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PubMed2002

P-selectin, and not E-selectin, negatively regulates murine megakaryocytopoiesis.

To assess the role of P-selectin and E-selectin in megakaryocytopoiesis, in vitro assays were performed in animal models deficient in both adhesion receptors. There was a significantly greater number of IL-3-responsive megakaryocyte progenitors CFU (CFU-MK) and an increase in immature megakaryoblasts in response to IL-6 in the P-selectin-null mice compared with the wild-type controls. Furthermore, P-selectin-null mice showed a greater number of CFU-MK colonies derived from CD34(+) cells in response to IL-3 or IL-3 plus stem cell factor. A significant shift in baseline ploidy with a reduction in 8N cells and an increase in 32N cells was also observed in the P-selectin-null mice. Secretion of the inhibitory growth factor TGF-beta1 and not TGF-beta2 was significantly lower in the supernatants of cultures containing bone marrow cells from P-selectin-deficient mice as compared with those from the wild-type control bone marrow cells. No differences in the responsiveness of murine CFU-MK, immature megakaryocytes, or 5-fluorouracil-selected stem cells to cytokines were observed in E-selectin-null mice as compared with the control mice. These studies indicate that the absence of P-selectin, and not E-selectin, resulted in an altered adhesion environment with subsequent expansion of megakaryocyte progenitors and immature megakaryoblasts, enhanced secretion of TGF-beta1, and apparent increased responsiveness to inflammatory cytokines.

Animals↗
PubMed1994

A sialyl-Le(x)-negative melanoma cell line binds to E-selectin but not to P-selectin.

The adhesion molecules E-selectin (ELAM-1) and P-selectin (GMP-140/CD62) recognize the carbohydrate motives sialyl-Le(x), sialyl-diLe(x), or sialyl-Lea, though with different affinity. We found that the melanoma cell line NKI-4 bound to E-selectin, but not to P-selectin. This melanoma cell line did not express sialyl-Le(x), but was positive for sialyl-diLe(x) and sialyl-Le(a). In contrast, 2 other melanoma cell lines, MeWo and SK-MEL-28, expressing either sialyl-diLe(x) or sialyl-Le(a) on the cell surface, bound neither E-selectin nor P-selectin. Transfection of the fucosyltransferases Fuc-TIII, Fuc-TIV, and Fuc-TV mediates cell surface expression of sialyl-Le(x) in many cell lines. We detected transcripts of the fucosyltransferases Fuc-TIII and Fuc-TV in 4 melanoma cell lines despite the absence of cell surface sialyl-Le(x). Our observations indicate that expression of fucosyltransferases (Fuc-TIII and -TV) and generation of cell-surface sialyl-diLe(x) are not sufficient to permit adherence to E-selectin or P-selectin. Furthermore, it seems possible that a yet undefined ligand different from sialyl-Le(x), sialyl-diLe(x), or sialyl-Le(a) enables melanoma cells to adhere to E-selectin.

Base Sequence↗
PubMed2001

Polymerized liposome assemblies: bifunctional macromolecular selectin inhibitors mimicking physiological selectin ligands.

Monomeric sialyl Lewis(X) (sLe(x)) and sLe(x)-like oligosaccharides are minimal structures capable of supporting selectin binding in vitro. However, their weak binding interactions do not correlate with the high-affinity binding interactions witnessed in vivo. The polyvalent display of carbohydrate groups found on cell surface glycoprotein structures may contribute to the enhanced binding strength of selectin-mediated adhesion. Detailed biochemical analyses of physiological selectin ligands have revealed a complicated composition of molecules that bind to the selectins in vivo and suggest that there are other requirements for tight binding beyond simple carbohydrate multimerization. In an effort to mimic the high-affinity binding, polyvalent scaffolds that contain multicomponent displays of selectin-binding ligands have been synthesized. Here, we demonstrate that the presentation of additional anionic functional groups in the form of sulfate esters, on a polymerized liposome surface containing a multimeric array of sLe(x)-like oligosaccharides, generates a highly potent, bifunctional macromolecular assembly. This assembly inhibits L-, E-, and P-selectin binding to GlyCAM-1, a physiological ligand better than sLe(x)-like liposomes without additional anionic charge. These multivalent arrays are 4 orders of magnitude better than the monovalent carbohydrate. Liposomes displaying 3'-sulfo Lewis(X)-like oligosaccharides, on the other hand, show slight loss of binding with introduction of additional anionic functional groups for E- and P-selectin and negligible change for L-selectin. The ability to rapidly and systematically vary the composition of these assemblies is a distinguishing feature of this methodology and may be applied to the study of other systems where composite binding determinants are important for high-affinity binding.

Binding, Competitive↗
PubMed1997

Failure to express the P-selectin gene or P-selectin blockade confers early pulmonary protection after lung ischemia or transplantation.

Endothelial P-selectin expression contributes to the first wave of neutrophil (polymorphonuclear leukocyte: PMN) influx in several inflammatory conditions. Although remote tissue ischemia, such as a crush injury to the hindlimb, may result in P-selectin-mediated pulmonary leukosequestration, it is not known whether the lungs exhibit a similar response after hypothermic preservation or when subjected to a direct ischemic insult. To determine if P-selectin may mediate early primary graft failure, left lungs harvested from male Lewis rats were preserved for 6 hr at 4 degrees C and transplanted orthotopically into isogeneic recipients. Recipients immunodepleted of PMNs before transplantation demonstrated improved graft function; pulmonary vascular resistance was reduced approximately 6-fold, arterial oxygenation was increased approximately 3-fold, and recipient survival was increased approximately 4-fold (P < 0.05, 0.05, and 0.005, respectively). Administration of a blocking anti-P-selectin IgG 10 min before reperfusion diminished graft PMN infiltration and resulted in improved graft function and recipient survival compared with controls. To establish the role of P-selectin in normothermic pulmonary ischemia, mice were subjected to temporary left pulmonary artery ligation. After functional removal of the nonischemic right lung, mice deletionally mutant for the P-selectin gene (P-selectin-/-) exhibited reduced PMN infiltration (approximately 2-fold), improved arterial oxygenation (approximately 2-fold), and improved survival (approximately 3-fold) compared with P-selectin +/+ control mice (P < 0.05, 0.01, and 0.05, respectively). These studies isolate and identify the central role of a single gene product (P-selectin) in early PMN recruitment and tissue injury after frank pulmonary ischemia and in the setting of lung transplantation after hypothermic preservation.

Animals↗
PubMed1998

Identification of N-terminal residues on P-selectin glycoprotein ligand-1 required for binding to P-selectin.

The major high affinity ligand for P-selectin on human leukocytes is P-selectin glycoprotein ligand-1 (PSGL-1). To bind P-selectin, PSGL-1 must be modified with tyrosine sulfate and sialylated, fucosylated, core-2 O-glycan(s). The required sites for these modifications on full-length PSGL-1 have not been defined. The N-terminal region of mature PSGL-1, which begins at residue 42, includes tyrosines at residues 46, 48, and 51, plus potential sites for Thr-linked O-glycans at residues 44 and 57. We expressed full-length PSGL-1 constructs with substitutions of these residues in transfected Chinese hamster ovary cells. The cells were co-transfected with cDNAs for the glycosyltransferases required to construct sialylated and fucosylated, core-2 O-glycans on PSGL-1. The transfected cells were assayed for their abilities to bind fluid-phase P-selectin and to support rolling adhesion of pre-B cells expressing P-selectin under hydrodynamic flow. In both assays, substitution of Thr-57 with alanine eliminated binding of PSGL-1 to P-selectin without affecting sulfation of PSGL-1, whereas substitution with serine, to which an O-glycan might also be attached, did not affect binding. Binding was not altered by substituting alanines for the two amino acids on either side of Thr-57, or by substituting alanine for Thr-44. Substitution of all three tyrosines with phenylalanines markedly reduced sulfation and prevented binding to P-selectin. However, all constructs in which one or two tyrosines were replaced with phenylalanines bound P-selectin. These results suggest that full-length PSGL-1 requires an O-glycan attached to Thr-57 plus sulfation of any one of its three clustered tyrosines to bind P-selectin.

Alanine↗
PubMed1997

Characterization of a novel adhesion function blocking monoclonal antibody to rat/mouse P-selectin generated in the P-selectin-deficient mouse.

P-selectin is an important adhesion molecule involved in leukocyte migration. However, to date, no monoclonal antibodies (MAb) generated against rat P-selectin have been identified which block P-selectin mediated leukocyte adhesion. Most studies in the rat have utilized crossreacting antibodies generated against P-selectin in higher species. In a P-selectin deficient mouse we generated an anti-rat/mouse P-selectin MAb, designated RMP-1, by immunization with activated rat platelets. This IgG2a MAb immunoprecipitates a 140 kDa protein under reducing conditions from rat platelet lysate. By ELISA and immunofluorescence flow cytometry, MAb RMP-1 reacts with thrombin-activated but not unactivated rat platelets. In addition, by ELISA MAb RMP-1 binds to activated mouse platelets and recombinant rat and mouse P-selectin. MAb RMP-1 inhibited adhesion of HL-60 myeloid cells to immobilized mouse P-selectin by 97% and to activated rat and mouse platelets by 100% under static conditions, confirming the adhesion function blocking activity of MAb RMP-1. This novel MAb should be useful for studying P-selectin function in vitro and in vivo in both rat and mouse inflammation models.

Animals↗
PubMed1995

Further studies of the binding specificity of the leukocyte adhesion molecule, L-selectin, towards sulphated oligosaccharides--suggestion of a link between the selectin- and the integrin-mediated lymphocyte adhesion systems.

This communication is concerned with the binding specificity of the leukocyte-adhesion molecule L-selectin (leukocyte homing receptor) towards structurally defined sulphated oligosaccharides of the blood group Le(a) and Le(x) series, and of the glycosaminoglycan series heparin, chondroitin sulphate and keratan sulphate. The recombinant soluble form of the rat L-selectin (L-selectin-IgG Fc chimera) investigated here was shown previously to bind to lipid-linked oligosaccharides 3-O, 4-O and 6-O sulphated at galactose, such as sulphatides and a mixture of 3-sulphated Le(a)/Le(x) type tetrasaccharides isolated from ovarian cystadenoma, as well as to the HNK-1 glycolipid with 3-O sulphated glucuronic acid. In the present study, the L-selectin investigated in both chromatogram binding and plastic microwell binding experiments using neoglycolipids was found to bind to the individual 3-sulphated Le(a) and Le(x) sequences (penta-, tetra- and trisaccharides), and with somewhat lower intensities to their non-fucosylated analogues. Glycosaminoglycan disaccharides of keratan sulphate, heparin and chondroitin sulphate types were also bound by L-selectin in one or both assay systems, leading to the conclusion that clustered glycosaminoglycan oligosaccharides with 6-O sulphation of N-acetylgalactosamine, N-acetylglucosamine or glucosamine, 4-O sulphation of N-acetylgalactosamine, 2-O sulphation of uronic acid, N-sulphation of glucosamine and, to a lesser extent, the non-sulphated uronic acid-containing disaccharides, can support L-selectin adhesion. As inflammatory chemokines (short-range stimulators of lymphocyte migration which trigger integrin activation) are known to bind to endothelial glycosaminoglycans, we propose that the binding of the lymphocyte membrane L-selectin to endothelial glycosaminoglycans may provide a link between the selectin-mediated and integrin-mediated adhesion systems in leukocyte extravasation cascades. The possibility is also raised that lymphocyte L-selectin interactions with glycosaminoglycans may contribute to pathologies of glycosaminoglycan-rich tissues, e.g. cartilage loss in rheumatoid arthritis and inflammatory lesions of the cornea.

Animals↗
PubMed2004

Association between the Thr715Pro P-selectin gene polymorphism and soluble P-selectin levels in a multiethnic population in South London.

The aim was to investigate whether the Thr715Pro P-selectin polymorphism is associated with soluble P-selectin (sP-selectin) levels in individuals from different ethnic groups. Plasma sP-selectin and Thr715Pro (A/C) P-selectin gene polymorphism were measured in 237 white (106 females), 177 black African origin (92 females) and 201 South Asian (94 females) individuals living in England. All were free from coronary heart disease (CHD), stroke and other cardiovascular disease, diabetes, drug therapy for hypertension or high lipids, hormone replacement therapy or oral contraceptive pill. The Thr715Pro C allele was rare in blacks (0.8%) and intermediate in South Asians (3.0%) compared to whites (11.2%; p <0.001). sP-selectin levels were significantly lower in the individuals with the AC or CC compared to the AA genotype in both whites (-25% (95% C.I. -33.3 to -16.9); p <0.001) and South Asians (-25.2% (-40.5 to -6.1); p <0.012). There was insufficient power for this analysis in blacks. In conclusion, in whites and South Asians the C allele of the Thr715Pro P-selectin polymorphism is associated with lower sP-selectin levels. Lower levels of sP-selectin were not accounted for by this polymorphism in blacks, in whom the C allele was very rare.

Age Factors↗
PubMed2006

Deficiency of P-selectin or P-selectin glycoprotein ligand-1 leads to accelerated development of glomerulonephritis and increased expression of CC chemokine ligand 2 in lupus-prone mice.

The selectins and their ligands mediate leukocyte rolling on endothelial cells, the initial step in the emigration cascade leading to leukocyte infiltration of tissue. These adhesion molecules have been shown to be key promoters of acute leukocyte emigration events; however, their roles in the development of long-term inflammatory responses, including those that occur during chronic inflammatory diseases such as systemic lupus erythematosus, are unclear. To assess participation of P-selectin in such disorders, we studied the progression of systemic lupus erythematosus-like disease in P-selectin-deficient and control MRL/MpJ-Fas(lpr) (Fas(lpr)) mice. Surprisingly, we found that P-selectin deficiency resulted in significantly earlier mortality, characterized by a more rapid development of glomerulonephritis and dermatitis. Expression of CCL2 (MCP-1) was increased in the kidneys of P-selectin mutant mice and in supernatants of LPS-stimulated primary renal endothelial cell cultures from these mice. A closely similar phenotype, including elevated renal expression of CCL2, was also observed in Fas(lpr) mice deficient in the major P-selectin ligand, P-selectin glycoprotein ligand-1. These results indicate that P-selectin and P-selectin glycoprotein ligand-1 are not required for leukocyte infiltration and the development of autoimmune disease in Fas(lpr) mice, but rather expression of these adhesion molecules is important for modulating the progression of glomerulonephritis, possibly through down-regulation of endothelial CCL2 expression.

Animals↗
PubMed2000

Role of P-selectin and anti-P-selectin monoclonal antibody in apoptosis during hepatic/renal ischemia reperfusion injury.

AIM:To evaluale the potential role of P-selectin and anti-P-selectin monoclonal antibody (mAb) in apoptosis during hepatic/renal ischemia-reperfusion injury.METHODS:Plasma P-selectin level, hepatic/renal P-selectin expression and cell apoptosis were detected in rat model of hepatic/renal ischemia-reperfusion injury.ELISA,immunohist ochemistry and TUNEL were used. Some ischemia-reperfusion rats were treated with anti-P-selectin mAb.RESULTS:Hepatic/renal function insuffic-iency, up-regulated expression of P-selectin in plasma and hepatic/renal tissue, hepatic/renal histopathological damages and cell apoptosis were found in rats with hepatic/renal ischemia-reperfusion injury, while these changes became less conspi-cuous in animals treated with anti-P-selectin mAb.CONCLUSION:P-selectin might mediate neutrophil infiltration and cell apoptosis and contribute to hepatic/renal ischemia-reperfusion injury, anti-P-selectin mAb might be an efficient approa-ch for the prevention and treatment of hepatic/renal ischemia reperfusion injury.

Journal Article↗
PubMed2002

E-selectin, L-selectin, ICAM-1 and IL-6 concentrations changes in the serum of patients with hyperthyroidism in the early period of radioiodine I-131 therapy.

BACKGROUND: Among cytokines- interleukins: -6 and -8 (IL-6, IL-8) and E-selectin (E-sel.), L-selectin (L-sel.) and intercellular cell adhesion molecule-1 (ICAM-1) are the most important links in the initiation of the inflammatory process. Taking into account that the inflammatory process is the basic stage of effective radioiodine therapy, we tried to compare the behaviour of the initial inflammatory factors in the early period of I-131 therapy (RAI) of hyperthyroidism. The aim of the study was to estimate the behaviour of IL-6, ICAM-1, E-selectin and L-selectin concentrations in the serum of patients with hyperthyroidism before and during I-131 therapy. MATERIAL AND METHODS: The groups of 26 patients with Graves' disease (GD) and 18 patients with toxic nodular goiter (TNG), aged 34-77, were studied. Control group (C) consisted of 10 healthy volunteers. For estimation of thyroid function serum concentrations of TSH, free T4 and free T3 were measured by IRMA or RIA kits (Polatom, Poland). IL-6, ICAM-1, E-selectin and L-selectin serum concentrations were determined using ELISA method by Bender kits (USA). Blood samples for all estimations were taken 10-12 days before and in 6th week after I-131 administration. Treatment dose of radioiodine was calculated, basing on modified equation for absorbed dose. RESULTS: Compared to control, no statistical differences in the levels of E-selectin (C--44.4 +/- 11 ng/ml) and L-selectin (C--842 +/- 168.9 ng/ml) were observed before treatment in the patients with GD (E-sel.--59.8 +/- 19.6 ng/ml; L-sel.--1288.2 +/- 273.5 ng/ml) and with TNG (E-sel.--61.5 +/- 18.4 ng/ml, L-sel.--1247.0 +/- 273.5 ng/ml) as well as in the 6th week after I-131 administration; values in GD group were: E-sel.--57.3 +/- 19.5 ng/ml, L-sel.--1142.4 +/- 193.4 ng/ml; in TNG group: E-sel.--62.1 +/- 20.6 ng/ml, L-sel.--1113.5 +/- 236.3 ng/ml. In comparison to control there was no difference in initial IL-6 levels either in GD or in TNG group, but a statistically important decrease was observed in the 6th week after I-131 administration in GD patients (C--2.07 +/- 0.2 ng/ml v. 1.79 +/- 0.16 ng/ml). ICAM-1 serum concentrations before treatment were elevated compared to control group (C--190.2 +/- 34.7 ng/ml) in both groups (GD--263.6 +/- 24.6 ng/ml, p < 0.05; TNG--251.4 +/- 36.1 ng/ml, p < 0.05). In GD patients a statistically significant increase of ICAM-1 was observed in the 6th week (301.1 +/- 33.2 ng/ml, p < 0.05) of RAI whereas in TNG group there was no statistical difference compared to initial values (249.7 +/- 42.6 ng/ml, N.S.). CONCLUSION: We conclude that ICAM-1 and IL-6 may be important factors in the estimation of the inflammatory processes in the thyroid gland during radioiodine therapy, especially GD disease. E- and L-selectins seem to be not helpful in the monitoring of the thyroid inflammatory changes during the early period of I-131 therapy.

Journal Article↗
PubMed1999

Expression of E-selectin, P-selectin, and intercellular adhesion molecule-1 during experimental murine listeriosis.

The expression of adhesion molecules E-selectin, P-selectin, and intercellular adhesion molecule-1 (ICAM-1) was immunohistochemically investigated during the course of experimental murine listeriosis. Infection was monitored by microbiological count of blood, liver, and spleen. After an early generalized expression of P-selectin and ICAM-1, a later regulation occurred specifically to areas of inflammation. Expression of E-selectin was faint and inconstantly detected in all of the studied organs. In the liver, typical lesions of murine listeriosis were related to the expression of ICAM-1 on sinusoidal endothelial cells and the biliary system and to the de novo expression of P-selectin in hepatic portal vessels. Inflammation in the spleen was related to the expression of ICAM-1 on red pulp sinusoidal cells, especially in the marginal sinus. High endothelial venules of inflamed lymph nodes also expressed P-selectin and ICAM-1. Lesions in the central nervous system appeared on day 3 after infection as a pyogranulomatous leptomeningitis associated with an intense expression of P-selectin and ICAM-1 in meningeal vessels, especially those in the hippocampal sulcus, suggesting a way through which inflammation initially reach the central nervous system during experimental murine listeriosis. Leptomeningitis was followed by the presence of ventriculitis, which was related to the up-regulation of ICAM-1 on choroid plexus epithelial cells, periventricular vessels and ependymal cells. Up-regulation of P-selectin and ICAM-1 during experimental murine listeriosis could play an important role in the recruitment of leukocytes, especially to the liver, lymphoid organs, and central nervous system.

Animals↗
PubMed2001

Effects of heparin and aspirin on circulating P-selectin, E-selectin and von Willebrand Factor levels in healthy men.

As thrombin stimulates P-selectin expression on platelets and its release into plasma, we hypothesized that enhancing antithrombin activity by unfractionated heparin (UFH) could decrease plasma levels of circulating (c)P-selectin, (c)E-selectin, and von Willebrand Factor (vWF). Hence the effect of UFH and aspirin were examined on these activation markers in healthy volunteers. UFH decreased cP-selectin levels by -10% (CI: -16 - (-4%); P = 0.005) at 24 h, but did not change levels of vWF-Ag. In contrast, aspirin did not affect cP-selectin levels but decreased vWF-Ag levels by -12% (CI: -18 - (-7%); P = 0.005) at 24 h. Neither drug affected cE-selectin levels. Thus, UFH decreases cP-selectin levels, which may reflect decreased platelet activation in vivo. An increase in cP-selectin under UFH therapy should alert the clinician to look for platelet destruction.

Adult↗
PubMed2000

Binding of a large chondroitin sulfate/dermatan sulfate proteoglycan, versican, to L-selectin, P-selectin, and CD44.

Here we show that a large chondroitin sulfate proteoglycan, versican, derived from a renal adenocarcinoma cell line ACHN, binds L-selectin, P-selectin, and CD44. The binding was mediated by the interaction of the chondroitin sulfate (CS) chain of versican with the carbohydrate-binding domain of L- and P-selectin and CD44. The binding of versican to L- and P-selectin was inhibited by CS B, CS E, and heparan sulfate (HS) but not by any other glycosaminoglycans tested. On the other hand, the binding to CD44 was inhibited by hyaluronic acid, chondroitin (CH), CS A, CS B, CS C, CS D, and CS E but not by HS or keratan sulfate. A cross-blocking study indicated that L- and P-selectin recognize close or overlapping sites on versican, whereas CD44 recognizes separate sites. We also show that soluble L- and P-selectin directly bind to immobilized CS B, CS E, and HS and that soluble CD44 directly binds to immobilized hyaluronic acid, CH, and all the CS chains examined. Consistent with these results, structural analysis showed that versican is modified with at least CS B and CS C. Thus, proteoglycans sufficiently modified with the appropriate glycosaminoglycans should be able to bind L-selectin, P-selectin, and/or CD44.

Animals↗
PubMed2000

Soluble adhesion molecules (sICAM-1, sL-Selectin, sE-Selectin, sCD44) in healthy allogenic peripheral stem-cell donors primed with recombinant G-CSF.

BACKGROUND: We analysed the effects of rhG-CSF (Amgen-Roche, USA) on serum changes of four soluble adhesion molecules (SAM) (sICAM-1, sL-Selectin, sE-Selectin and sCD44) in healthy peripheral allogeneic stem-cell transplantation donors and their correlation with acute GvHD and effect on engraftment kinetics. METHODS: Serum SAM of 15 consecutive healthy HLA identical-sibling donors (median age 30 years, male:female ratio, 7:8) were monitored using a commercial ELISA Kit (Bender Med, Austria) prior to, on the day of first apheresis and 24 h after the cessation of rhG-CSF (10 microg/kg/day s.c. on 5 days) administration. Leukapheresis was started on the fifth day of rhG-CSF administration, using a continuous-flow blood separator (Cobe Spectra, COBE BCT, Inc, Lakewood, CO). Apheresis cycles were continued daily until a target of 4.0 x 10(6) CD34(+) cells/kg was reached. RESULTS: The results indicate a steady rise of sL-Selectin, sE-Selectin, and sCD44, but not of sICAM-1. Median number of mononuclear cells (MNC) and CD34(+) cells transfused were 7.7x 10(8)/kg and 6.0 x 10(6)/kg, respectively. There was a near-significant correlation between the sL-Selectin levels and CD34(+) cell yield (r = 0.49, 0.06). Median granulocyte and platelet engraftment days were 11 (10-18) and 12 (9-33), respectively. There was a significant inverse correlation between the CD34(+) cell dose and granulocyte levels (r = -0.68, p = 0.022), but not for platelet engraftment. The only correlation between SAM levels and engraftment was for sICAM-1 levels. Increasing sICAM-1 levels were a sign of prolonged neutropenia (r = 0.72, p = 0.011). No correlation between the apheresis day serum levels of adhesion molecules and acute GvHD was documented. DISCUSSION: Analysis of sICAM-1, sL-Selectin, sE-Selectin and sCD44 levels during allogeneic PBSC apheresis did not reveal any significant effect on engraftment and GvHD, except the correlation of sL-Selectin levels and collected CD34(+) cells. More research and data about the role of not only SAM levels, but also antigenic expression of SAM are required to enlighten leukocyte-endothelial cell interactions and egress of stem cells during G-CSF administration.

Adult↗
PubMed1995

Serum concentrations of E-selectin, P-selectin, ICAM-1 and interleukin 6 in acute leukaemia patients with chemotherapy-induced leucopenia and bacterial infections.

Serum concentrations of E-selectin (CD62E), P-selectin (CD62P), ICAM-1 (CD54) and interleukin 6 were investigated in acute leukaemia patients with chemotherapy-induced leucopenia and complicating bacterial infections. Serum concentrations of both E-selectin and P-selectin were decreased in the leucopenic patients without infections when compared with levels before chemotherapy; and serum concentrations of both E-selectin and P-selectin showed a further decrease during complicating bacterial infections. In contrast to the leukaemia patients, previously healthy individuals with meningococcal disease showed markedly elevated serum concentrations of E-selectin and normal levels of P-selectin during infection. Serum concentrations of ICAM-1 and interleukin 6 increased during bacterial infections in the acute leukaemia patients with chemotherapy-induced leucopenia. The alterations in serum concentrations of soluble adhesion molecules and interleukin 6 reversed when clinical signs of bacterial infections resolved during antibiotic therapy. Our results demonstrate that acute leukaemia patients with chemotherapy-induced cytopenia show altered levels of both soluble adhesion molecules and interleukin 6 during complicating bacterial infections.

Adolescent↗
PubMed2003

Trafficking of Th1 cells to lung: a role for selectins and a P-selectin glycoprotein-1-independent ligand.

Trafficking of lymphocytes to lung is a critical component of pulmonary immune defense and surveillance. Selectins, expressed on vascular endothelium, regulate T lymphocyte emigration into tissues, such as skin, but the role of the selectins in trafficking of T cells to lung has not been well characterized. Here, we used a model of lung inflammation induced by adoptive transfer of alloreactive Th1 cells to analyze the role of P- and E-selectin in Th1 cell trafficking to lung in vivo. We found that both P- and E-selectin play an important role in Th1 lymphocyte migration to lung. We confirmed that the Th1 cells express P-selectin glycoprotein ligand-1, which was functional in binding to P- and E-selectin in vitro. However, our studies reveal that a ligand distinct from P-selectin glycoprotein-1 also binds these selectins in vitro and appears to play a physiologic role in in vivo emigration of Th1 lymphocytes into the lung.

Adoptive Transfer↗
PubMed2005

[Effects of dipfluzine on expressions of E-selectin, P-selectin, and ICAM-1 in brain ischemia-reperfusion rats].

AIM: To evaluate the effects of dipfluzine on the expressions of E-selectin, P-selectin, and ICAM-1 and the infiltration of polymorphonuclear leukocytes in brain ischemia-reperfusion rats. METHODS: The model of focal cerebral ischemia was established with the Zea-Longa occluding suture. Dipfluzine (0.25, 0.5 and 1 mg x kg(-1)), flunarizine 0.5 mg x kg(-1) and solvent were injected separately into lingual vein at 30 min after ischemia. The occluding suture was slowly taken away to cause reperfusion at 1 h after ischemia. Rats were decapitated under anesthesia at 24 h after ischemia-reperfusion and brains were immediately removed to do the following procedures. Effects of dipfluzine on morphology of the brain tissue were observed through hematoxylin-eosin (HE) staining. By immunohistochemistry and flow cytometry technique and biochemical method, effects of dipfluzine on P-selectin, E-selectin, ICAM-1 and myeloperoxidase (MPO) were observed. RESULTS: Dipfluzine could relieve pathological damages in the brain tissue after ischemia-reperfusion, and reduce the expressions of E-selectin, P-selectin and ICAM-1 and activities of MPO in dose-dependent manner. CONCLUSION: Dipfluzine depresses the expressions of P-selectin, E-selectin, and ICAM-1, which are correlated with their effects on the activities of MPO, suggesting that dipfluzine has anti-inflammation effect in certain extent and could protect brain tissue from ischemia-reperfusion injury.

Animals↗