P‐selectin glycoprotein ligand‐1 modulates immune inflammatory responses in the enteric lamina propria

Núñez-Andrade, N.; Lamana, Amalia; Sancho, David; Gisbert, Javier P.; González‐Amaro, Roberto; Sánchez‐Madrid, Francisco; Urzainqui, Ana

doi:10.1002/path.2850

Cited by 30 publications

(30 citation statements)

References 43 publications

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Section: Selectin Ligand-mediated Signalingmentioning

confidence: 99%

“…There is also evidence that engagement of PSGL-1 by P-selectin or E-selectin can trigger proliferative and differentiation signals in hematopoietic cells, including hematopoietic progenitors 88 and dendritic cells, 89 with functional consequences during inflammation. 90 The signaling pathways controlling these processes have not been described.Little is known about the possible pathophysiologic roles of ESL-1, but a potential contribution to vascular occlusion in sickle cell disease has been recently described. 85 In a murine model of sickle cell disease after challenge with tumor necrosis factor-␣, interactions between sickle-shaped erythrocytes and neutrophils generate intravascular cell aggregates that trigger the vasoocclusive episodes characteristic of patients with this disease.…”

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confidence: 99%

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Leukocyte ligands for endothelial selectins: specialized glycoconjugates that mediate rolling and signaling under flow

Zarbock

Ley

McEver

et al. 2011

Blood

418

393

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Reversible interactions of glycoconjugates on leukocytes with P-and E-selectin on endothelial cells mediate tethering and rolling of leukocytes in inflamed vascular beds, the first step in their recruitment to sites of injury. Although selectin ligands on hematopoietic precursors have been identified, here we review evidence that PSGL-1, CD44, and ESL-1 on mature leukocytes are physiologic glycoprotein ligands for endothelial selectins. Each ligand has specialized adhesive functions during tethering and rolling. Furthermore, PSGL-1 and CD44 induce signals that activate the ␤2 integrin LFA-1 and promote slow rolling, whereas ESL-1 induces signals that activate the ␤2 integrin Mac-1 in adherent neutrophils. We also review evidence for glycolipids, CD43, L-selectin, and other glycoconjugates as potential physiologic ligands for endothelial selectins on neutrophils or lymphocytes. Although the physiologic characterization of these ligands has been obtained in mice, we also note reported similarities and differences with human selectin ligands. (Blood. 2011;118(26):6743-6751) IntroductionThe selectins mediate adhesion of hematopoietic cells to vascular surfaces and to each other. 1 These interactions are important for host defense, hematopoiesis, immune cell surveillance, hemostasis, and inflammation. Each of the 3 selectins is a type I transmembrane protein with an N-terminal C-type lectin domain, an epidermal growth factor-like domain, a series of consensus repeats, a transmembrane domain, and a short cytoplasmic tail. L-selectin is constitutively expressed on most leukocytes. P-selectin is rapidly mobilized from secretory granules to the plasma membranes of platelets and endothelial cells on stimulation. E-selectin expression on endothelial cells is regulated at the transcriptional level by inflammatory mediators, such as tumor necrosis factor-␣.The rolling cell adhesion mediated by selectins is a dynamic process that requires rapid formation and breakage of bonds under flow. 2 Rolling enables cells to receive signals that activate integrins, another class of adhesion receptors, which cause the cells to roll slower and to arrest. 3 Here we discuss how leukocytes, particularly neutrophils, interact with endothelial selectins during inflammation. We review evidence that surprisingly few neutrophil glycoproteins are physiologic selectin ligands, defined by their ability to mediate rolling adhesion. Rolling can be studied with flow chambers in vitro or ex vivo and in transparent tissues or by epifluorescence in vivo.The selectins are Ca 2ϩ -dependent lectins. The minimal glycan determinant for selectin binding is sialyl Lewis x (sLe x ; NeuAc␣2,3Gal␤1,4[Fuc␣1,3]GlcNAc␤1-R). 1 The fucose moiety of sLe x expressed on selectin ligands forms critical interactions with the Ca 2ϩ -coordination site on the lectin domain of selectins. 2 Leukocytes from mice lacking the 2 ␣1,3-fucosyltransferases that add fucose to form sLe x on hematopoietic cells cannot roll on Pand E-selectin. 4 Because sLe x can potentially cap N-and O-gl...

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Section: Selectin Ligand-mediated Signalingmentioning

confidence: 99%

mentioning

confidence: 99%

Leukocyte ligands for endothelial selectins: specialized glycoconjugates that mediate rolling and signaling under flow

Zarbock

Ley

McEver

et al. 2011

Blood

418

393

View full text Add to dashboard Cite

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“…The administration of anti-PSGL-1 antibodies in mice reduced the total number of macrophages, dendritic cells, and B lymphocytes in the lamina propria, and decreased the expression of MHC-II on dendritic cells and macrophages (25).…”

Section: Discussionmentioning

confidence: 95%

Soluble P-selectin glycoprotein ligand – a possible new target in ulcerative colitis

Ajdukovic¹,

Salamunić²,

Hozo³

et al. 2015

BLL

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Background:The main characteristic of active infl ammatory bowel disease (IBD) is the neutrophil infi ltration into the intestinal lamina propria, where neutrophils usually do not reside. Selectins are cell surface glycoproteins responsible for binding the leukocytes to vascular cells and their extravasation into the surrounding tissue. They show high affi nity to P-selectin glycoprotein ligand-1 (PSGL-1) receptors. PSGL-1 is expressed on the surface of all leukocytes and they mediate the rolling of neutrophils on P-selectin. Soluble PSGL-1 acts competitively with cellular PSGL in many physiological and pathological processes. The aim of our study was to compare serum sPSGL-1 concentration in the blood of patients with ulcerative colitis (UC) and healthy control subjects. Methods: Serum concentrations of sPSGL-1 were measured in 20 patients with UC and 20 control subjects. Two-layer immunoenzyme procedure (ELISA) was used. Results: The mean (± standard deviation) serum concentrations of sPSGL-1 in patients with UC and controls were 349.97±75.40 U/mL and 284.39±52.40 U/mL, respectively (p=0.003). Conclusion:In the present study, we showed that patients with UC had signifi cantly higher sPSGL-1 blood values in comparison with healthy subjects. A short-term blockade with anti-PSGL-1 antibodies could block the transport of neutrophils and decrease UC activity. Thus it could possibly be employed in a new therapeutic approach to the treatment of UC (Fig. 1, Ref. 25). Text in PDF www.elis.sk.

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“…Autoantibodies (mainly anti-Ro-SS-A and anti-La-SS-B) contribute to playing roles in its clinical pictures (2). Central and peripheral nervous system involvement may be seen as different sign, symptoms and varying its frequencies (2). Objectives: The aim of this study is to investigate the frequency of neurological and other involvement patterns of the Sjögren's syndrome (SjS).…”

Section: Ab0127 the Frequency Of Nuerological Involvement Inmentioning

confidence: 99%

“…Plasmacytoid DCs (pDCs) are potent type I interferon (IFN) producers and myeloid DCs (mDCs) are professional antigen-presenting cells. Clinically, the level of serum interferon alpha (IFNa) correlates with the severity of disease with pDC infiltration in nephritic kidney suggested that pDCs may contribute to SLE pathogenesis [1,2]. Moreover, monocyte-derived mDCs from SLE patients also display activated phenotypes [3].…”

mentioning

confidence: 99%

AB0126 Comparison of Serum Apelin, Fetuin-A Levels and Carotid Intima-Media Thickness in Patients with Sjögren's Syndrome and Healthy Subjects

Şahin

Seven²,

Demirpençe³

et al. 2016

Ann Rheum Dis

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BackgroundApelin is a glycoprotein, adipocytokine that plays an important role in decreasing the vascular inflammation on cardiovascular and metabolic disorders (1). Fetuin-A is also another glycoprotein that can be an acute phase protein negatively correlates with inflammation (2). Carotid intima-media thickness (C-IMT) may indicate vascular inflammation in primary Sjögren's syndrome (3). However, we do not know the relationship between serum apelin, fetuin-a levels and C-IMT in patients with Sjögren's syndrome.ObjectivesTo compare of the serum Apelin, Fetuin-A levels and C-IMT in patients with Sjögren's syndrome (SjS) and healthy controls.MethodsSixty-SjS patients and sixty healthy subjects were enrolled to this study. Serum apelin, fetuin-a levels were measured by ELISA. Concomitant C-IMT evaluations of the participants were performed. The BMI, insulin, HOMA-IR, lipid profiles were studied. Other laboratory parameters, autoantibody profiles, minor salivary gland biopsy scores (Chisholm) were obtained from patient's record files. The study was approved by the local ethics committee.ResultsThe median levels of apelin were 178.02±55.23 ng/mL in healthy subjects and 98.66±37.25 ng/mL in SjS (p<0.05) (Figure 1). The median levels of fetuin-a were 1370.3±81.74 ng/mL in control group and 1613±64.49 ng/mL in SjS group (p=0.021) (Figure 1). The C-IMT was negatively correlated with apelin levels in SjS patients (r= - 0.209, p=0.02). There was no significant correlation between fetuin-a levels and C-IMT in SjS (p=0.08). However, there were significant correletions between C-IMT and hemoglobin-A1c (r=0.353, p=0.005), C3 (r=0.36, p=0.004), C4 (r=0.351, p=0.005).ConclusionsWe found lower serum apelin and higher fetuin-a levels in SjS patients than in healthy subjects. Apelin and fetuin-a may be a new possible surrogate biomarker of inflammation in Sjögren's syndrome.ReferencesGualillo O, Gonzalez-Juanatey JR, Lago F. The emerging role of adipokines as mediators of cardiovascular function: physiologic and clinical perspectives. Trends Cardiovasc Med 2007 Nov;17(8):275–83.Harman H, Tekeoğlu İ, Gürol G, et al. Comparison of fetuin-A and transforming growth factor beta 1 levels in patients with spondyloarthropathies and rheumatoid arthritis. Int J Rheum Dis. 2016 Jan 22. doi: 10.1111/1756-185X.12791. [Epub ahead of print].Gravani F, Papadaki I, Antypa E, et al. Subclinical atherosclerosis and impaired bone health in patients with primary Sjogren's syndrome: prevalence, clinical and laboratory associations. Arthritis Res Ther 2015 Apr 11;17:99. doi: 10.1186/s13075-015-0613-6.AcknowledgementWe would like to thank to “Cumhuriyet University Scientific Researches Project Unit (CUBAP)” for funding this project.Disclosure of InterestNone declared

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P‐selectin glycoprotein ligand‐1 modulates immune inflammatory responses in the enteric lamina propria

Cited by 30 publications

References 43 publications

Leukocyte ligands for endothelial selectins: specialized glycoconjugates that mediate rolling and signaling under flow

Leukocyte ligands for endothelial selectins: specialized glycoconjugates that mediate rolling and signaling under flow

Soluble P-selectin glycoprotein ligand – a possible new target in ulcerative colitis

AB0126 Comparison of Serum Apelin, Fetuin-A Levels and Carotid Intima-Media Thickness in Patients with Sjögren's Syndrome and Healthy Subjects

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