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At least 199 records · Page 11Linked to original sources
PubMed2003

Migration of human blood dendritic cells across endothelial cell monolayers: adhesion molecules and chemokines involved in subset-specific transmigration.

Distinct subsets of dendritic cells (DCs) are present in blood, probably "en route" to different tissues. We have investigated the chemokines and adhesion molecules involved in the migration of myeloid (CD11c(+)) and plasmacytoid (CD123(+)) human peripheral blood DCs across vascular endothelium. Among blood DCs, the CD11c(+) subset vigorously migrated across endothelium in the absence of any chemotactic stimuli, whereas spontaneous migration of CD123(+) DCs was limited. In bare cell migration assays, myeloid DCs responded with great potency to several inflammatory and homeostatic chemokines, whereas plasmacytoid DCs responded poorly to all chemokines tested. In contrast, the presence of endothelium greatly favored transmigration of plasmacytoid DCs in response to CXCL12 (stromal cell-derived factor-1) and CCL5 (regulated on activation, normal T expressed and secreted). Myeloid DCs exhibited a very potent transendothelial migration in response to CXCL12, CCL5, and CCL2 (monocyte chemoattractant protein-1). Furthermore, we explored whether blood DCs acutely switch their pattern of migration to the lymph node-derived chemokine CCL21 (secondary lymphoid-tissue chemokine) in response to microbial stimuli [viral double-stranded (ds)RNA or bacterial CpG-DNA]. A synthetic dsRNA rapidly enhanced the response of CD11c(+) DCs to CCL21, whereas a longer stimulation with CpG-DNA was needed to trigger CD123(+) DCs responsive to CCL21. Use of blocking monoclonal antibodies to adhesion molecules revealed that both DC subsets used platelet endothelial cell adhesion molecule-1 to move across activated endothelium. CD123(+) DCs required beta(2) and beta(1) integrins to transmigrate, whereas CD11c(+) DCs may use integrin-independent mechanisms to migrate across activated endothelium.

Antibodies, Monoclonal↗
PubMed2001

IFN-beta decreases adhesion and transmigration capacities of lymphocytes in Guillain-Barré syndrome.

The adhesion capacities, transmigration capacities, and integrin expression of lymphocytes from patients with Guillain-Barré syndrome incubated with interferon-beta were studied. Interferon-beta induced a dose-dependent inhibition of lymphocyte adhesion to recombinant vascular adhesion molecule-1 (p < 0.0001) and recombinant intercellular adhesion molecule-1 (rICAM-1) (p < 0.01) without modulation of very late activation molecule-4 and lymphocyte function-associated antigen-1 expressions and a dose-dependent decrease of lymphocyte transmigration across fibronectin (p < 0.0001). Inhibition of adhesion to rICAM-1 was similar after long (18 hours) or short (5 minutes) incubation time. These results support the potential therapeutic benefit of interferon-beta in Guillain-Barré syndrome.

Adjuvants, Immunologic↗
PubMed2004

Peptide-mediated inhibition of neutrophil transmigration by blocking CD47 interactions with signal regulatory protein alpha.

CD47, a cell surface transmembrane Ig superfamily member, is an extracellular ligand for signal regulatory protein (SIRPalpha). Interactions between CD47 and SIRPalpha regulate many important immune cell functions including neutrophil (PMN) transmigration. Here we report identification of a novel function-blocking peptide, CERVIGTGWVRC, that structurally mimics an epitope on CD47 and binds to SIRPalpha. The CERVIGTGWVRC sequence was identified by panning phage display libraries on the inhibitory CD47 mAb, C5D5. In vitro PMN migration assays demonstrated that peptide CERVIGTGWVRC specifically inhibited PMN migration across intestinal epithelial monolayers and matrix in a dose-dependent fashion. Further studies using recombinant proteins indicated that the peptide specifically blocks CD47 and SIRPalpha binding in a dose-dependent fashion. Protein binding assays using SIRPalpha domain-specific recombinant proteins demonstrated that this peptide directly bound to the distal-most Ig loop of SIRPalpha, the same loop where CD47 binds. In summary, these findings support the relevance of CD47-SIRPalpha interactions in regulation of PMN transmigration and provide structural data predicting the key residues involved on the surface of CD47. Such peptide reagents may be useful for studies on experimental models of inflammation and provide a template for the design of anti-inflammatory agents.

Amino Acid Sequence↗
PubMed1992

Off-farm employment in Indonesian transmigration: case studies from south Sumatra.

The authors assess the impact of off-farm employment in the context of Indonesia's transmigration program. "The central objective...is to explore and generalize transmigrant households' employment behavior with respect to off-farm activities.... The specific intent...is to focus upon the individuals participating in off-farm employment: the conditions which lead to the development of their employment behavior as well as the nature of the employment itself." (SUMMARY IN IND)

Agriculture↗
PubMedDate not supplied

Transmigration of blood leukocytes into the peritoneal cavity is related to the upregulation of ICAM-1 (CD54) and Mac-1 (CD11b/CD18) adhesion molecules.

BACKGROUND: Migration of blood leukocytes into the peritoneal cavity of patients treated with peritoneal dialysis appears to be an important mechanism to prevent and fight peritonitis. To study the role of adhesion molecules in the process of leukocyte transmigration, we compared the expression of several adhesion receptors between peripheral blood monocytes and macrophages isolated from overnight dwell effluents. METHODS: The study was performed in 12, stable, infection-free patients treated with continuous ambulatory peritoneal dialysis (CAPD) and in 9 patients during peritonitis. In another set of experiments, we analyzed the expression of these molecules on blood leukocytes in 10 predialysis chronic renal failure (CRF) patients and 9 healthy controls. Peritoneal cells from an 8-hour dwell were isolated by centrifugation. Expression of adhesion receptors CD11a, CD11b, CD18, CD49d, and CD54 on blood and peritoneal leukocytes was measured using flow cytometry. RESULTS: In macrophages from the uninfected effluents, expression of both subunits of Mac-1 integrin receptor (CD11b and CD18) and intercellular adhesion molecule (ICAM)-1 receptor (CD54) was upregulated compared to peripheral blood monocytes from the same patients. The median value of mean fluorescence intensity in blood and effluent was 760.3 versus 1085.8 for CD11b (p = 0.013), 288.8 versus 448.6 for CD18 (p = 0.003), and 186.1 versus 365.7 for CD54 (p = 0.001). The same adhesion receptors were also significantly upregulated on peritoneal macrophages and neutrophils during peritonitis compared to blood leukocytes. Blood leukocytes from CAPD and CRF patients showed higher expression of CD54 and CD49d molecules compared to leukocytes from healthy controls. CONCLUSIONS: These data suggest that transmigration of blood leukocytes into the peritoneal cavity during uncomplicated dialysis and in peritonitis is related to selective upregulation of ICAM-1 (CD54) and Mac-1 (CD18/CD11b) receptors.

Adult↗
PubMed2006

Transmigration of impacted mandibular canines--report of 4 cases.

Impacted canines are not uncommon in clinical practice, but intraosseous movement of impacted canines crossing the midline (transmigration) is a rare phenomenon. We report 4 cases of mandibular canine transmigration to emphasize the need to supplement periapical radiographs with a panoramic radiographic examination in patients with over-retained deciduous canines or missing permanent canines.

Adult↗
PubMed1985

SEM observations on the cellular transmigration through the wall of blood vessels in cancer of the human larynx.

Human larynges, removed surgically for advanced planoepithelial carcinoma were used for study. After employing appropriate preparation procedure the obtained material was examined in scanning electron microscope (SEM). The predominant findings were: the human cancer cells transmigrate through the venule lining at/or near the sites of the endothelial intercellular junction, capillaries and postcapillary venules constitute a territory within the transmigration of lymphocytes, piercing the body of the endothelial cell, occur in both directions, the cellular elements of the immune system are relatively more numerous gathered in the peripheral areas of the primary tumor, the obtained results are consistent with in vivo and in vitro experimental data.

Carcinoma↗
PubMed1983

Transmigration and health in connection with tropical diseases in Indonesia.

Health aspects of the Indonesian transmigration programme has been described through review of studies conducted before and after the implementation of the programme of different population groups. The problem of development of economic centres and low health status of manpower has been discussed. To back up the transmigration programme in the future it has been suggested to conduct health studies using multidisciplinary and multiinstitutional approach. More efforts should be done to develop multidisciplinary and multiinstitutional cooperation.

Adolescent↗
PubMed1994

Extreme transmigration of mandibular cuspid: report of two cases.

Transmigration of impacted mandibular cuspid to the opposite side seems unhypothetical due to the presence of symphyseal cartilage. Two such rare cases of extreme transmigration were radiographically discovered when patient reported for orthodontic therapy.

Child↗
PubMed1996

Transforming growth factor-beta 1 inhibits the production of IL-8 and the transmigration of neutrophils through activated endothelium.

A central mechanism of inflammation is the activation of vascular endothelium by the inflammatory cytokines TNF-alpha and IL-1. These cytokines induce the expression of adhesion molecules, the elaboration of chemokines, and the transendothelial migration of white cells. TGF-beta 1 has anti-inflammatory properties, is expressed in the vessel wall, and has previously been shown to inhibit leukocyte adhesiveness to the endothelium at least in part by inhibiting the expression of E-selectin. We now show that TGF-beta 1 also inhibits the migration of neutrophils through endothelial monolayers activated by TNF-alpha. At a dose of 10 U/ml TNF-alpha, the transmigration of neutrophils was inhibited 42.7 +/- 7.9% (n = 8) by 0.2 ng/ml TGF-beta 1. Furthermore, TGF-beta 1 inhibited, in a time- and dose-dependent fashion, the elaboration of IL-8 by TNF-activated endothelial cells by between 33 and 78% (TNF doses from 100 down to 0.1 U/ml) and the elaboration of mRNA for IL-8 by 69%. TGF-beta 1 treatment did not significantly alter the TNF-induced IL-8 mRNA stability, suggesting that the mechanism of action of TGF-beta 1 is on gene transcription. Neutrophil transmigration through cytokine-activated endothelium involves both IL-8-dependent and IL-8-independent mechanisms. Using an anti-IL-8 Ab, we show that TGF-beta 1 inhibits only the IL-8-dependent pathway, but does not affect the IL-8-independent transendothelial migration mechanism. These and our previous results show that TGF-beta1, achieves its anti-inflammatory properties by inhibiting the expression of at least two genes, E-selectin and IL-8, which are essential in the inflammatory pathway.

Cell Movement↗
PubMed1996

Neutrophil rolling, arrest, and transmigration across activated, surface-adherent platelets via sequential action of P-selectin and the beta 2-integrin CD11b/CD18.

Platelets bound to thrombogenic surfaces have been shown to support activation-dependent firm adhesion of neutrophils in flow following selectin-mediated tethering and rolling. The specific receptor(s) responsible for mediating adhesion-strengthening interactions between neutrophils and platelets has not previously been identified. Furthermore, the ability of adherent platelets to support the migration of bound neutrophils has not been tested. We studied neutrophil interactions with activated, surface-adherent platelets as a model for leukocyte binding in vascular shear flow and emigration at thrombogenic sites. Our results demonstrate that the beta 2-integrin Mac-1 (CD11b/CD18) is required for both firm attachment to and transmigration of neutrophils across surface-adherent platelets. In flow assays, neutrophils from patients with leukocyte adhesion deficiency-1 (LAD-I), which lack beta 2-integrin receptors, formed P-selectin-mediated rolling interactions, but were unable to develop firm adhesion to activated platelets, in contrast to healthy neutrophils, which developed firm adhesion within 5 to 30 seconds after initiation of rolling. Furthermore, the adhesion-strengthening interaction observed for healthy neutrophils could be specifically inhibited by monoclonal antibodies (mAbs) to Mac-1, but not to lymphocyte function-associated antigen-1 (LFA-1; CD11a/CD18) or intercellular adhesion molecule-2 (ICAM-2; CD102). Further evidence for a beta 2-integrin-dependent neutrophil/platelet interaction is demonstrated by the complete inhibition of interleukin (IL)-8-induced neutrophil transmigration across platelets bound to fibronectin-coated polycarbonate filters by mAbs to Mac-1. Thus, Mac-1 is required for firm adhesion of neutrophils to activated, adherent platelets and may play an important role in promoting neutrophil accumulation on and migration across platelets deposited at sites of vascular injury.

Blood Platelets↗
PubMed1997

Synergy between L-selectin signaling and chemotactic activation during neutrophil adhesion and transmigration.

L-selectin enables capture and rolling of neutrophils on inflamed endothelium. This may facilitate the binding of agonists such as IL-8 and platelet-activating factor (PAF), which signal CD18-mediated firm adhesion and transmigration. Recent studies demonstrate that L-selectin can mediate transmembrane signaling. However, the functional effects of costimulation through agonist and L-selectin require further study. Here, we quantify cell adhesion, motility, and transmigration in response to co-activation through L-selectin and agonist. The surface expression of CD11b/CD18 increased and L-selectin decreased in proportion to the extent of L-selectin cross-linking. A flow cytometric assay was used to measure CD11b/CD18-dependent adhesion to fluorescent beads adsorbed with albumin. Neutrophil adhesion was detected within seconds of adding PAF (20 pM), IL-8 (50 pM), or cross-linking L-selectin. Costimulation through agonist and L-selectin potentiated by up to threefold the rate and extent of bead capture. Stimulation through L-selectin induced membrane ruffling, whereas PAF or IL-8 induced bipolar shape change. L-selectin cross-linking sustained the transient shape change induced by low concentrations (10-50 pM) of agonist. Chemokinesis stimulated by IL-8 was inhibited in the presence of cross-linking L-selectin. This was attributed to enhanced cell spreading following costimulation. Migration across HUVEC monolayers stimulated with IL-1 was also potentiated in the presence of L-selectin cross-linking. We propose that cross-linking of L-selectin and binding of agonist receptors may act synergistically to amplify neutrophil activation and emigration in the inflamed vasculature.

Cell Adhesion↗
PubMed1998

Differential regulation of eosinophil adhesion and transmigration by pulmonary microvascular endothelial cells.

In bronchial asthma, eosinophils (EOS) adhere to, and migrate across, the lung microvasculature to exert their effector functions in the airways. This study was conducted to determine the effect of cytokines on adhesion molecule expression on human pulmonary microvascular endothelial cells (HPMEC) and the influence of these molecules on EOS adhesion and transmigration in vitro. Unlike ICAM-1 expression (>80% positive cytokine-treated HPMEC by flow cytometry), VCAM-1 expression varied with the cytokine(s) pretreatment; the order of potency was: TNF-alpha + IL-4 (82.2 +/- 4.2% positive cells) > TNF-alpha (41.8 +/- 5.1%) > IL-1beta (20.8 +/- 4.7%). IL-4 alone had no effect on either ICAM-1 or VCAM-1 expression. EOS adhesion to cytokine-treated HPMEC followed the same order as that observed for VCAM-1 expression. Interestingly, EOS migration across cytokine-treated HPMEC varied inversely with VCAM-1 expression on, and EOS adhesion to, HPMEC; IL-1beta (21.2 +/- 1.4% migration) > TNF-alpha (12.6 +/- 2.6%) > TNF-alpha + IL-4 (9.1 +/- 2.0%). EOS adhesion was greatest with TNF-alpha + IL-4-treated HPMEC, was dependent on VCAM-1, and inhibited with anti-alpha4 integrin mAb (67.7 +/- 7.5% inhibition, p < 0.0005). In contrast, the highest EOS migration occurred across IL-1beta-treated HPMEC and was inhibited by anti-beta2 integrin mAb (40.4 +/- 2.5% inhibition, p < 0.005). Viable HPMEC were required for EOS migration but not adhesion. Our results suggest that EOS adhesion and transmigration are differentially regulated by VCAM-1 and ICAM-1 expression and the interaction of these adhesion proteins with their respective counterligands, i.e., alpha4 and beta2 integrins on EOS.

Adult↗
PubMed1999

Differential immobilization and hierarchical involvement of chemokines in monocyte arrest and transmigration on inflamed endothelium in shear flow.

Monocyte extravasation into areas of inflammation involves sequential interactions of multiple adhesion molecules. However, differential contribution of chemokines produced by cytokine-stimulated endothelium and their receptors to leukocyte attachment and transmigration under flow conditions remains to be elucidated. The activation of endothelial cells with TNF-alpha up-regulated mRNA and protein expression of the CXC chemokine GRO-alpha and the CC chemokine monocyte chemotactic protein (MCP)-1, which act through the receptors CXCR2 and CCR2 expressed on monocytes, respectively. Whereas GRO-alpha was immobilized to endothelial cells via heparan sulfate proteoglycans, MCP-1 was secreted in a soluble form. Consequently, inhibition experiments with blocking peptide analogues and monoclonal antibodies revealed that GRO-alpha and its receptor CXCR2 but not MCP-1 and its receptors substantially contributed to conversion of rolling into firm, shear-resistant arrest of monocytes to TNF-alpha-stimulated endothelium in physiological flow. In contrast, MCP-1 and CCR2 but not GRO-alpha and CXCR2 mediated spreading, shape change and subsequent transendothelial migration, which was evident in flow but rarely in stasis and may thus require the establishment of a diffusible MCP-1 gradient. Differential patterns of presentation may determine a functional specialization and hierarchy of chemokines and their receptors in sequential steps of monocyte emigration on inflamed endothelium and shear flow.

Antigen Presentation↗
PubMed1993

Chemotaxins inhibit neutrophil adherence to and transmigration across cytokine-activated endothelium: correlation to the expression of L-selectin.

Non-activated neutrophils strongly adhere to cytokine-activated human umbilical vein endothelial cells (HUVE). However, activation of neutrophils by different chemotactic mediators led to potent inhibition of this endothelial-dependent interaction. For different formylated peptides, concentrations leading to maximal adherence inhibition coincided with those known for inducing maximal chemotactic migration of neutrophils. In terms of maximal adherence inhibition, a rank list was found in the order of N-formyl-Met-Leu-Phe > C5adesArg > interleukin-8 > C5a > or = leukotriene B4, whereas platelet-activating factor, and lipopolysaccharide showed no inhibition. This rank order was congruent to that of down-regulation of neutrophil L-selectin detected by the monoclonal antibody Leu-8. Moreover, the dose-dependent increase of neutrophil adherence inhibition corresponded to the loss of L-selectin expression. Concentrations higher than that required for maximal inhibition led to a dose-dependent decrease of inhibition, which was accompanied by increasing expression of neutrophil CD11/CD18. In contrast to the capacity of non-activated neutrophils to migrate across interleukin-1-activated HUVE monolayers, transmigration was significantly impaired after chemotactic activation.

Antigens, CD↗
PubMed2005

Transmigration of human ovarian adenocarcinoma cells through endothelial extracellular matrix involves alphav integrins and the participation of MMP2.

The growth of ovarian carcinoma is dependent upon their vascularistion, but the interaction of ovarian cancer cells with the endothelium and their invasion through an endothelial environment remain poorly understood at the molecular level. To investigate adhesive events underlying this process with focusing on the role of alphav integrins and MT1MMP-MMP2 proteinases, we used in vitro models of cocultures of human ovarian adenocarcinoma cell lines (IGROV1 and SKOV3) with human umbilical vein endothelial cells (HUVECs). Immunostaining of HUVECs revealed the network organisation of fibrillar fibronectin (Fn) and pericellular vitronectin (Vn). During coculture, IGROV1 and SKOV3 cells gain access to subendothelial basement membrane of HUVECs and dislocated endothelial Fn without affecting endothelial Vn. Transmigration assays revealed that tumour cells invade Vn and, with an higher efficiency, Fn. Our data also highlighted that ovarian carcinoma cells migrated through the Fn-rich HUVEC-ECM. The expression of MMP2 and MT1-MMP was revealed in tumour cells within an endothelial environment. Furthermore, we found that cell migration through the endothelial ECM was almost totally dependent on alphav integrin function, whereas beta1 integrins were not solicited. In addition, inhibitors of MMP2 activity (alone or combined with anti-alphav integrin MAb) or TSRI265 (which blocks MMP2-alphavbeta3 association) were found to impede this process. Finally, alphav integrins, MT1-MMP and MMP2 were found in ovarian carcinoma cells within the 3-dimensional architecture of intraperitoneal tumour nodes collected from nude mice xenografted with IGROV1 or SKOV3 cell lines or within human tumour tissues. alphav integrins therefore appear as essential to the migration properties of human ovarian carcinoma cells, especially in an endothelial environment, with MMP2 participating to this process.

Animals↗
PubMed2003

Chlamydia pneumoniae infection promotes the transmigration of monocytes through human brain endothelial cells.

We have investigated the effects of Chlamydia pneumoniae on human brain endothelial cells (HBMECs) and human monocytes as a mechanism for breaching the blood-brain barrier (BBB) in Alzheimer's disease (AD). HBMECs and peripheral blood monocytes may be key components in controlling the entry of C. pneumoniae into the human brain. Our results indicate that C. pneumoniae infects blood vessels and monocytes in AD brain tissues compared with normal brain tissue. C. pneumoniae infection stimulates transendothelial entry of monocytes through HBMECs. This entry is facilitated by the up-regulation of VCAM-1 and ICAM-1 on HBMECs and a corresponding increase of LFA-1, VLA-4, and MAC-1 on monocytes. C. pneumoniae infection in HBMECs and THP-1 monocytes up-regulates monocyte transmigration threefold in an in vitro brain endothelial monolayer. In this way, C. pneumoniae infection in these cell types may contribute to increased monocyte migration and promote inflammation within the CNS resulting from infection at the level of the vasculature. Thus, infection at the level of the vasculature may be a key initiating factor in the pathogenesis of neurodegenerative diseases such as sporadic AD.

Alzheimer Disease↗