend on the combinatorial effect of specific adhesion molecules. As a preliminary step to determining their role in T-cell development, we have studied the distribution of LFA-1/ICAM-1, CD2/LFA-3, VLA-4/VCAM-1, and HECA 452-antigen/E-Selectin ligand pairs on frozen sections of human thymus. Using two color-immunohistochemistry, and a variety of cell-lineage markers that reveal the nature of the cells on which these adhesion molecules are located, we find a differential distribution of adhesion molecules, with some being shared by both endothelial and epithelial cells. We also identify the VCAM-1-positive subpopulation as cortical macrophages. The relevance of these findings to thymopoiesis is discussed.
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Amari, Masao, Katsuji Taguchi, Minoru Iwahara, Toshiaki Oharaseki, Yuki Yokouchi, Shiro Naoe, and Kei Takahashi. "Interaction between mesothelial cells and macrophages in the initial process of pleural adhesion: ultrastructural studies using adhesion molecules." Medical Molecular Morphology 39, no. 4 (December 21, 2006): 187–92. http://dx.doi.org/10.1007/s00795-006-0340-9.
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Liberek, Tomasz, Michal Chmielewski, Monika Lichodziejewska–Niemierko, Krzysztof Lewandowski, and Boleslaw Rutkowski. "Transmigration of Blood Leukocytes into the Peritoneal Cavity is Related to the Upregulation of ICAM-1 (CD54) and MAC-1 (CD11b/CD18) Adhesion Molecules." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 24, no. 2 (March 2004): 139–46. http://dx.doi.org/10.1177/089686080402400204.
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Background Migration of blood leukocytes into the peritoneal cavity of patients treated with peritoneal dialysis appears to be an important mechanism to prevent and fight peritonitis. To study the role of adhesion molecules in the process of leukocyte transmigration, we compared the expression of several adhesion receptors between peripheral blood monocytes and macrophages isolated from overnight dwell effluents. Methods The study was performed in 12, stable, infection-free patients treated with continuous ambulatory peritoneal dialysis (CAPD) and in 9 patients during peritonitis. In another set of experiments, we analyzed the expression of these molecules on blood leukocytes in 10 predialysis chronic renal failure (CRF) patients and 9 healthy controls. Peritoneal cells from an 8-hour dwell were isolated by centrifugation. Expression of adhesion receptors CD11a, CD11b, CD18, CD49d, and CD54 on blood and peritoneal leukocytes was measured using flow cytometry. Results In macrophages from the uninfected effluents, expression of both subunits of Mac-1 integrin receptor (CD11b and CD18) and intercellular adhesion molecule (ICAM)-1 receptor (CD54) was upregulated compared to peripheral blood monocytes from the same patients. The median value of mean fluorescence intensity in blood and effluent was 760.3 versus 1085.8 for CD11b ( p = 0.013), 288.8 versus 448.6 for CD18 ( p = 0.003), and 186.1 versus 365.7 for CD54 ( p = 0.001). The same adhesion receptors were also significantly upregulated on peritoneal macrophages and neutrophils during peritonitis compared to blood leukocytes. Blood leukocytes from CAPD and CRF patients showed higher expression of CD54 and CD49d molecules compared to leukocytes from healthy controls. Conclusions These data suggest that transmigration of blood leukocytes into the peritoneal cavity during uncomplicated dialysis and in peritonitis is related to selective upregulation of ICAM-1 (CD54) and Mac-1 (CD18/CD11b) receptors.
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Di Sciullo, Gino, Tim Donahue, Melitta Schachner, and Steven A. Bogen. "L1 Antibodies Block Lymph Node Fibroblastic Reticular Matrix Remodeling In Vivo." Journal of Experimental Medicine 187, no. 12 (June 15, 1998): 1953–63. http://dx.doi.org/10.1084/jem.187.12.1953.
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L1 is an immunoglobulin superfamily adhesion molecule highly expressed on neurons and involved in cell motility, neurite outgrowth, axon fasciculation, myelination, and synaptic plasticity. L1 is also expressed by nonneural cells, but its function outside of the nervous system has not been studied extensively. We find that administration of an L1 monoclonal antibody in vivo disrupts the normal remodeling of lymph node reticular matrix during an immune response. Ultrastructural examination reveals that reticular fibroblasts in mice treated with L1 monoclonal antibodies fail to spread and envelop collagen fibers with their cellular processes. The induced defect in the remodeling of the fibroblastic reticular system results in the loss of normal nodal architecture, collapsed cortical sinusoids, and macrophage accumulation in malformed sinuses. Surprisingly, such profound architectural abnormalities have no detectable effects on the primary immune response to protein antigens.
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Krishnatry, Anu Shilpa, Daniel A. Brazeau, and Ho-Leung Fung. "Broad regulation of matrix and adhesion molecules in THP-1 human macrophages by nitroglycerin." Nitric Oxide 22, no. 1 (January 2010): 11–17. http://dx.doi.org/10.1016/j.niox.2009.10.004.
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Prieto, Jacqueline, Anders Eklund, and Manuel Patarroyo. "Regulated Expression of Integrins and Other Adhesion Molecules during Differentiation of Monocytes into Macrophages." Cellular Immunology 156, no. 1 (June 1994): 191–211. http://dx.doi.org/10.1006/cimm.1994.1164.
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Vargas García, Cynthia E., Mariya Petrova, Ingmar J. J. Claes, Ilke De Boeck, Tine L. A. Verhoeven, Ellen Dilissen, Ingemar von Ossowski, et al. "Piliation of Lactobacillus rhamnosus GG Promotes Adhesion, Phagocytosis, and Cytokine Modulation in Macrophages." Applied and Environmental Microbiology 81, no. 6 (January 9, 2015): 2050–62. http://dx.doi.org/10.1128/aem.03949-14.
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ABSTRACTRecently,spaCBA-encoded pili on the cell surface ofLactobacillus rhamnosusGG were identified to be key molecules for binding to human intestinal mucus and Caco-2 intestinal epithelial cells. Here, we investigated the role of the SpaCBA pilus ofL. rhamnosusGG in the interaction with macrophagesin vitroby comparing the wild type with surface mutants. Our results show that SpaCBA pili play a significant role in the capacity for adhesion to macrophages and also promote bacterial uptake by these phagocytic cells. Interestingly, our data suggest that SpaCBA pili also mediate anti-inflammatory effects by induction of interleukin-10 (IL-10) mRNA and reduction of interleukin-6 (IL-6) mRNA in a murine RAW 264.7 macrophage cell line. These pili appear to mediate these effects indirectly by promoting close contact with the macrophages, facilitating the exertion of anti-inflammatory effects by other surface molecules via yet unknown mechanisms. Blockage of complement receptor 3 (CR3), previously identified to be a receptor for streptococcal pili, significantly decreased the uptake of pilus-expressing strains in RAW 264.7 cells, while the expression of IL-10 and IL-6 mRNA by these macrophages was not affected by this blocking. On the other hand, blockage of Toll-like receptor 2 (TLR2) significantly reduced the expression of IL-6 mRNA irrespective of the presence of pili.
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Xu, H., J. A. Gonzalo, Y. St Pierre, I. R. Williams, T. S. Kupper, R. S. Cotran, T. A. Springer, and J. C. Gutierrez-Ramos. "Leukocytosis and resistance to septic shock in intercellular adhesion molecule 1-deficient mice." Journal of Experimental Medicine 180, no. 1 (July 1, 1994): 95–109. http://dx.doi.org/10.1084/jem.180.1.95.
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Intercellular adhesion molecule 1 (ICAM-1) is one of three immunoglobulin superfamily members that bind to the integrins lymphocyte function associated 1 (LFA-1) and Mac-1 on leukocytes. We have generated mice that are genetically and functionally deficient in ICAM-1. These mice have elevated numbers of circulating neutrophils and lymphocytes, as well as diminished allogeneic T cell responses and delayed type hypersensitivity. Mutant mice are resistant to lethal effects of high doses of endotoxin (lipopolysaccharide [LPS]), and this correlates with a significant decrease in neutrophil infiltration in the liver. Production of inflammatory cytokines such as tumor necrosis factor alpha or interleukin 1 is normal in ICAM-1-deficient mice, and thus protection appears to be related to a diminution in critical leukocyte-endothelial interactions. After sensitization with D-galactosamine (D-Gal), ICAM-1-deficient mice are resistant to the lethal effect of low doses of exotoxin (Staphylococcus aureus enterotoxin B [SEB]), which has been shown to mediate its toxic effects via the activation of specific T cells. In this model, ICAM-1-mediated protection against SEB lethality correlates with a decrease in the systemic release of inflammatory cytokines, as well as with prevention of extensive hepatocyte necrosis and hemorrhage. ICAM-1-deficient mice sensitized with D-Gal, however, are not protected from lethality when challenged with low doses of endotoxin (LPS). These studies show that the different contribution of ICAM-1 in the activation of either T cells or macrophages is decisive for the fatal outcome of the shock in these two models. This work suggests that anti-ICAM-1 therapy may be beneficial in both gram-positive and -negative septic shock, either by reducing T cell activation or by diminishing neutrophil infiltration.
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Fabriek, Babs O., Machteld M. J. Polfliet, Rianka P. M. Vloet, Roel C. van der Schors, Antoon J. M. Ligtenberg, Lehn K. Weaver, Christiaan Geest, et al. "The macrophage CD163 surface glycoprotein is an erythroblast adhesion receptor." Blood 109, no. 12 (June 15, 2007): 5223–29. http://dx.doi.org/10.1182/blood-2006-08-036467.
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Abstract Erythropoiesis occurs in erythroblastic islands, where developing erythroblasts closely interact with macrophages. The adhesion molecules that govern macrophage-erythroblast contact have only been partially defined. Our previous work has implicated the rat ED2 antigen, which is highly expressed on the surface of macrophages in erythroblastic islands, in erythroblast binding. In particular, the monoclonal antibody ED2 was found to inhibit erythroblast binding to bone marrow macrophages. Here, we identify the ED2 antigen as the rat CD163 surface glycoprotein, a member of the group B scavenger receptor cysteine-rich (SRCR) family that has previously been shown to function as a receptor for hemoglobin-haptoglobin (Hb-Hp) complexes and is believed to contribute to the clearance of free hemoglobin. CD163 transfectants and recombinant protein containing the extracellular domain of CD163 supported the adhesion of erythroblastic cells. Furthermore, we identified a 13–amino acid motif (CD163p2) corresponding to a putative interaction site within the second scavenger receptor domain of CD163 that could mediate erythroblast binding. Finally, CD163p2 promoted erythroid expansion in vitro, suggesting that it enhanced erythroid proliferation and/or survival, but did not affect differentiation. These findings identify CD163 on macrophages as an adhesion receptor for erythroblasts in erythroblastic islands, and suggest a regulatory role for CD163 during erythropoiesis.
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Sfacteria, Alessandra, Ettore Napoli, Claudia Rifici, Daria Commisso, Giada Giambrone, Giuseppe Mazzullo, and Gabriele Marino. "Immune Cells and Immunoglobulin Expression in the Mammary Gland Tumors of Dog." Animals 11, no. 5 (April 21, 2021): 1189. http://dx.doi.org/10.3390/ani11051189.
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Inflammatory cells have a role in tumor progression and have prognostic and therapeutic potential. The immunohistochemical expression for Mast Cell Tryptase, Macrophage Marker, CD79a, IgA, IgM and IgG on 43 cases of canine mammary gland lesions was analyzed. In hyperplasia, a few B cells (BCs) and Tumor-Associated Macrophages (TAMs) were observed, while the number of Tumor-Associated Mast Cells (TAMCs) was the highest. In the peritumoral stroma of malignant lesions, low number of TAMCs and a high number of TAMAs and BCs were present. Immune cells of each type were always lower in the intratumoral than peritumoral stroma. Positivity to CD79a was also detected in the epithelial cells of simple and micropapillay carcinomas. Immunoglobulin reactivity was mainly located in the epithelial cells where an intense positivity to IgA and IgG and a weak positivity for IgM were detectable. On the basis of our preliminary results and literature data, we suggest that such cells and molecules could be directly involved in the biology of canine mammary gland tumors. In breast cancer, stromal inflammatory cells and cancer derived immunoglobulins have been correlated with the progression, malignancy and poor prognosis of the tumor. The results herein reported show that the dog’s mammary gland epithelium also expresses immunoglobulins, and they mostly show a direct relationship with the infiltration of macrophages. In addition, this study shows that the infiltration of mast cells, B-cells and macrophages varies depending on the degree of malignancy of neoplasia.
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Takenaka, Katsuto, Tatiana K. Prasolava, Jean C. Y. Wang, Steven M. Mortin-Toth, Sam Khalouei, Olga I. Gan, John E. Dick, and Jayne S. Danska. "Identification of a New Genetic Determinant Controlling Human Hematopoietic Stem Cell Engraftment." Blood 110, no. 11 (November 16, 2007): 175. http://dx.doi.org/10.1182/blood.v110.11.175.175.
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Abstract Transplantation of human hematopoietic stem cells (HSC) has been the most important clinical application of stem cell biology. A key discovery enabling successful HSC transplantation was the recognition that HSC engraftment is controlled by human leukocyte antigen (HLA) polymorphism. Although HLA disparity plays a key role in graft rejection, graft failure can occur even in patients receiving an HLA-identical transplant, suggesting that additional, as yet uncharacterized, factors modulate engraftment. We have identified a new genetic determinant that controls the outcome of human HSC transplantation. Xenotransplantation in the non-obese diabetic/severe combine immune-deficient (NOD.SCID) mouse is the best functional assay for human HSC, based on their ability to repopulate recipient animals. We show that NOD.SCID mice provide significantly better support for human hematopoietic grafts than mice of different strain backgrounds carrying equivalent immunodeficiency mutations. To identify the molecular basis for this strain-specificity, we used positional genetics combined with in vitro and in vivo assays of human hematopoiesis. We generated reciprocal congenic strains between NOD and the related non-obese diabetes resistant (NOR) strain which is 88% identical to NOD, and found that support of human hematopoiesis is conferred by variation in a single gene, signal regulatory protein α (Sirpα) on chromosome 2. Human HSC were unable to engraft NOD.SCID mice carrying the NOR allele of Sirpα. NOD SIRPα displays 24 amino acid variations compared to NOR and C57BL/6, concentrated in the immunoglobulin IgV-like domain of this Ig-superfamily member. SIRPα is expressed on myeloid cells and mediates signals that modulate diverse macrophage functions. Indeed, lentiviral gene transfer of the NOD Sirpα variant into NOR macrophages restored their ability to support human hematopoiesis in long-term chimeric stroma-based assays. CD47, the only known cellular ligand of SIRPα, is ubiquitously expressed and modulates multiple cellular actions on hematopoietic cells including platelet activation and adhesion, and leukocyte adhesion and cytokine production. NOD SIRPα demonstrates enhanced binding to human CD47 compared to the NOR protein, suggesting that differential interaction with CD47 underlies the strong effect of Sirpα variation on support of human hematopoiesis in vitro and in vivo. Our findings reveal a novel SIRPα-dependent, macrophage-mediated mechanism critical in HSC transplantation. Future analysis of Sirpα variants within human populations could identify alleles associated with hematopoietic support in BM failure syndromes or correlated with outcomes in clinical transplantation.
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Hoffer, E., Y. Baum, A. Tabak, and C. Frevert. "Adhesion molecules of blood polymorphonuclear leukocytes and alveolar macrophages in rats: modulation by exposure to ozone." Human & Experimental Toxicology 18, no. 9 (September 1999): 547–51. http://dx.doi.org/10.1191/096032799678845089.
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1 Exposure to elevated levels of ozone results in an infiltration of polymorphonuclear leukocytes (PMNs) into the lungs. The purpose of this study was to investigate whether the ozone-induced inflammatory process is preceded by a change in the expression of adhesion molecules (integrins and selectins) in peripheral blood PMNs and alveolar macrophages in rats. 2 Female Sprague Dawley rats were exposed to air or ozone (1 p.p.m., 2 h). Bronchoalveolar lavage (BAL) was carried out and blood was collected via intracardiac puncture at 0 or 18 h after the exposure. There were no PMN in the BAL fluid at time 0 after the 2 h exposure to ozone. The expression of cell adhesion molecules from the integrin family (represented by CD18) on alveolar macrophages (AM) was lowered. The expression of cell adhesion molecules from the selectin family (represented by CD62L) on blood PMN was not affected by exposure to ozone, while the expression of integrins (CD11b) on blood PMN was lowered. 3 This effect was confirmed by experiments in which plasma of ozone-exposed animals was incubated with PMN from peripheral blood obtained from nonexposed animals. In these experiments, the expression of CD11b on PMNs of non-exposed animals was lower after incubation with plasma from ozone-exposed animals. 4 Our experiments suggest the presence of factor(s) in blood, which cause a decrease in the expression of CD11b on PMNs.
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Ofori-Acquah, Solomon F. "Essential Role for Activated Leukocyte Cell Adhesion Molecule in Transendothelial Migration." Blood 106, no. 11 (November 16, 2005): 3691. http://dx.doi.org/10.1182/blood.v106.11.3691.3691.
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Abstract Activated leukocyte cell adhesion molecule (ALCAM/CD166) is a member of the immunoglobulin cell adhesion super family, which has been implicated in diverse physiological and pathophysiological events involving cell migration. Hitherto, ALCAM’s role in inflammation has not been determined. In this study, we show ALCAM is involved in controlling migration of mononuclear leukocytes across the pulmonary endothelium. We demonstrated that ALCAM is localized at intercellular junctions in pulmonary microvascular endothelial cells in vitro and in vivo. ALCAM co-localized with multiple adherens junction molecules including cadherins, catenins and Dlg, as determined by confocal microscopy, and these observations were confirmed by co-immunoprecipitation and co-distribution assays. Treatment of endothelial cultures with EGTA and cytochalasin D translocated ALCAM from intercellular junctions to the cytosol indicating a requirement for homotypic cadherin adhesion and an intact endothelial cytoskeleton for maintaining ALCAM at endothelial cell junctions. Collectively, these data supports the conclusion that ALCAM contributes to the adherens junction complex in endothelial cells. To determine ALCAM’s role in leukocyte-endothelial cell interactions, adult Sprague Dawley rats were intratracheally instilled with macrophage inflammatory protein-1, and this treatment caused acute expression of ALCAM exclusively in newly recruited mononuclear but not polymorphonuclear leukocytes in the alveolar airway. Given that no ALCAM reactivity was observed in peripheral blood leukocytes, we concluded ALCAM is activated as part of the phenotypic switch by mononuclear leukocytes transitioning from circulation to interstitial tissue compartments. To determine the physiological relevance of this finding we examined whether ALCAM was required for transendothelial migration using monocyte chemoattractant protein 1 (MCP-1). MCP-1 dose- and time-dependently increased the number of transmigrated THP-1 monocytes across pulmonary microvascular endothelial monolayers. Recombinant soluble ALCAM dose-dependently reduced the number of transmigrated THP-1 monocytes, whereas in control experiments recombinant soluble vascular endothelial cadherin had no effect on transmigration. This study shows for the first time that ALCAM is located at endothelial cell junctions where it is intimately involved in controlling the number of monocytes that pass through endothelial barriers. ALCAM may therefore play an essential role in the response to inflammation by enhancing recruitment of mononuclear leukocytes by inflamed tissues.
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Brittingham, Andrew, Gang Chen, Bradford S. McGwire, Kwang-Poo Chang, and David M. Mosser. "Interaction of Leishmania gp63 with Cellular Receptors for Fibronectin." Infection and Immunity 67, no. 9 (September 1, 1999): 4477–84. http://dx.doi.org/10.1128/iai.67.9.4477-4484.1999.
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ABSTRACT The most abundant protein on the surface of the promastigote form of the protozoan parasites Leishmania spp. is a 63-kDa molecule, designated gp63 or leishmanolysin. Because gp63 has been shown to possess fibronectin-like properties, we examined the interaction of gp63 with the cellular receptors for fibronectin. We measured the direct binding of Leishmania to human macrophages or to transfected mammalian cells expressing human fibronectin receptors. Leishmania expressing gp63 exhibited modest but reproducible adhesion to human macrophages and to transfected CHO cells expressing α4/β1 fibronectin receptors. In both cases, this interaction depended on gp63 but occurred independently of the SRYD sequence of gp63, because parasites expressing gp63 with a mutated SRYD sequence bound to macrophages and α4/β1 receptor-expressing cells as well as did wild-type parasites. The contribution of gp63 to parasite adhesion was more pronounced when the assays were performed in the presence of complement, suggesting that the receptors for complement and fibronectin may cooperate to mediate the efficient adhesion of parasites to macrophages. The interaction of gp63 with fibronectin receptors may also play an important role in parasite internalization by macrophages. Erythrocytes to which gp63 was cross-linked were efficiently phagocytized by macrophages, whereas control erythrocytes opsonized with complement alone bound to macrophages but remained peripherally attached to the outside of the cell. Similarly, parasites expressing wild-type gp63 were rapidly and efficiently phagocytized by resting macrophages, whereas parasites lacking gp63 were internalized more slowly. This rapid internalization of gp63-expressing parasites was dependent on the β1 integrins, because pretreatment of macrophages with monoclonal antibodies to the β1 integrins decreased the internalization of gp63-expressing parasites. These observations indicate that complement receptors are the primary mediators of parasite adhesion; however, maximal parasite adhesion and internalization may require the participation of the β1 integrins, which recognize fibronectin-like molecules such as gp63 on the surface of the parasite.
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Ballana, Ester, Eduardo Pauls, Jordi Senserrich, Bonaventura Clotet, Françoise Perron-Sierra, Gordon C. Tucker, and José A. Esté. "Cell adhesion through αV-containing integrins is required for efficient HIV-1 infection in macrophages." Blood 113, no. 6 (February 5, 2009): 1278–86. http://dx.doi.org/10.1182/blood-2008-06-161869.
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AbstractMonocytes and macrophages are an important reservoir of human immunodeficiency virus (HIV) and may represent the largest reservoir of this virus in tissues. Differentiation of monocytes into macrophages leads to cell attachment and susceptibility to infection and replication of HIV. Among other cell-surface molecules, integrins are overexpressed during monocyte-macrophage differentiation and may play a role in the replication cycle of envelope viruses including HIV. Here, we show that inhibition of αV integrin in monocyte-derived macrophages, by RNA interference or their inhibition by a selective small heterocyclic RGD-mimetic nonpeptide compound, inhibited the replication of HIV in the absence of cytotoxicity. Interference or inhibition of αV integrins triggered a signal transduction pathway, leading to down-regulation of nuclear factor-κB–dependent HIV-1 transcription. Such inhibition was mediated by a MAP-kinase signaling cascade, probably involving ERK1/2, p38-mitogen–activated protein kinases, and HSP27. In conclusion, our results reveal a significant role of integrin αV-mediated adhesion in HIV-1 infection of macrophages.
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Keréveur, A., D. McIlroy, A. Samri, E. Oksenhendler, J. P. Clauvel, and B. Autran. "Up-regulation of adhesion and MHC molecules on splenic monocyte/macrophages in adult haemophagocytic syndrome." British Journal of Haematology 104, no. 4 (March 1999): 871–77. http://dx.doi.org/10.1046/j.1365-2141.1999.01247.x.
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Faull, R. J., J. Wang, and W. Stavros. "Changes in the expression of adhesion molecules as peripheral blood monocytes differentiate into peritoneal macrophages." Nephrology Dialysis Transplantation 11, no. 10 (October 1, 1996): 2037–44. http://dx.doi.org/10.1093/oxfordjournals.ndt.a027093.
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Chu, Ya-Ting, Chiou-Feng Lin, Chih-Peng Chang, Trai-Ming Yeh, Robert Anderson, Shu-Wen Wan, Yi-Wen Yang, and Yee-Shin Lin. "Anti-dengue virus nonstructural protein 1 antibodies contribute to platelet phagocytosis by macrophages." Thrombosis and Haemostasis 115, no. 03 (2016): 646–56. http://dx.doi.org/10.1160/th15-06-0498.
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SummaryThrombocytopenia is an important clinical manifestation of dengue disease. The hypotheses concerning the pathogenesis of thrombocytopenia include decreased production and increased destruction or consumption of platelets. We previously suggested a mechanism of molecular mimicry in which antibodies (Abs) directed against dengue virus (DENV) nonstructural protein 1 (NS1) cross-react with platelets. Furthermore, several lines of evidence show activation of endothelial cells (ECs) and macrophages are related to dengue disease severity. Previous studies also suggested that Ab-opsonised platelets facilitate the engulfment of platelets by macrophages. Here we show that TNF-α-activated ECs upregulate adhesion molecule expression to enhance the binding of platelets and macrophages and lead to anti-DENV NS1 Ab-mediated platelet phagocytosis. We further demonstrate that the interaction between macrophages and TNF-α-activated ECs requires binding of FcγR with the Fc region of platelet-bound anti-DENV NS1 Abs. Importantly, the binding of anti-DENV NS1 Abs to platelets did not interfere with platelet adhesion to ECs. The adhesion molecules ICAM-1 and β3 integrin expressed on ECs as well as the FcγR expressed on macrophages were critical in anti-DENV NS1 Ab-mediated platelet phagocytosis on activated ECs. Moreover, anti-DENV NS1 Abs dramatically enhanced platelet engulfment by macrophages in a murine model of DENV infection. Our study provides evidence for a novel role for anti-DENV NS1 Abs in the pathogenesis of thrombocytopenia in dengue disease by enhancing platelet phagocytosis by macrophages.
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Bazzoni, Gianfranco, Maria Grazia Lampugnani, and Elisabetta Dejana. "The Role of Endothelial Cell-to-Cell Junctions in Vascular Morphogenesis." Thrombosis and Haemostasis 82, no. 08 (1999): 755–61. http://dx.doi.org/10.1055/s-0037-1615908.
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IntroductionAdhesion of endothelial cells (ECs) to one another and to the extracellular matrix is mediated by various surface receptors These surface receptors belong to several families of ubiquitously expressed cell adhesion molecules, such as cadherins integrins, immunoglobulins, and proteoglycans. Besides merely providing attachment sites, most adhesive receptors interac with cytoskeletal and cytoplasmic molecules and, thus, contribute to the regulation of cell morphology and signaling.Adhesion requires refined modulation to sustain the process of new vessel formation or angiogenesis. Adjoining cells mus act in concert to finalize migration and proliferation and organize into a three-dimensional network of patent tubes. Some of the molecules involved in these cell-to-extracellular matrix and cell-to-cell interactions have now been characterized. The intracellular signaling pathways activated by these molecules are, on the contrary, still rather obscure. Moreover, the adhesive systems to matrix and neighboring cells can communicate,1-4 adding complexity and coordination to the process.
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Cho, Jae Youl. "Suppressive Effect of Hydroquinone, a Benzene Metabolite, on In Vitro Inflammatory Responses Mediated by Macrophages, Monocytes, and Lymphocytes." Mediators of Inflammation 2008 (2008): 1–11. http://dx.doi.org/10.1155/2008/298010.
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We investigated the inhibitory effects of hydroquinone on cytokine release, phagocytosis, NO production, ROS generation, cell-cell/cell fibronectin adhesion, and lymphocyte proliferation. We found that hydroquinone suppressed the production of proinflammatory cytokines [tumor necrosis factor (TNF)-, interleukin (IL)-1, and IL-6], secretion of toxic molecules [nitric oxide (NO) and reactive oxygen species (ROS)], phagocytic uptake of FITC-labeled dextran, upregulation of costimulatory molecules, U937 cell-cell adhesion induced by CD18 and CD29, and the proliferation of lymphocytes from the bone marrow and spleen. Considering that (1) environmental chemical stressors reduce the immune response of chronic cigarette smokers and children against bacterial and viral infections and that (2) workers in petroleum factories are at higher risk for cancer, our data suggest that hydroquinone might pathologically inhibit inflammatory responses mediated by monocytes, macrophages, and lymphocytes.
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El-Bassiouni, Nora E. I., Ola Mahmoud Mahmoud, Eman G. El Ahwani, Raafat A. Ibrahim, and Azza E. I. El Bassiouny. "MONOCYTE ADHESION MOLECULES EXPRESSION IN PATIENTS WITH CHRONIC HEPATITIS C AND LIVER CIRRHOSIS." Mediterranean Journal of Hematology and Infectious Diseases 5, no. 1 (September 1, 2013): e2013054. http://dx.doi.org/10.4084/mjhid.2013.054.
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Abstract: Introduction: Chronic viral hepatitis is histologically characterized by predominantly periportal infiltration of mononuclear cells, including monocytes/macrophages. Intralobular infiltration of these inflammatory cells is an ominous sign of deterioration and a criterion for disease activity. We aimed to study the expression of monocytes adhesion molecules and their endothelial ligands in patients with chronic hepatitis C (CHC) and liver cirrhosis (LC). The influence of cytokines and chemokine on monocyte adhesion was also taken into account. Material and Methods: The current study included 30 cases of CHC, 30 cases of LC and 15 normal healthy controls. Flow cytometric quantification of CD11a, CD11b and CD49d monocyte surface antigen expression was performed. Circulating sE-selectin, sICAM-1, sVCAM-1, TNF-α, IL-1 and MCP-1 were measured by ELISA kits. Results: The expression of CD11b, CD49d, and the serum level of sICAM-1, sVCAM-1, TNF-α showed progressive increase from non-cirrhotic to cirrhotic patients. correlation was found between monocyte adhesion molecules CD11a, CD11b and CD49d and each of sICAM-1 and sVCAM-1 Conclusions: These findings suggest that the modulation of monocyte-subset recruitment into the liver via adhesion molecules or cytokines/cytokine receptors may represent promising approaches for therapeutic interventions in human liver fibrosis. Measurement of serum soluble adhesion molecules may be useful for monitoring progression of liver inflammation and fibrosis during CHC.
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Horn, S., N. Bashan, and J. Gopas. "Phagocytosis of phenylhydrazine oxidized and G-6-PD-deficient red blood cells: the role of cell-bound immunoglobulins." Blood 78, no. 7 (October 1, 1991): 1818–25. http://dx.doi.org/10.1182/blood.v78.7.1818.1818.
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Abstract In this study, the role of Igs in the recognition and removal of oxidatively damaged human red blood cells (RBCs) was investigated. Phagocytosis of normal RBCs exposed to the oxidative hemolytic agent phenylhydrazine (Phz) and of glucose-6-phosphate dehydrogenase (G6PD)- deficient RBCs by murine macrophages was examined. A 40-fold increase in phagocytosis of RBCs treated with 3 mmol/L Phz was obtained both in the absence and presence of autologous serum, indicating that binding of autologous antibodies to the oxidized cells is not essential for phagocytosis. Yet, a basal number of IgG molecules was found to be present on the RBCs, as determined both by binding of 125I protein A and fluorescein isothiocyanate-antihuman Ig to the cells. Macrophage Fc receptors were found to be involved in the recognition of the RBCs, because phagocytosis was partially inhibited by incubating macrophages with bovine serum albumin (BSA) anti-BSA complexes, aIg (aggregated Igs), and anti-Fc receptor II monoclonal antibodies. Galactose/mannose inhibited phagocytosis of oxidized RBCs additively to aIg. Because phagocytosis was decreased when Phz-RBCs were incubated with F(ab')2 fragments of antihuman antibodies, it is suggested that the basal amount of Igs bound to the cells plays a role in the recognition of Phz- RBCs. G6PD-deficient RBCs were recognized and phagocytosed by murine macrophages without preexposure to oxidants in vitro (mean of 19 RBCs/100 macrophages). This phagocytosis was not affected by the addition of serum and was inhibited by incubating macrophages with galactose/mannose and the various Fc receptor blockers. A positive correlation between hemoglobin content and the number of cell-bound Igs to each patient erythrocytes was found. These results support the involvement of both an Fc and a lectin-like macrophage receptor in the recognition and phagocytosis of Phz-oxidized and G6PD-deficient RBCs and suggest opsonization as a possible physiologic process for the removal of severe damaged RBCs.
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Horn, S., N. Bashan, and J. Gopas. "Phagocytosis of phenylhydrazine oxidized and G-6-PD-deficient red blood cells: the role of cell-bound immunoglobulins." Blood 78, no. 7 (October 1, 1991): 1818–25. http://dx.doi.org/10.1182/blood.v78.7.1818.bloodjournal7871818.
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In this study, the role of Igs in the recognition and removal of oxidatively damaged human red blood cells (RBCs) was investigated. Phagocytosis of normal RBCs exposed to the oxidative hemolytic agent phenylhydrazine (Phz) and of glucose-6-phosphate dehydrogenase (G6PD)- deficient RBCs by murine macrophages was examined. A 40-fold increase in phagocytosis of RBCs treated with 3 mmol/L Phz was obtained both in the absence and presence of autologous serum, indicating that binding of autologous antibodies to the oxidized cells is not essential for phagocytosis. Yet, a basal number of IgG molecules was found to be present on the RBCs, as determined both by binding of 125I protein A and fluorescein isothiocyanate-antihuman Ig to the cells. Macrophage Fc receptors were found to be involved in the recognition of the RBCs, because phagocytosis was partially inhibited by incubating macrophages with bovine serum albumin (BSA) anti-BSA complexes, aIg (aggregated Igs), and anti-Fc receptor II monoclonal antibodies. Galactose/mannose inhibited phagocytosis of oxidized RBCs additively to aIg. Because phagocytosis was decreased when Phz-RBCs were incubated with F(ab')2 fragments of antihuman antibodies, it is suggested that the basal amount of Igs bound to the cells plays a role in the recognition of Phz- RBCs. G6PD-deficient RBCs were recognized and phagocytosed by murine macrophages without preexposure to oxidants in vitro (mean of 19 RBCs/100 macrophages). This phagocytosis was not affected by the addition of serum and was inhibited by incubating macrophages with galactose/mannose and the various Fc receptor blockers. A positive correlation between hemoglobin content and the number of cell-bound Igs to each patient erythrocytes was found. These results support the involvement of both an Fc and a lectin-like macrophage receptor in the recognition and phagocytosis of Phz-oxidized and G6PD-deficient RBCs and suggest opsonization as a possible physiologic process for the removal of severe damaged RBCs.
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Tan, Fang, Flaubert Mbeunkui, Crystal Harris, and Solomon F. Ofori-Acquah. "Mechanisms for Transcriptional Activation of the Human Activated Leukocyte Cell Adhesion Molecule Gene and Its Silencing by Immunosuppressive Toxins." Blood 108, no. 11 (November 16, 2006): 1637. http://dx.doi.org/10.1182/blood.v108.11.1637.1637.
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Abstract Activated leukocyte cell adhesion molecule (ALCAM/CD166) is a member of the immunoglobulin super-family. It is expressed on the surfaces of activated monocytes, dendritic cells and macrophages. These immune cells use ALCAM through homotypic and heterotypic adhesions to control multiple stages in the inflammatory response. Indeed, anti-ALCAM antibodies and recombinant soluble ALCAM significantly inhibit monocyte transendothelial migration, stabilization of the immunological synapse and dendritic cell-mediated T-lymphocyte proliferation. Despite this significance, there is currently no understanding of how the human ALCAM gene is regulated. In this study, we identified the mechanisms for transcription, basal transcriptional activation and immunosuppressive silencing of the ALCAM gene. A common site for transcription of the ALCAM gene was identified 350 base pairs (bp) upstream from the translational start site. Multiple truncated fragments of the ALCAM promoter was cloned from genomic DNA and sub-cloned upstream of a promoterless luciferase vector. A proximal 650-bp promoter sequence conferred tissue-independent activation in hematopoietic, epithelial and endothelial cells. A canonical Sp1 binding sequence at −550 upstream of the translational start site was mapped within this proximal positive regulatory promoter region. Site-directed mutagenesis revealed this sequence was essential for optimum ALCAM promoter activity. Importantly, Sp1 occupied the cognate sequence in vivo as determined by chromatin immunoprecipitation assays. Over-expression of Sp1 significantly increased ALCAM promoter activity whereas a control expression vector had no impact. DNA sequences in the interval −600 to −800 negatively influenced promoter activity in a tissue-specific manner. This region contained a putative binding sequence for the aryl hydrocarbon receptor (Ahr), which highlighted ALCAM as a potential target of the immunosuppressing ligand dioxin. This hypothesis was tested by examination of whether ALCAM activation is blocked by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) in monocytes differentiating into macrophages and dendritic cells. Expression of ALCAM was increased 3–5-fold in HL-60 and THP-1 monocytes treated with the differentiating agent phorbol 12-myristate 13-acetate. TCDD dose dependently blocked this activation, indeed, the highest concentration of TCDD (25 nM) used in this study completely blocked ALCAM activation in both monocytic cells. In conclusion, we have unveiled for the first time, the molecular basis for transcription and basal trans-activation of the human ALCAM gene, and identified the Ahr-pathway as a powerful silencer of ALCAM gene activation. Further studies of the ALCAM promoter, may clarify how this gene is up-regulated as part of the inflammatory response, and how it is silenced by immunotoxins. Heterologous expression of ALCAM may be a potential strategy to mitigate the immunosuppressive effects of dioxins and polycyclic aromatic hydrocarbons.
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Regezi, J. A., L. A. Macphail, D. W. Richards, and J. S. Greenspan. "A Study of Macrophages, Macrophage-related Cells, and Endothelial Adhesion Molecules in Recurrent Aphthous Ulcers in HIV-positive Patients." Journal of Dental Research 72, no. 12 (December 1993): 1549–53. http://dx.doi.org/10.1177/00220345930720120301.
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The purpose of this immunohistochemical study was to investigate the presence and distribution of macrophages (CDllc+ and CD68+) and macrophage-related dendritic cells (factor XIIIa+ and CD36+) in early and late aphthous ulcers associated with HIV infection. To substantiate a mechanism by which these cells may move from the vascular compartment to tissue spaces, we also investigated expression of ELAM (endothelial leukocyte adhesion molecule), ICAM-1 (intercellular adhesion molecule), and CD18 (leukocyte function antigen). Numerous CD 1 lc+ and CD68+ macrophages were seen in early lesions, though larger numbers of CD68+ cells were present in older lesions. No significant increases in factor XIIIa+ dendrocytes were seen in either early or late lesions, though dendrocytes appeared enlarged. CD36+ cells and CD18+ leukocytes were more numerous in early than in late aphthous ulcers. ELAM and ICAM expression was most intense on endothelial cells in early aphthous ulcers, with staining intensity fading toward the lesion periphery. Control specimens showed weaker ELAM and ICAM staining than did the ulcer specimens. Keratinocytes did not express ICAM. By virtue of their numbers, macrophages and macrophage subtypes appear to have a significant role in both the early and late stages of this disease. Although factor XIIIa-expressing dendrocytes may not have been more numerous in the ulcers, they appeared to be "activated" because of their prominence in the lesions and their occasional co-expression of CD68 antigen (KP1+). They may have a minor role in antigen processing, phagocytosis, and fibroplasia. ELAM and ICAM expression by endothelial cells provides a mechanism by which macrophages and other leukocytes can be recruited to the site of the lesion. This mechanism appears to be functional in HIV-positive patients.
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Kozień, Dawid, Bożena Szermer-Olearnik, Andrzej Rapak, Agnieszka Szczygieł, Natalia Anger-Góra, Janusz Boratyński, Elżbieta Pajtasz-Piasecka, Mirosław M. Bućko, and Zbigniew Pędzich. "Boron-Rich Boron Carbide Nanoparticles as a Carrier in Boron Neutron Capture Therapy: Their Influence on Tumor and Immune Phagocytic Cells." Materials 14, no. 11 (June 2, 2021): 3010. http://dx.doi.org/10.3390/ma14113010.
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The aim of the work was to study the interaction between boron-rich boron carbide nanoparticles and selected tumor and immune phagocytic cells. Experiments were performed to investigate the feasibility of the application of boron carbide nanoparticles as a boron carrier in boron neutron capture therapy. Boron carbide powder was prepared by the direct reaction between boron and soot using the transport of reagents through the gas phase. The powder was ground, and a population of nanoparticles with an average particle size about 80 nm was selected by centrifugation. The aqueous suspension of the nanoparticles was functionalized with human immunoglobulins or FITC-labeled human immunoglobulins and was then added to the MC38 murine colon carcinoma and to the RAW 264.7 cell line of mouse macrophages. Flow cytometry analysis was used to determine interactions between the functionalized boron carbide nanoparticles and respective cells. It was shown that B4C–IgG nanoconjugates may bind to phagocytic cells to be internalized by them, at least partially, whereas such nanoconjugates can only slightly interact with molecules on the cancer cells’ surface.
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Chanez, P., A. M. Vignola, P. Lacoste, F. B. Michel, P. Godard, and J. Bousquet. "Increased expression of adhesion molecules (ICAM-1 and LFA-1) on alveolar macrophages from asthmatic patients." Allergy 48, no. 8 (November 1993): 576–80. http://dx.doi.org/10.1111/j.1398-9995.1993.tb00751.x.
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