Статті в журналах: "Leukocyte-endothelial"

1

Harlan, JM. "Leukocyte-endothelial interactions." Blood 65, no. 3 (March 1, 1985): 513–25. http://dx.doi.org/10.1182/blood.v65.3.513.513.

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2

Harlan, JM. "Leukocyte-endothelial interactions." Blood 65, no. 3 (March 1, 1985): 513–25. http://dx.doi.org/10.1182/blood.v65.3.513.bloodjournal653513.

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3

MIYASAKA, Masayuki. "Leukocyte-Endothelial Cell Interactions." Japanese Journal of Thrombosis and Hemostasis 1, no. 6 (1990): 465–74. http://dx.doi.org/10.2491/jjsth.1.465.

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4

Carlos, TM, and JM Harlan. "Leukocyte-endothelial adhesion molecules." Blood 84, no. 7 (October 1, 1994): 2068–101. http://dx.doi.org/10.1182/blood.v84.7.2068.2068.

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Abstract In the 9 years since the last review on leukocyte and endothelial interactions was published in this journal many of the critical structures involved in leukocyte adherence to and migration across endothelium have been elucidated. With the advent of cell and molecular biology approaches, investigations have progressed from the early descriptions by intravital microscopy and histology, to functional and immunologic characterization of adhesion molecules, and now to the development of genetically deficient animals and the first phase I trial of “anti-adhesion” therapy in humans. The molecular cloning and definition of the adhesive functions of the leukocyte integrins, endothelial members of the Ig gene superfamily, and the selectins has already provided sufficient information to construct an operative paradigm of the molecular basis of leukocyte emigration. The regulation of these adhesion molecules by chemoattractants, cytokines, or chemokines, and the interrelationships of adhesion pathways need to be examined in vitro and, particularly, in vivo. Additional studies are required to dissect the contribution of the individual adhesion molecules to leukocyte emigration in various models of inflammation or immune reaction. Certainly, new adhesion structures will be identified, and the current paradigm of leukocyte emigration will be refined. The promise of new insights into the biology and pathology of the inflammatory and immune response, and the potential for new therapies for a wide variety of diseases assures that this will continue to be an exciting area of investigation.

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5

Carlos, TM, and JM Harlan. "Leukocyte-endothelial adhesion molecules." Blood 84, no. 7 (October 1, 1994): 2068–101. http://dx.doi.org/10.1182/blood.v84.7.2068.bloodjournal8472068.

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In the 9 years since the last review on leukocyte and endothelial interactions was published in this journal many of the critical structures involved in leukocyte adherence to and migration across endothelium have been elucidated. With the advent of cell and molecular biology approaches, investigations have progressed from the early descriptions by intravital microscopy and histology, to functional and immunologic characterization of adhesion molecules, and now to the development of genetically deficient animals and the first phase I trial of “anti-adhesion” therapy in humans. The molecular cloning and definition of the adhesive functions of the leukocyte integrins, endothelial members of the Ig gene superfamily, and the selectins has already provided sufficient information to construct an operative paradigm of the molecular basis of leukocyte emigration. The regulation of these adhesion molecules by chemoattractants, cytokines, or chemokines, and the interrelationships of adhesion pathways need to be examined in vitro and, particularly, in vivo. Additional studies are required to dissect the contribution of the individual adhesion molecules to leukocyte emigration in various models of inflammation or immune reaction. Certainly, new adhesion structures will be identified, and the current paradigm of leukocyte emigration will be refined. The promise of new insights into the biology and pathology of the inflammatory and immune response, and the potential for new therapies for a wide variety of diseases assures that this will continue to be an exciting area of investigation.

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6

Wild, Martin K., and M. Gabriele Bixel. "Leukocyte?endothelial cell interactions." FEBS Journal 273, no. 19 (October 2006): 4375–76. http://dx.doi.org/10.1111/j.1742-4658.2006.05436.x.

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7

Harlan, John. "Leukocyte-Mediated Endothelial Injury." Journal of Vascular and Interventional Radiology 9, no. 4 (July 1998): 675–77. http://dx.doi.org/10.1016/s1051-0443(98)70352-5.

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8

McEver, Rodger P. "Leukocyte—endothelial cell interactions." Current Biology 2, no. 11 (November 1992): 620. http://dx.doi.org/10.1016/0960-9822(92)90185-d.

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9

McEver, Rodger P. "Leukocyte—endothelial cell interactions." Current Opinion in Cell Biology 4, no. 5 (October 1992): 840–49. http://dx.doi.org/10.1016/0955-0674(92)90109-p.

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10

Bevilacqua, M. P. "Endothelial-Leukocyte Adhesion Molecules." Annual Review of Immunology 11, no. 1 (April 1993): 767–804. http://dx.doi.org/10.1146/annurev.iy.11.040193.004003.

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11

Hossain, Mokarram, Syed M. Qadri, Yang Su, and Lixin Liu. "ICAM-1-mediated leukocyte adhesion is critical for the activation of endothelial LSP1." American Journal of Physiology-Cell Physiology 304, no. 9 (May 1, 2013): C895—C904. http://dx.doi.org/10.1152/ajpcell.00297.2012.

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Leukocyte-endothelial interaction triggers signaling events in endothelial cells prior to transendothelial migration of leukocytes. Leukocyte-specific protein 1 (LSP1), expressed in endothelial cells, plays a pivotal role in regulating subsequent recruitment steps following leukocyte adhesion. In neutrophils, LSP1 is activated by phosphorylation of its serine residues by molecules downstream of p38 MAPK and PKC. Whether leukocyte adhesion to endothelial cells is required for endothelial LSP1 activation remains elusive. In addition, discrepancies in the functions of endothelial and leukocyte LSP1 in leukocyte adhesion prevail. We demonstrate that adhesion of wild-type ( Lsp1+/+) neutrophils to LSP1-deficient ( Lsp1−/−) endothelial cells was significantly reduced compared with adhesion to Lsp1+/+endothelial cells. Immunoblotting revealed increased phosphorylated endothelial LSP1 in the presence of adherent Lsp1−/−neutrophils [stimulated by macrophage inflammatory protein-2 (CXCL2), TNF-α, or thapsigargin], but not cytokine or chemokine alone. Pharmacological inhibition of p38 MAPK by SB-203580 (10 μM) significantly blunted the phosphorylation of endothelial LSP1. Functionally blocking endothelial ICAM-1 or neutrophil β2-integrins diminished neutrophil adhesion and phosphorylation of endothelial LSP1. The engagement of endothelial ICAM-1 cross-linking, which mimics leukocyte adhesion, resulted in phosphorylation of endothelial LSP1. In neutrophil-depleted Lsp1+/+mice, administration of ICAM-1 cross-linking antibody resulted in increased phosphorylation of LSP1 and p38 MAPK in TNF-α-stimulated cremaster muscle. In conclusion, endothelial LSP1 participates in leukocyte adhesion in vitro, and leukocyte adhesion through ICAM-1 fosters the activation of endothelial LSP1, an effect at least partially mediated by the activation of p38 MAPK. Endothelial LSP1, in contrast to neutrophil LSP1, is not phosphorylated by cytokine or chemokine stimulation alone.

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12

SAINANI, Gurmukh S., and Vibhuti G. MARU. "The endothelial leukocyte adhesion molecule." Acta Cardiologica 60, no. 5 (November 1, 2005): 501–7. http://dx.doi.org/10.2143/ac.60.5.2004971.

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13

Langer, Harald F., and Triantafyllos Chavakis. "Leukocyte - endothelial interactions in inflammation." Journal of Cellular and Molecular Medicine 13, no. 7 (July 2009): 1211–20. http://dx.doi.org/10.1111/j.1582-4934.2009.00811.x.

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14

Wautier, Jean-Luc, Hendra Setiadi, Didier Vilette, Dominique Weill, and Marie-Paule Wautier. "Leukocyte adhesion to endothelial cells." Biorheology 27, no. 3-4 (August 1, 1990): 425–32. http://dx.doi.org/10.3233/bir-1990-273-419.

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15

Hordijk, Peter L. "Endothelial Signaling in Leukocyte Transmigration." Cell Biochemistry and Biophysics 38, no. 3 (2003): 305–22. http://dx.doi.org/10.1385/cbb:38:3:305.

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16

Ni, Xiang, Kurt R. Gritman, Toby K. Eisenstein, Martin W. Adler, Karl E. Arfors, and Ronald F. Tuma. "Morphine Attenuates Leukocyte/Endothelial Interactions." Microvascular Research 60, no. 2 (September 2000): 121–30. http://dx.doi.org/10.1006/mvre.2000.2253.

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17

Doulet, Nicolas, Emmanuel Donnadieu, Marie-Pierre Laran-Chich, Florence Niedergang, Xavier Nassif, Pierre Olivier Couraud, and Sandrine Bourdoulous. "Neisseria meningitidis infection of human endothelial cells interferes with leukocyte transmigration by preventing the formation of endothelial docking structures." Journal of Cell Biology 173, no. 4 (May 22, 2006): 627–37. http://dx.doi.org/10.1083/jcb.200507128.

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Neisseria meningitidis elicits the formation of membrane protrusions on vascular endothelial cells, enabling its internalization and transcytosis. We provide evidence that this process interferes with the transendothelial migration of leukocytes. Bacteria adhering to endothelial cells actively recruit ezrin, moesin, and ezrin binding adhesion molecules. These molecules no longer accumulate at sites of leukocyte–endothelial contact, preventing the formation of the endothelial docking structures required for proper leukocyte diapedesis. Overexpression of exogenous ezrin or moesin is sufficient to rescue the formation of docking structures on and leukocyte migration through infected endothelial monolayers. Inversely, expression of the dominant-negative NH2-terminal domain of ezrin markedly inhibits the formation of docking structures and leukocyte diapedesis through noninfected monolayers. Ezrin and moesin thus appear as pivotal endothelial proteins required for leukocyte diapedesis that are titrated away by N. meningitidis. These results highlight a novel strategy developed by a bacterial pathogen to hamper the host inflammatory response by interfering with leukocyte–endothelial cell interaction.

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18

Hickey, M. J., P. H. Reinhardt, L. Ostrovsky, W. M. Jones, M. A. Jutila, D. Payne, J. Elliott, and P. Kubes. "Tumor necrosis factor-alpha induces leukocyte recruitment by different mechanisms in vivo and in vitro." Journal of Immunology 158, no. 7 (April 1, 1997): 3391–400. http://dx.doi.org/10.4049/jimmunol.158.7.3391.

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Abstract It is well established that E-selectin is the endothelial adhesion molecule that is primarily responsible for mediating leukocyte rolling on TNF-alpha-stimulated cultured endothelial cells. Despite this, few studies in in vivo inflammatory models have observed reduced leukocyte accumulation using mAbs against E-selectin. The objective of this study was to compare the function of E-selectin on endothelial cells in vitro with its role in TNF-alpha-induced leukocyte recruitment in vivo using EL246, a mAb that blocks the function of E-selectin on activated feline endothelial cells. In vitro experiments using feline endothelial cells showed that EL246 functionally inhibits E-selectin-dependent leukocyte recruitment induced by TNF-alpha, without affecting the function of other rolling mechanisms. Intravital microscopy of single 25- to 40-microm venules in the feline mesentery was then used to examine leukocyte rolling and adhesion in response to superfusion with TNF-alpha. TNF-alpha treatment significantly increased the number of both rolling and adherent leukocytes and significantly decreased leukocyte rolling velocity. Treatment with EL246 (1 mg/kg), either i.v. at the start of the TNF-alpha protocol or directly into the superior mesenteric artery after 3 h of TNF-alpha treatment, had no effect on leukocyte rolling, adhesion, or rolling velocity. However, treatment with the selectin-binding carbohydrate, fucoidan, reduced leukocyte rolling to below baseline levels. These results suggest that in contrast to its prominent role on cultured endothelial cells, E-selectin does not contribute to leukocyte recruitment in TNF-alpha-stimulated feline mesenteric venules in vivo.

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19

Dole, Vandana S., Wolfgang Bergmeier, Heather A. Mitchell, Sarah C. Eichenberger, and Denisa D. Wagner. "Activated platelets induce Weibel-Palade–body secretion and leukocyte rolling in vivo: role of P-selectin." Blood 106, no. 7 (October 1, 2005): 2334–39. http://dx.doi.org/10.1182/blood-2005-04-1530.

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AbstractThe presence of activated platelets and platelet-leukocyte aggregates in the circulation accompanies major surgical procedures and occurs in several chronic diseases. Recent findings that activated platelets contribute to the inflammatory disease atherosclerosis made us address the question whether activated platelets stimulate normal healthy endothelium. Infusion of activated platelets into young mice led to the formation of transient platelet-leukocyte aggregates and resulted in a several-fold systemic increase in leukocyte rolling 2 to 4 hours after infusion. Rolling returned to baseline levels 7 hours after infusion. Infusion of activated P-selectin-/- platelets did not induce leukocyte rolling, indicating that platelet P-selectin was involved in the endothelial activation. The endothelial activation did not require platelet CD40L. Leukocyte rolling was mediated solely by the interaction of endothelial P-selectin and leukocyte P-selectin glycoprotein ligand 1 (PSGL-1). Endothelial P-selectin is stored with von Willebrand factor (VWF) in Weibel-Palade bodies. The release of Weibel-Palade bodies on infusion of activated platelets was indicated by both elevation of plasma VWF levels and by an increase in the in vivo staining of endothelial P-selectin. We conclude that the presence of activated platelets in circulation promotes acute inflammation by stimulating secretion of Weibel-Palade bodies and P-selectin–mediated leukocyte rolling.

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20

GIMBRONE, Michael A., M. Elyse WHEELER, and Michael P. BEVILACQUA. "Endothelial-Dependent Mechanisms of Leukocyte Adhesion." Journal of Japan Atherosclerosis Society 16, no. 8 (1989): 1101–4. http://dx.doi.org/10.5551/jat1973.16.8_1101.

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21

Granger, D. Neil. "Regulation of Leukocyte-Endothelial Cell Interactions." Inflammatory Bowel Diseases 3, no. 2 (1997): 155. http://dx.doi.org/10.1097/00054725-199706000-00022.

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22

Luscinskas, Francis W., Jennifer Allport, Han Ding, Tucker Collins, and Mary E. Gerritsen. "Endothelial Cell Regulation of Leukocyte Transmigration." Inflammatory Bowel Diseases 3, no. 2 (1997): 156–57. http://dx.doi.org/10.1097/00054725-199706000-00023.

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23

Hordijk, Peter L. "Endothelial signalling events during leukocyte transmigration." FEBS Journal 273, no. 19 (October 2006): 4408–15. http://dx.doi.org/10.1111/j.1742-4658.2006.05440.x.

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24

Pinsky, David J. "Transcriptional basis for leukocyte–endothelial interactions." Trends in Molecular Medicine 7, no. 9 (September 2001): 425–26. http://dx.doi.org/10.1016/s1471-4914(01)01995-5.

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25

Reglero-Real, Natalia, Beatriz Marcos-Ramiro, and Jaime Millán. "Endothelial membrane reorganization during leukocyte extravasation." Cellular and Molecular Life Sciences 69, no. 18 (May 10, 2012): 3079–99. http://dx.doi.org/10.1007/s00018-012-0987-4.

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26

Vaporciyan, Ara A., Michael L. Jones, and Peter A. Ward. "Rapid analysis of leukocyte-endothelial adhesion." Journal of Immunological Methods 159, no. 1-2 (February 1993): 93–100. http://dx.doi.org/10.1016/0022-1759(93)90145-w.

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27

McIntyre, Thomas M., Stephen M. Prescott, Andrew S. Weyrich, and Guy A. Zimmerman. "Cell-cell interactions: leukocyte-endothelial interactions." Current Opinion in Hematology 10, no. 2 (March 2003): 150–58. http://dx.doi.org/10.1097/00062752-200303000-00009.

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28

van Buul, Jaap, and Peter Hordijk. "Endothelial adapter proteins in leukocyte transmigration." Thrombosis and Haemostasis 101, no. 04 (2009): 649–55. http://dx.doi.org/10.1160/th08-11-0714.

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SummaryLeukocyte transendothelial migration (TEM) requires endothelial signalling. This signalling is initiated by clustering of cell-surface adhesion molecules and transmitted into the endothelium by a group of associated or co-clustered adapter proteins. These adapter proteins, such as cortactin and filamin, connect the adhesion molecules to the actin cytoskeleton as well as to signalling enzymes and downstream pathways. This short review aims to define common themes in adapter protein binding in endothelial cells and to propose critical functions that are exerted by these adapters in leukocyte transendothelial migration.

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29

Jain, Rakesh K., Lance L. Munn, and Dai Fukumura. "Measuring Leukocyte-Endothelial Interactions in Mice." Cold Spring Harbor Protocols 2013, no. 6 (June 2013): pdb.prot075085. http://dx.doi.org/10.1101/pdb.prot075085.

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30

Mesri, Mehdi, and Dario C. Altieri. "Endothelial Cell Activation by Leukocyte Microparticles." Journal of Immunology 161, no. 8 (October 15, 1998): 4382–87. http://dx.doi.org/10.4049/jimmunol.161.8.4382.

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Abstract The ability of polymorphonuclear leukocytes (PMNs) to modulate endothelial cell (EC) activation was investigated. Adding PMNs to cultured HUVECs resulted in a release of IL-6 (888 ± 71 pg/ml, a 35-fold increase over release by the two cell types alone) and IL-8 (45.2 ± 14.5 ng/ml, a 6.4-fold over PMN release alone and a 173-fold increase over EC release alone). In contrast, the release of TNF-α, IL-1β, and platelet-derived growth factor was not affected by the EC-PMN coculture. Neutralizing mAbs to ICAM-1 or β2 integrins or a physical segregation of PMNs and ECs did not reduce EC stimulation. In contrast, cell-free supernatants of PMNs recapitulated EC activation with an 18-fold up-regulation of EC IL-6 mRNA. The filtration of PMN supernatant or PMN pretreatment with metabolic antagonists or membrane cross-linking agents all suppressed EC activation. By flow cytometry, PMNs released in the supernatant, heterogeneous membrane-derived microparticles containing discrete proteins of 28 to 250 kDa as resolved by SDS-PAGE. PMN microparticle formation was enhanced by inflammatory stimuli, including formyl peptide and phorbol ester, and was time-dependent, reaching a plateau after a 1-h incubation from stimulation. Purified PMN microparticles induced EC IL-6 release in a reaction that was quantitatively indistinguishable from that observed with unfractionated PMN supernatant and unaffected by a neutralizing Ab to soluble IL-6R. These findings demonstrate that membrane microparticles released from stimulated PMNs are competent inflammatory mediators to produce EC activation and cytokine gene induction.

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31

Schnoor, Michael, Pilar Alcaide, Mathieu-Benoit Voisin, and Jaap D. van Buul. "Crossing the Vascular Wall: Common and Unique Mechanisms Exploited by Different Leukocyte Subsets during Extravasation." Mediators of Inflammation 2015 (2015): 1–23. http://dx.doi.org/10.1155/2015/946509.

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Leukocyte extravasation is one of the essential and first steps during the initiation of inflammation. Therefore, a better understanding of the key molecules that regulate this process may help to develop novel therapeutics for treatment of inflammation-based diseases such as atherosclerosis or rheumatoid arthritis. The endothelial adhesion molecules ICAM-1 and VCAM-1 are known as the central mediators of leukocyte adhesion to and transmigration across the endothelium. Engagement of these molecules by their leukocyte integrin receptors initiates the activation of several signaling pathways within both leukocytes and endothelium. Several of such events have been described to occur during transendothelial migration of all leukocyte subsets, whereas other mechanisms are known only for a single leukocyte subset. Here, we summarize current knowledge on regulatory mechanisms of leukocyte extravasation from a leukocyte and endothelial point of view, respectively. Specifically, we will focus on highlighting common and unique mechanisms that specific leukocyte subsets exploit to succeed in crossing endothelial monolayers.

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32

Casadevall, Maria, Esteban Saperas, Julián Panés, Azucena Salas, Donald C. Anderson, Juan R. Malagelada, and Josep M. Piqué. "Mechanisms underlying the anti-inflammatory actions of central corticotropin-releasing factor." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 4 (April 1, 1999): G1016—G1026. http://dx.doi.org/10.1152/ajpgi.1999.276.4.g1016.

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Immune activation of hypothalamic corticotropin-releasing factor (CRF) provides a negative feedback mechanism to modulate peripheral inflammatory responses. We investigated whether central CRF attenuates endothelial expression of intercellular adhesion molecule 1 (ICAM-1) and leukocyte recruitment during endotoxemia in rats and determined its mechanisms of action. As measured by intravital microscopy, lipopolysaccharide (LPS) induced a dose-dependent increase in leukocyte rolling, adhesion, and emigration in mesenteric venules, which was associated with upregulation of endothelial ICAM-1 expression. Intracisternal injection of CRF abrogated both the increased expression of ICAM-1 and leukocyte recruitment. Intravenous injection of the specific CRF receptor antagonist astressin did not modify leukocyte-endothelial cell interactions induced by a high dose of LPS but enhanced leukocyte adhesion induced by a low dose. Blockade of endogenous glucocorticoids but not α-melanocyte-stimulating hormone (α-MSH) receptors reversed the inhibitory action of CRF on leukocyte-endothelial cell interactions during endotoxemia. In conclusion, cerebral CRF blunts endothelial upregulation of ICAM-1 and attenuates the recruitment of leukocytes during endotoxemia. The anti-inflammatory effects of CRF are mediated by adrenocortical activation and additional mechanisms independent of α-MSH.

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33

Preissner, Klaus, Sentot Santoso, and Triantafyllos Chavakis. "Leukocyte trans-endothelial migration: JAMs add new pieces to the puzzle." Thrombosis and Haemostasis 89, no. 01 (2003): 13–17. http://dx.doi.org/10.1055/s-0037-1613537.

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SummaryThe molecular details of leukocyte transmigration through the endothelial barrier (also called diapedesis), which is the final step of leukocyte extravasation from the circulation to a given site of inflammation, are by far not well understood. The present review will focus on the different mechanisms potentially involved in leukocyte trans-endothelial migration. Both homophilic and heterophilic interactions between leukocyte and endothelial cell receptors will be covered, with a particular focus on the growing gene family of junctional adhesion molecules (JAM). Deciphering their mechanisms of interaction will also allow to unravel novel strategies for therapeutic intervention in inflammatory or atherothrombotic diseases.

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34

Biedermann, Barbara C. "Vascular Endothelium: Checkpoint for Inflammation and Immunity." Physiology 16, no. 2 (April 2001): 84–88. http://dx.doi.org/10.1152/physiologyonline.2001.16.2.84.

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Vascular endothelial cells play a threefold role in the interaction with leukocytes. First, they are gatekeepers in leukocyte recruitment to inflammatory foci and lymphocyte homing to secondary lymphoid organs. Second, they modulate leukocyte activation. Finally, they are targets of leukocyte-derived molecules, resulting either in endothelial cell activation or death.

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35

Luscinskas, F. W., J. M. Kiely, H. Ding, M. S. Obin, C. A. Hébert, J. B. Baker, and M. A. Gimbrone. "In vitro inhibitory effect of IL-8 and other chemoattractants on neutrophil-endothelial adhesive interactions." Journal of Immunology 149, no. 6 (September 15, 1992): 2163–71. http://dx.doi.org/10.4049/jimmunol.149.6.2163.

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Abstract We have previously reported that cytokine- or LPS-activated human umbilical vein endothelial cell (HUVEC) monolayers secrete IL-8 that can act as a neutrophil-selective adhesion inhibitor. In our study we investigated the mechanisms involved in the leukocyte adhesion inhibitory action of IL-8. The leukocyte adhesion inhibitory effect appears to be mediated by the action of IL-8 on the neutrophil, does not involve down-regulation of relevant endothelial adhesion molecules such as endothelial-leukocyte adhesion molecule-1 or intercellular adhesion molecule-1, and is quantitatively similar in different endothelial activation states that are predominantly endothelial-leukocyte adhesion molecule-1 dependent or intercellular adhesion molecule-1 dependent. In addition to inhibiting the attachment of freshly isolated peripheral blood neutrophils to cytokine-activated HUVEC monolayers, IL-8 also promoted a rapid detachment of tightly adherent neutrophils from activated HUVEC, and abolished neutrophil transendothelial migration. Certain other chemoattractants, including FMLP and C5a, had similar inhibitory actions, indicating IL-8 was not unique in its ability to inhibit various neutrophil-endothelial interactions. In contrast, two other neutrophil agonists 1-0-alkyl-2-acetyl sn-glycero-3-phosphocholine and granulocyte-macrophage-CSF, which, like IL-8, are produced by activated HUVEC, as well as the leukocyte-derived chemoattractant leukotriene B4, exerted minimal inhibitory effects on adhesion. Regardless of their ability to modulate neutrophil-endothelial cell adhesion, all these agents induced altered leukocyte surface expression of functionally important adhesion molecules, including loss of L-selectin (leukocyte adhesion molecule-1, LECAM-1) and increase in CD11b/CD18. Thus, although the above agonists have been characterized primarily as chemoattractants, our findings demonstrate that these agents can exert a wide range of modulatory effects on neutrophil-endothelial adhesive interactions.

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36

Moore, T. M., P. Khimenko, W. K. Adkins, M. Miyasaka, and A. E. Taylor. "Adhesion molecules contribute to ischemia and reperfusion-induced injury in the isolated rat lung." Journal of Applied Physiology 78, no. 6 (June 1, 1995): 2245–52. http://dx.doi.org/10.1152/jappl.1995.78.6.2245.

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Leukocyte adherence to the endothelium after ischemia and reperfusion contributes to microvascular injury in most organs. The purpose of this study was to evaluate the leukocyte and endothelial cell adhesion molecules involved with ischemia-reperfusion (I/R)-induced pulmonary microvascular injury in the isolated rat lung. After 45 min of ischemia and 30 min of reperfusion, microvascular permeability was significantly increased and lung retention of leukocytes occurred. Pretreatment with monoclonal antibodies against the leukocyte adhesion molecule CD18 or the endothelial cell adhesion molecules intercellular adhesion molecule 1 and P-selectin significantly attenuated the I/R-induced permeability increase and lung sequestration of neutrophils, mononuclear leukocytes, and eosinophils. In contrast, immunoneutralization of the rat leukocyte adhesion molecule L-selectin neither protected against the I/R-induced permeability increase nor prevented lung sequestration of neutrophils and eosinophils. We conclude that leukocyte adherence in the pulmonary, microvasculature and subsequent permeability increase after I/R is dependent on the integrin CD18, its endothelial cell ligand intercellular adhesion molecule 1, and the endothelial cell rolling factor P-selectin but not the leukocyte rolling factor L-selectin.

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37

Alon, R., R. C. Fuhlbrigge, E. B. Finger, and T. A. Springer. "Interactions through L-selectin between leukocytes and adherent leukocytes nucleate rolling adhesions on selectins and VCAM-1 in shear flow." Journal of Cell Biology 135, no. 3 (November 1, 1996): 849–65. http://dx.doi.org/10.1083/jcb.135.3.849.

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We demonstrate an additional step and a positive feedback loop in leukocyte accumulation on inflamed endothelium. Leukocytes in shear flow bind to adherent leukocytes through L-selectin/ligand interactions and subsequently bind downstream and roll on inflamed endothelium, purified E-selectin, P-selectin, L-selectin, VCAM-1, or peripheral node addressin. Thus adherent leukocytes nucleate formation of strings of rolling cells and synergistically enhance leukocyte accumulation. Neutrophils, monocytes, and activated T cell lines, but not peripheral blood T lymphocytes, tether to each other through L-selectin. L-selectin is not involved in direct binding to either E- or P-selectin and is not a major counterreceptor of endothelial selectins. Leukocyte-leukocyte tethers are more tolerant to high shear than direct tethers to endothelial selectins and, like other L-selectin-mediated interactions, require a shear threshold. Synergism between leukocyte-leukocyte and leukocyte-endothelial interactions introduces novel regulatory mechanisms in recruitment of leukocytes in inflammation.

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38

Muller, William A. "Leukocyte–endothelial-cell interactions in leukocyte transmigration and the inflammatory response." Trends in Immunology 24, no. 6 (June 2003): 326–33. http://dx.doi.org/10.1016/s1471-4906(03)00117-0.

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39

Perry, M. A., and D. N. Granger. "Leukocyte adhesion in local versus hemorrhage-induced ischemia." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 3 (September 1, 1992): H810—H815. http://dx.doi.org/10.1152/ajpheart.1992.263.3.h810.

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The objective of this study was to compare the leukocyte-endothelial cell adhesive interactions elicited in postcapillary venules by either local ischemia-reperfusion or hemorrhage-reperfusion. Leukocyte rolling, adherence, and emigration were monitored in cat mesenteric venules exposed to an 85% reduction in blood flow (induced by either hemorrhage or local restriction of arterial inflow) for 1 h, followed by 1 h reperfusion. Leukocyte-endothelial cell interactions, venular diameter, and red blood cell velocity were measured during baseline, ischemia, and reperfusion periods. Both local and hemorrhage-induced ischemia reperfusion caused a reduction in leukocyte rolling velocity and increases in leukocyte adherence and emigration. Quantitatively, the adherence and emigration responses in both ischemia models were nearly identical. However, the two models differed in their response to immunoneutralization of the leukocyte adhesion glycoprotein CD11/CD18 with monoclonal antibody (MAb) IB4. The MAb had a more profound effect in attenuating leukocyte adherence and emigration in the local ischemia model. These results indicate that different factors may contribute to leukocyte-endothelial cell adhesive interactions observed in local vs. systemic models of ischemia-reperfusion.

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40

Abdala-Valencia, Hiam, Sergejs Berdnikovs, Christine A. McCary, Daniela Urick, Riti Mahadevia, Michelle E. Marchese, Kelsey Swartz, Lakiea Wright, Gökhan M. Mutlu, and Joan M. Cook-Mills. "Inhibition of allergic inflammation by supplementation with 5-hydroxytryptophan." American Journal of Physiology-Lung Cellular and Molecular Physiology 303, no. 8 (October 15, 2012): L642—L660. http://dx.doi.org/10.1152/ajplung.00406.2011.

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Clinical reports indicate that patients with allergy/asthma commonly have associated symptoms of anxiety/depression. Anxiety/depression can be reduced by 5-hydroxytryptophan (5-HTP) supplementation. However, it is not known whether 5-HTP reduces allergic inflammation. Therefore, we determined whether 5-HTP supplementation reduces allergic inflammation. We also determined whether 5-HTP decreases passage of leukocytes through the endothelial barrier by regulating endothelial cell function. For these studies, C57BL/6 mice were supplemented with 5-HTP, treated with ovalbumin fraction V (OVA), house dust mite (HDM) extract, or IL-4, and examined for allergic lung inflammation and OVA-induced airway responsiveness. To determine whether 5-HTP reduces leukocyte or eosinophil transendothelial migration, endothelial cells were pretreated with 5-HTP, washed and then used in an in vitro transendothelial migration assay under laminar flow. Interestingly, 5-HTP reduced allergic lung inflammation by 70–90% and reduced antigen-induced airway responsiveness without affecting body weight, blood eosinophils, cytokines, or chemokines. 5-HTP reduced allergen-induced transglutaminase 2 (TG2) expression and serotonylation (serotonin conjugation to proteins) in lung endothelial cells. Consistent with the regulation of endothelial serotonylation in vivo, in vitro pretreatment of endothelial cells with 5-HTP reduced TNF-α-induced endothelial cell serotonylation and reduced leukocyte transendothelial migration. Furthermore, eosinophil and leukocyte transendothelial migration was reduced by inhibitors of transglutaminase and by inhibition of endothelial cell serotonin synthesis, suggesting that endothelial cell serotonylation is key for leukocyte transendothelial migration. In summary, 5-HTP supplementation inhibits endothelial serotonylation, leukocyte recruitment, and allergic inflammation. These data identify novel potential targets for intervention in allergy/asthma.

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41

Gimbrone, M., M. Obin, A. Brock, E. Luis, P. Hass, C. Hebert, Y. Yip, et al. "Endothelial interleukin-8: a novel inhibitor of leukocyte-endothelial interactions." Science 246, no. 4937 (December 22, 1989): 1601–3. http://dx.doi.org/10.1126/science.2688092.

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42

Chavakis, Emmanouil, Eun Choi, and Triantafyllos Chavakis. "Novel aspects in the regulation of the leukocyte adhesion cascade." Thrombosis and Haemostasis 102, no. 08 (2009): 191–97. http://dx.doi.org/10.1160/th08-12-0844.

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SummaryLeukocyte recruitment plays a major role in the immune response to infectious pathogens and during inflammatory and autoimmune disorders. The process of leukocyte extravasation from the blood into the inflamed tissue requires a complex cascade of adhesive events between the leukocytes and the endothelium including leukocyte rolling, adhesion and transendothelial migration. Leukocyte-endothelial interactions are mediated by tightly regulated binding interactions between adhesion receptors on both cells. In this regard, leukocyte adhesion onto the endothelium is governed by leukocyte integrins and their endothelial counter-receptors of the immunoglobulin superfamily. The present review will focus on novel aspects with respect to the modulation of the leukocyte adhesion cascade.

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43

Kuhlencordt, Peter J., Eva Rosel, Robert E. Gerszten, Manuel Morales-Ruiz, David Dombkowski, William J. Atkinson, Fred Han, et al. "Role of endothelial nitric oxide synthase in endothelial activation: insights from eNOS knockout endothelial cells." American Journal of Physiology-Cell Physiology 286, no. 5 (May 2004): C1195—C1202. http://dx.doi.org/10.1152/ajpcell.00546.2002.

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The objective of this study was to determine whether absence of endothelial nitric oxide synthase (eNOS) affects the expression of cell surface adhesion molecules in endothelial cells. Murine lung endothelial cells (MLECs) were prepared by immunomagnetic bead selection from wild-type and eNOS knockout mice. Wild-type cells expressed eNOS, but eNOS knockout cells did not. Expression of neuronal NOS and inducible NOS was not detectable in cells of either genotype. Upon stimulation, confluent wild-type MLECs produced significant amounts of NO compared with Nω-monomethyl-l-arginine-treated wild-type cells. eNOS knockout and wild-type cells showed no difference in the expression of E-selectin, P-selectin, intracellular adhesion molecule-1, and vascular cell adhesion molecule-1 as measured by flow cytometry on the surface of platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31)-positive cells. Both eNOS knockout and wild-type cells displayed the characteristics of resting endothelium. Adhesion studies in a parallel plate laminar flow chamber showed no difference in leukocyte-endothelial cell interactions between the two genotypes. Cytokine treatment induced endothelial cell adhesion molecule expression and increased leukocyte-endothelial cell interactions in both genotypes. We conclude that in resting murine endothelial cells, absence of endothelial production of NO by itself does not initiate endothelial cell activation or promote leukocyte-endothelial cell interactions. We propose that eNOS derived NO does not chronically suppress endothelial cell activation in an autocrine fashion but serves to counterbalance signals that mediate activation.

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44

Nwariaku, Fiemu E., Zijuan Liu, Xudong Zhu, Dorit Nahari, Christine Ingle, Ru Feng Wu, Ying Gu, George Sarosi, and Lance S. Terada. "NADPH oxidase mediates vascular endothelial cadherin phosphorylation and endothelial dysfunction." Blood 104, no. 10 (November 15, 2004): 3214–20. http://dx.doi.org/10.1182/blood-2004-05-1868.

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Abstract Vascular endothelial activation is an early step during leukocyte/endothelial adhesion and transendothelial leukocyte migration in inflammatory states. Leukocyte transmigration occurs through intercellular gaps between endothelial cells. Vascular endothelial cadherin (VE-cadherin) is a predominant component of endothelial adherens junctions that regulates intercellular gap formation. We found that tumor necrosis factor (TNF) caused tyrosine phosphorylation of VE-cadherin, separation of lateral cell-cell junctions, and intercellular gap formation in human umbilical vein endothelial cell (HUVEC) monolayers. These events appear to be regulated by intracellular oxidant production through endothelial NAD(P)H (nicotinamide adenine dinucleotide phosphate) oxidase because antioxidants and expression of a transdominant inhibitor of the NADPH oxidase, p67(V204A), effectively blocked the effects of TNF on all 3 parameters of junctional integrity. Antioxidants and p67(V204A) also decreased TNF-induced JNK activation. Dominant-negative JNK abrogated VE-cadherin phosphorylation and junctional separation, suggesting a downstream role for JNK. Finally, adenoviral delivery of the kinase dead PAK1(K298A) decreased TNF-induced JNK activation, VE-cadherin phosphorylation, and lateral junctional separation, consistent with the proposed involvement of PAK1 upstream of the NADPH oxidase. Thus, PAK-1 acts in concert with oxidase during TNF-induced oxidant production and loss of endothelial cell junctional integrity.

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45

Johnson-Leger, C., M. Aurrand-Lions, and B. A. Imhof. "The parting of the endothelium: miracle, or simply a junctional affair?" Journal of Cell Science 113, no. 6 (March 15, 2000): 921–33. http://dx.doi.org/10.1242/jcs.113.6.921.

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Leukocyte extravasation from the blood across the endothelium is vital for the functioning of the immune system. Our understanding of the early steps of this process has developed rapidly. However, it is still unclear how leukocytes undergo the final step, migrating through the junctions that mediate adhesion between adjacent endothelial cells, while preserving the barrier function of the endothelium. The first stage of transmigration - tethering and rolling - is mediated by interactions between selectins on the surface of leukocytes and glycosylated proteins such as GlyCAM-1 on the surface of endothelial cells. Stimulation of the leukocyte by chemokines then induces tight adhesion, which involves binding of activated leukocyte integrins to endothelial ICAM-1/VCAM-1 molecules. Passage of the leukocyte across the endothelium appears to require delocalization of certain endothelial cell molecules and proteolytic degradation of junctional complexes.

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46

Middleton, Jim, Angela M. Patterson, Lucy Gardner, Caroline Schmutz, and Brian A. Ashton. "Leukocyte extravasation: chemokine transport and presentation by the endothelium." Blood 100, no. 12 (December 1, 2002): 3853–60. http://dx.doi.org/10.1182/blood.v100.12.3853.

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At sites of inflammation and in normal immune surveillance, chemokines direct leukocyte migration across the endothelium. Many cell types that are extravascular can produce chemokines, and for these mediators to directly elicit leukocyte migration from the blood, they would need to reach the luminal surface of the endothelium. This article reviews the evidence that endothelial cells are active in transcytosing chemokines to their luminal surfaces, where they are presented to leukocytes. The endothelial binding sites that transport and present chemokines include glycosaminoglycans (GAGs) and possibly the Duffy antigen/receptor for chemokines (DARC). The binding residues on chemokines that interact with GAGs are discussed, as are the carbohydrate structures on GAGs that bind these cytokines. The expression of particular GAG structures by endothelial cells may lend selectivity to the type of chemokine presented in a given tissue, thereby contributing to selective leukocyte recruitment. At the luminal surface of the endothelium, chemokines are preferentially presented to blood leukocytes on the tips of microvillous processes. Similarly, certain adhesion molecules and chemokine receptors are also preferentially distributed on leukocyte and endothelial microvilli, and evidence suggests an important role for these structures in creating the necessary surface topography for leukocyte migration. Finally, the mechanisms of chemokine transcytosis and presentation by endothelial cells are incorporated into the current model of chemokine-driven leukocyte extravasation.

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47

Yun, Peter L. W., Arthur A. DeCarlo, and Neil Hunter. "Gingipains of Porphyromonas gingivalis Modulate Leukocyte Adhesion Molecule Expression Induced in Human Endothelial Cells by Ligation of CD99." Infection and Immunity 74, no. 3 (March 2006): 1661–72. http://dx.doi.org/10.1128/iai.74.3.1661-1672.2006.

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ABSTRACT Porphyromonas gingivalis has been implicated as a key etiologic agent in the pathogenesis of destructive chronic periodontitis. Among virulence factors of this organism are cysteine proteinases, or gingipains, that have the capacity to modulate host inflammatory defenses. Intercellular adhesion molecule expression by vascular endothelium represents a crucial process for leukocyte transendothelial migration into inflamed tissue. Ligation of CD99 on endothelial cells was shown to induce expression of endothelial leukocyte adhesion molecule 1, vascular cell adhesion molecule 1, intercellular adhesion molecule 1, and major histocompatibility complex class II molecules and to increase adhesion of leukocytes. CD99 ligation was also found to induce nuclear translocation of NF-κB. These results indicate that endothelial cell activation by CD99 ligation may lead to the up-regulation of adhesion molecule expression via NF-κB activation. However, pretreatment of endothelial cells with gingipains caused a dose-dependent reduction of adhesion molecule expression and leukocyte adhesion induced by ligation of CD99 on endothelial cells. The data provide evidence that the gingipains can reduce the functional expression of CD99 on endothelial cells, leading indirectly to the disruption of adhesion molecule expression and of leukocyte recruitment to inflammatory foci.

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48

Tsujikawa, Akitaka, Junichi Kiryu, Atsushi Nonaka, Kenji Yamashiro, Hirokazu Nishiwaki, Yoshihito Honda, and Yuichiro Ogura. "Leukocyte-endothelial cell interactions in diabetic retina after transient retinal ischemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 3 (September 1, 2000): R980—R989. http://dx.doi.org/10.1152/ajpregu.2000.279.3.r980.

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Diabetes is associated with increased neural damage after transient cerebral ischemia. Recently, leukocytes, which are thought to play a central role in ischemia-reperfusion injury, have been suggested to be involved in exacerbated damage after transient ischemia in diabetic animals. The present study was designed to clarify whether the anticipated worse outcome after transient cerebral ischemia in diabetic animals was due to augmented leukocyte-mediated neural injury. Using rats with streptozotocin-induced diabetes of 4-wk duration, we investigated leukocyte-endothelial cell interactions during reperfusion after a transient 60-min period of retinal ischemia. Unexpectedly, postischemic diabetic retina showed no active leukocyte-endothelial cell interactions during reperfusion. The maximal numbers of rolling and accumulating leukocytes in diabetic retina were reduced by 73.6 and 41.2%, respectively, compared with those in nondiabetic rats. In addition, neither preischemic insulin treatment of diabetic rats nor preischemic glucose infusion of nondiabetic rats significantly influenced leukocyte-endothelial cell interactions during reperfusion. The present study demonstrated that high blood glucose concentration before induction of ischemia did not exacerbate leukocyte involvement in the postischemic retinal injury. Furthermore, diabetic retina showed suppressed leukocyte-endothelial cells interactions after transient ischemia, perhaps due to an adaptive mechanism that developed during the period of induced diabetes.

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49

Davenpeck, Kelly L., John Zagorski, Robert P. Schleimer, and Bruce S. Bochner. "Lipopolysaccharide-Induced Leukocyte Rolling and Adhesion in the Rat Mesenteric Microcirculation: Regulation by Glucocorticoids and Role of Cytokines." Journal of Immunology 161, no. 12 (December 15, 1998): 6861–70. http://dx.doi.org/10.4049/jimmunol.161.12.6861.

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Abstract A common side effect of high dose glucocorticoid therapy is increased susceptibility to bacterial infection, an effect that is in part mediated through inhibition of leukocyte recruitment to infected areas. However, the sites at which glucocorticoids act to prevent the multistep process of leukocyte recruitment have not been fully established. In this study, the effects of the glucocorticoid dexamethasone (DEX) on leukocyte-endothelial interactions, in response to bacterial LPS, were examined utilizing a model of rat mesenteric intravital microscopy. Pretreatment of rats with DEX (0.5 mg/kg) for 18 h or 30 min before stimulation with LPS significantly inhibited LPS-induced leukocyte rolling and adhesion in mesenteric postcapillary venules. Pretreatment with DEX also inhibited LPS-induced changes in expression of L-selectin and a shared epitope of CD11b/c on circulating neutrophils. These effects of DEX may be due to DEX inhibition of IL-1, TNF, and cytokine-induced neutrophil chemoattractant-1 (CINC-1) generation, since antagonists to these mediators were able to mimic DEX effects on leukocyte-endothelial interactions and circulating leukocyte phenotype. These data indicate that inhibition of cytokine- and chemokine-induced leukocyte-endothelial interactions may be a primary mechanism by which glucocorticoids inhibit leukocyte recruitment to bacterial agents and thus increase susceptibility to infection.

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50

Cotran, R. S., J. S. Pober, M. A. Gimbrone, T. A. Springer, E. A. Wiebke, A. A. Gaspari, S. A. Rosenberg, and M. T. Lotze. "Endothelial activation during interleukin 2 immunotherapy. A possible mechanism for the vascular leak syndrome." Journal of Immunology 140, no. 6 (March 15, 1988): 1883–88. http://dx.doi.org/10.4049/jimmunol.140.6.1883.

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Abstract A major sequela of immunotherapy with interleukin 2 (IL-2) is development of a vascular leak syndrome. The pathogenesis of this toxic effect is not known. We have examined pre- and post-treatment skin biopsies from 14 patients undergoing systemic administration of IL-2 for evidence of endothelial cell activation. Specifically, we have used the immunoperoxidase technique to detect the expression of three different activation antigens: endothelial-leukocyte adhesion molecule 1, detected with monoclonal antibody H4/18; intercellular adhesion molecule 1, detected with antibody RR1/1; and histocompatibility leukocyte antigen-DQ, detected with antibody Leu 10. Each of these antigens may be induced on cultured endothelial cells by various cytokines (although not by IL-2) and is expressed during endothelial cell activation in vivo at sites of delayed hypersensitivity and other immune responses. Pretreatment biopsies from each patient showed no endothelial expression of endothelial-leukocyte adhesion molecule 1 and only weak to moderate expression of intercellular adhesion molecule 1 and histocompatibility leukocyte antigen-DQ (except for one specimen unreactive with Leu 10). After 5 days of treatment, every patient showed marked endothelial expression of all three antigens (except for the same patient who remained unreactive with Leu 10). Endothelial-leukocyte adhesion molecule-1 expression was confined to postcapillary venular endothelium whereas intercellular adhesion molecule-1 and Leu 10 also were expressed on stromal cells and mononuclear cells. Thus, we conclude that i.v. administration of IL-2 leads to endothelial cell activation. Because IL-2 fails to induce the same antigens on cultured endothelial cells, we infer that IL-2 acts in vivo by inducing the production of other cytokines (e.g., interleukin 1, tumor necrosis factor, lymphotoxin, and interferon-gamma). Finally, since endothelial cell activation at sites of cell-mediated immune responses is well known to result in vascular leakiness to macromolecules, we propose that the vascular leak syndrome accompanying IL-2 therapy may arise from widespread inappropriate endothelial cell activation.

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