The Adhesion and Transendothelial Migration of Human T Lymphocytes

Oppenheimer‐Marks, Nancy; Lipsky, Peter E.

doi:10.1007/978-1-4613-9266-8_19

Cited by 145 publications

(202 citation statements)

References 29 publications

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“…We found that high insulin directly enhanced endothelial PECAM-1 expression leading to increased PMN transendothelial migration, whereas many reports have indicated that surface expression of endothelial PECAM-1 is not altered by inflammatory mediators [14,28]. Conversely, ICAM-1 and E-selectin were reported to have roles in transendothelial migration of lymphocytes and eosinophils [29,30].…”

Section: Discussionmentioning

confidence: 83%

High insulin enhances neutrophil transendothelial migration through increasing surface expression of platelet endothelial cell adhesion molecule-1 via activation of mitogen activated protein kinase

et al. 2002

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Aims/hypothesis. There is increasing evidence that hyperinsulinaemia is linked with the development of atherosclerosis in patients with diabetes. However, the mechanisms by which hyperinsulinaemia causes accelerated atherosclerosis, especially with respect to leukocytes transendothelial migration, are poorly understood. We examined whether hyperinsulinaemia directly affects neutrophil transendothelial migration and surface expression of related endothelial adhesion molecules. Methods. Experiments on the transmigration of neutrophils from healthy volunteers and from patients with Type II (non-insulin-dependent) diabetes mellitus across human umbilical vein endothelial cells cultured in insulin-rich medium using cell-culture inserts were carried out. Migrated neutrophils were quantified by measuring their myeloperoxidase activities, and the surface expression of endothelial adhesion molecules was examined using an enzyme immunoassay. Results. High insulin (over 50 µU/ml for 24 h) enhanced neutrophil transendothelial migration in a dose-dependent manner. This was associated with increased expression of platelet endothelial cell adhesion molecule-1 (PECAM-1) but not of intercellular adhesion molecule-1 (ICAM-1), P-selectin or E-selectin. Both phenomena were attenuated by pretreatment with a tyrosine kinase inhibitor, especially a mitogenactivated protein kinase inhibitor, but not by inhibitors of other second messengers. In addition, a mitogenactivated protein kinase activator, anisomycin, by itself enhanced both neutrophil transendothelial migration and PECAM-1 expression within 3 h in a dosedependent manner. Pretreatment with nitric oxide synthase inhibitors had no effect on these events. Conclusion/interpretation. These results suggest that hyperinsulinaemia could accelerate atherosclerosis by directly enhancing neutrophil transendothelial migration through increasing endothelial PECAM-1 expression via mitogen-activated protein kinase activation.

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Section: Discussionmentioning

confidence: 83%

High insulin enhances neutrophil transendothelial migration through increasing surface expression of platelet endothelial cell adhesion molecule-1 via activation of mitogen activated protein kinase

et al. 2002

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“…Van Epps [13] also reported that lymphocyte transendothelial migration was suppressed by PGE 2 only when the drug was present in the assay. Oppenheimer-Marks et al [3] also suggested that following adherence, there is a cAMPsensitive second signal which stimulated migration.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the transendothelial migration of human lymphocytes but not monocytes by phosphodiesterase inhibitors

Lidington

Nöhammer

Dominguez

et al. 1996

Clinical and Experimental Immunology

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SUMMARYThis study describes an in vitro model of peripheral blood mononuclear cell (PBMC) migration through human endothelial cells, held on polycarbonate inserts, which allows automatic differential counting of migrated cells as lymphocytes and monocytes. Using this system it was found that treatment of PBMC with the phosphodiesterase (PDE) inhibitors theophylline (at 1 and 10 ¹ g/ml) and RO-20-1724 inhibited the migration of the lymphocyte component to 64 . 2 6 16 . 4%, 48 . 9 6 3 . 0% and 47 . 5 6 5 . 8% of the control values, respectively, while the migration of the monocytes component was largely unaffected. The PDE inhibitors needed to be present during the assay to inhibit migration, whereas pre-treatment of either the endothelium or the PBMC did not consistently effect lymphocyte migration. The drugs also inhibited the migration of lymphocytes through control inserts, either uncoated or coated with fibronectin, suggesting that some of the inhibition is an effect on lymphocyte motility rather than lymphocyte-endothelial interactions. Lymphocyte migration through fibronectin-coated filters was significantly enhanced compared with uncoated filters. Activation of the PBMC by anti-CD3 MoAb increased motility and migration by up to 300%. This migration appeared to be greatly inhibited by the PDE inhibitors, although the effect was complicated by problems of lymphocyte aggregation. This study provides a novel method of measuring mononuclear cell transendothelial migration, and suggests a possible role of PDE inhibitors in reducing this process.

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“…In fact, in one of the early studies approaching eosinophil function in allergy, Hubsher (1975a, b) demonstrated that immunologically-stimulated human eosinophils could inhibit in vitro histamine release through a prostaglandinmediated mechanism. Interestingly, recent studies have provided evidence that prostaglandins of E series are indeed able to exert a negative control on the function of pivotal pro-inflammatory cell targets, including mast cells (Hogaboam et al 1993), lymphocytes (Oppenheimer-Marks et al 1994, Garrone et al 1994, neutrophils (Ham et al 1983) and macrophages (Christman et al 1993).…”

Section: Involvement Of Prostaglandins In the Eosi-nophil-mediated Inmentioning

confidence: 99%

Modulatory role of eosinophils in allergic inflammation: new evidence for a rather outdated concept

Bandeira‐Melo¹,

Cordeiro²,

Silva³

et al. 1997

Mem. Inst. Oswaldo Cruz

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The Adhesion and Transendothelial Migration of Human T Lymphocytes

Cited by 145 publications

References 29 publications

High insulin enhances neutrophil transendothelial migration through increasing surface expression of platelet endothelial cell adhesion molecule-1 via activation of mitogen activated protein kinase

High insulin enhances neutrophil transendothelial migration through increasing surface expression of platelet endothelial cell adhesion molecule-1 via activation of mitogen activated protein kinase

Inhibition of the transendothelial migration of human lymphocytes but not monocytes by phosphodiesterase inhibitors

Modulatory role of eosinophils in allergic inflammation: new evidence for a rather outdated concept

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