Monocyte Adhesion to Activated Aortic Endothelium: Role of L-Selectin and Heparan Sulfate Proteoglycans

Giuffrè, Laura; Cordey, A S; Monai, N.; Tardy, Yves; Schapira, Marc; Spertini, Olivier

doi:10.1083/jcb.136.4.945

Cited by 120 publications

(49 citation statements)

References 98 publications

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“…The carbohydrates involved in this latter interaction have not been identified. However, it is thought that sulfation is important for high affinity binding to L-selectin (54)(55)(56)(57)(58), and, specifically, that heparan sulfate proteoglycans serve as ligands for monocyte L-selectin (59). Our study suggests that fucose is not an important saccharide for L-selectin-mediated rolling on systemic endothelium.…”

Section: Discussionmentioning

confidence: 61%

Leukocyte Adhesion Deficiency Type II is a generalized defect of de novo GDP-fucose biosynthesis. Endothelial cell fucosylation is not required for neutrophil rolling on human nonlymphoid endothelium.

Karsan¹,

Cornejo²,

Winn³

et al. 1998

J. Clin. Invest.

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Leukocyte Adhesion Deficiency Type II (LAD II) is a recently described syndrome and the two patients with this defect lack fucosylated glycoconjugates. These glycoconjugates include the selectin ligand, sialyl Lewis X , and various fucosylated blood group antigens. To date, the molecular anomaly in these patients has not been identified. We localized the defect in LAD II to the de novo pathway of GDPfucose biosynthesis, by inducing cell-surface expression of fucosylated glycoconjugates after exposure of lymphoblastoid cell lines from the LAD II patients to exogenous fucose. This defect is not restricted to hematopoietic cells, since similar findings were elicited in both human umbilical vein endothelial cells (HUVEC) and fibroblasts derived from an affected abortus. We have used these LAD II endothelial cells to examine the consequence of fucosylation of endothelial cells on the rolling of normal neutrophils in an in vitro assay. Neutrophil rolling on LPS-treated normal and LAD II HUVEC was inhibited by an E-selectin monoclonal antibody at both high and low shear rates. LAD II HUVEC lacking fucosylated glycoproteins supported leukocyte rolling to a similar degree as normal HUVEC or LAD II cells that were fucose-fed. At low shear rates, an L-selectin antibody inhibited neutrophil rolling to a similar degree whether the LAD II cells had been fucose-fed or not. These findings suggest that fucosylation of nonlymphoid endothelial cells does not play a major role in neutrophil rolling and that fucose is not a critical moiety on the L-selectin ligand(s) on endothelial cells of the systemic vasculature. ( J. Clin. Invest.

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Section: Discussionmentioning

confidence: 61%

Leukocyte Adhesion Deficiency Type II is a generalized defect of de novo GDP-fucose biosynthesis. Endothelial cell fucosylation is not required for neutrophil rolling on human nonlymphoid endothelium.

Karsan¹,

Cornejo²,

Winn³

et al. 1998

J. Clin. Invest.

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“…However, adhesion was not completely inhibited by the addition of blocking antibodies, suggesting that other adhesion molecules may be involved in this process. In addition to integrins, L-selectins are expressed on myeloid cells and have been shown to play an important role in the initial interaction with or tethering of monocytes to the endothelium (31,32). Unfortunately, there is no antibody available against L-selectin that cross-reacts specifically with equine monocytes to allow further experiments.…”

Section: Discussionmentioning

confidence: 99%

Equine Herpesvirus Type 1 Enhances Viral Replication in CD172a ⁺ Monocytic Cells upon Adhesion to Endothelial Cells

Laval

Favoreel

Poelaert

et al. 2015

J Virol

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Equine herpesvirus type 1 (EHV-1) is a main cause of respiratory disease, abortion, and encephalomyelopathy in horses. Monocytic cells (CD172a ؉ ) are the main carrier cells of EHV-1 during primary infection and are proposed to serve as a "Trojan horse" to facilitate the dissemination of EHV-1 to target organs. However, the mechanism by which EHV-1 is transferred from CD172a ؉ cells to endothelial cells (EC) remains unclear. The aim of this study was to investigate EHV-1 transmission between these two cell types. We hypothesized that EHV-1 employs specific strategies to promote the adhesion of infected CD172a ؉ cells to EC to facilitate EHV-1 spread. Here, we demonstrated that EHV-1 infection of CD172a؉ cells resulted in a 3-to 5-fold increase in adhesion to EC. Antibody blocking experiments indicated that ␣ 4 ␤ 1 , ␣ L ␤ 2 , and ␣ V ␤ 3 integrins mediated adhesion of infected CD172a ؉ cells to EC. We showed that integrin-mediated phosphatidylinositol 3-kinase (PI3K) and ERK/MAPK signaling pathways were involved in EHV-1-induced CD172a؉ cell adhesion at early times of infection. EHV-1 replication was enhanced in adherent CD172a؉ cells, which correlates with the production of tumor necrosis factor alpha (TNF-␣). In the presence of neutralizing antibodies, approximately 20% of infected CD172a؉ cells transferred cytoplasmic material to uninfected EC and 0.01% of infected CD172a؉ cells transmitted infectious virus to neighboring cells. Our results demonstrated that EHV-1 infection induces adhesion of CD172a؉ cells to EC, which enhances viral replication, but that transfer of viral material from CD172a ؉ cells to EC is a very specific and rare event. These findings give new insights into the complex pathogenesis of EHV-1. IMPORTANCEEquine herpesvirus type 1 (EHV-1) is a highly prevalent pathogen worldwide, causing frequent outbreaks of abortion and myeloencephalopathy, even in vaccinated horses. After primary replication in the respiratory tract, EHV-1 disseminates via cell-associated viremia in peripheral blood mononuclear cells (PBMC) and subsequently infects the endothelial cells (EC) of the pregnant uterus or central nervous system, leading in some cases to abortion and/or neurological disorders. Recently, we demonstrated that CD172a؉ monocytic carrier cells serve as a "Trojan horse" to facilitate EHV-1 spread from blood to target organs. Here, we investigated the mechanism underlying the transmission of EHV-1 from CD172a ؉ cells to EC. We demonstrated that EHV-1 infection induces cellular changes in CD172a؉ cells, promoting their adhesion to EC. We found that both cell-to-cell contacts and the secretion of soluble factors by EC activate EHV-1 replication in CD172a ؉ cells. This facilitates transfer of cytoplasmic viral material to EC, resulting mainly in a nonproductive infection. Our findings give new insights into how EHV-1 may spread to EC of target organs in vaccinated horses. E quine herpesvirus type 1 (EHV-1), a member of the subfamily Alphaherpesvirinae, is a ubiquitous pathogen in horses, causing...

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“…Lymphocytes were isolated by blood centrifugation on Ficoll-Hypaque and monocyte depletion by adherence on plastic (43). Neutrophils were isolated from Ficoll-Hypaque pellets by dextran sedimentation and erythrocyte hypotonic lysis.…”

Section: Methodsmentioning

confidence: 99%

Molecular Basis of Leukocyte Rolling on PSGL-1

Bernimoulin¹,

Zeng²,

Abbal³

et al. 2003

Journal of Biological Chemistry

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Interactions between the leukocyte adhesion receptor L-selectin and P-selectin glycoprotein ligand-1 play an important role in regulating the inflammatory response by mediating leukocyte tethering and rolling on adherent leukocytes. In this study, we have examined the effect of post-translational modifications of PSGL-1 including Tyr sulfation and presentation of sialylated and fucosylated O-glycans for L-selectin binding. The functional importance of these modifications was determined by analyzing soluble L-selectin binding and leukocyte rolling on CHO cells expressing various glycoforms of PSGL-1 or mutant PSGL-1 targeted at Nterminal Thr or Tyr residues. Simultaneous expression of core-2 ␤1,6-N-acetylglucosaminyltransferase and fucosyltransferase VII was required for optimal L-selectin binding to PSGL-1. Substitution of Thr-57 by Ala but not of Thr-44, strongly decreased L-selectin binding and leukocyte rolling on PSGL-1. Substitution of Tyr by Phe revealed that PSGL-1 Tyr-51 plays a predominant role in mediating L-selectin binding and leukocyte rolling whereas Tyr-48 has a minor role, an observation that contrasts with the pattern seen for the interactions between PSGL-1 and P-selectin where Tyr-48 plays a key role. Molecular modeling analysis of L-selectin and Pselectin interactions with PSGL-1 further supported these observations. Additional experiments showed that core-2 O-glycans attached to Thr-57 were also of critical importance in regulating the velocity and stability of leukocyte rolling. These observations pinpoint the structural characteristics of PSGL-1 that are required for optimal interactions with L-selectin and may be responsible for the specific kinetic and mechanical bond properties of the L-selectin-PSGL-1 adhesion receptorcounterreceptor pair.Selectins play a major role in regulating leukocyte migration in inflammatory lesions by mediating leukocyte rolling along vascular wall at site of inflammation (1-8). L-selectin is expressed by most leukocytes whereas P-selectin and E-selectin expression is induced on activated platelets and/or endothelial cells (1,2,4,5,7,9). E-, P-, and L-selectin function at different although overlapping phases of the inflammatory reaction (10).P-selectin interacts with its major ligand P-selectin glycoprotein ligand-1 (PSGL-1) 1 and supports leukocyte rolling along postcapillary venules at the earliest phase of inflammation (11-13). Several studies have indicated that L-selectin mediates both primary leukocyte-endothelial interactions (14, 15) and secondary interactions between circulating and adherent leukocytes, which both participate in leukocyte recruitment in inflammatory lesions. Secondary interactions are mainly supported by the interaction of PSGL-1 with L-selectin (16 -18).PSGL-1 is a mucin-like glycoprotein expressed as a homodimer on leukocyte microvilli (4, 19 -21). P-selectin binds with relatively high affinity (K d ϳ300 nM) (22) to PSGL-1 by reacting with N-terminal tyrosine sulfate residues and with the sLe x tetrasaccharide determinants presented...

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Monocyte Adhesion to Activated Aortic Endothelium: Role of L-Selectin and Heparan Sulfate Proteoglycans

Cited by 120 publications

References 98 publications

Leukocyte Adhesion Deficiency Type II is a generalized defect of de novo GDP-fucose biosynthesis. Endothelial cell fucosylation is not required for neutrophil rolling on human nonlymphoid endothelium.

Leukocyte Adhesion Deficiency Type II is a generalized defect of de novo GDP-fucose biosynthesis. Endothelial cell fucosylation is not required for neutrophil rolling on human nonlymphoid endothelium.

Equine Herpesvirus Type 1 Enhances Viral Replication in CD172a ⁺ Monocytic Cells upon Adhesion to Endothelial Cells

Molecular Basis of Leukocyte Rolling on PSGL-1

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Monocyte Adhesion to Activated Aortic Endothelium: Role of L-Selectin and Heparan Sulfate Proteoglycans

Cited by 120 publications

References 98 publications

Leukocyte Adhesion Deficiency Type II is a generalized defect of de novo GDP-fucose biosynthesis. Endothelial cell fucosylation is not required for neutrophil rolling on human nonlymphoid endothelium.

Leukocyte Adhesion Deficiency Type II is a generalized defect of de novo GDP-fucose biosynthesis. Endothelial cell fucosylation is not required for neutrophil rolling on human nonlymphoid endothelium.

Equine Herpesvirus Type 1 Enhances Viral Replication in CD172a + Monocytic Cells upon Adhesion to Endothelial Cells

Molecular Basis of Leukocyte Rolling on PSGL-1

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Product

Resources

About

Equine Herpesvirus Type 1 Enhances Viral Replication in CD172a ⁺ Monocytic Cells upon Adhesion to Endothelial Cells