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At least 235 records · Page 13Linked to original sources
PubMed2001

Dual role of H-Ras in regulation of lymphocyte function antigen-1 activity by stromal cell-derived factor-1alpha: implications for leukocyte transmigration.

We investigated the role of H-Ras in chemokine-induced integrin regulation in leukocytes. Stimulation of Jurkat T cells with the CXC chemokine stromal cell-derived factor-1alpha (SDF-1alpha) resulted in a rapid increase in the phosphorylation, i.e., activation of extracellular signal receptor-activated kinase (ERK) but not c-Jun NH(2)-terminal kinase or p38 kinase, and phosphorylation of Akt, reflecting phosphatidylinositol 3-kinase (PI3-K) activation. Phosphorylation of ERK in Jurkat cells was enhanced and attenuated by expression of dominant active (D12) or inactive (N17) forms of H-Ras, respectively, while N17 H-Ras abrogated SDF-1alpha-induced Akt phosphorylation. SDF-1alpha triggered a transient regulation of adhesion to intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 mediated by lymphocyte function antigen-1 (LFA-1) and very late antigen-4 (VLA-4), respectively, and a rapid increase in LFA-1 binding to soluble ICAM-1.Ig, which was inhibited by D12 but not N17 H-Ras. Both D12 and N17 H-Ras abrogated the regulation of LFA-1 but not VLA-4 avidity, and impaired LFA-1-mediated transendothelial chemotaxis but not VLA-4-dependent transmigration induced by SDF-1alpha. Analysis of the mutant Jurkat J19 clone revealed LFA-1 with constitutively high affinity and reduced ERK phosphorylation, which were partially restored by expression of active H-Ras. Inhibition of PI3-K blocked the up-regulation of Jurkat cell adhesion to ICAM-1 by SDF-1alpha, whereas inhibition of mitogen-activated protein kinase kinase impaired the subsequent down-regulation and blocking both pathways abrogated LFA-1 regulation. Our data suggest that inhibition of initial PI3-K activation by inactive H-Ras or sustained activation of an inhibitory ERK pathway by active H-Ras prevail to abolish LFA-1 regulation and transendothelial migration induced by SDF-1alpha in leukocytes, establishing a complex and bimodal involvement of H-Ras.

Cell Movement↗
PubMed2002

Targeting leukocyte MMPs and transmigration: minocycline as a potential therapy for multiple sclerosis.

Multiple sclerosis is characterized by the infiltration of leukocytes into the CNS. As matrix metalloproteinases (MMPs) facilitate the passage of leukocytes across matrix barriers, we tested the hypothesis that targeting MMPs could attenuate neuro-inflammation. We report that minocycline, a widely used generic drug with a good safety record, inhibited MMP activity, reduced production of MMP-9 and decreased the transmigration of T lymphocytes across a fibronectin matrix barrier. In addition, minocycline was efficacious against both mild and severe experimental autoimmune encephalomyelitis (EAE) in mice, an animal model of multiple sclerosis. When severe EAE was produced, minocycline pre-treatment delayed the course of the disease: when maximal disease activity occurred in vehicle-treated EAE mice, minocycline animals were relatively normal and had minimal signs of inflammation and demyelination in the CNS. When tested in mice afflicted with mild EAE, minocycline attenuated the clinical severity of disease throughout the course of treatment. These results indicate that minocycline may constitute a safe and inexpensive therapy for multiple sclerosis.

Animals↗
PubMed1999

Amoxycillin/clavulanic acid combinations increase transmigration of leucocytes through endothelial cell monolayers: endothelial cells play a key role.

Postoperative inflammation is still viewed as an unresolved problem. During inflammation, leucocytes play a tremendous role and migrate from intravascular spaces into the tissue to attack microorganisms. Different agents, e.g. anaesthetic drugs, are able to influence leucocyte recruitment. Previous studies have investigated the influence of amoxycillin on chemotaxis of leucocytes alone. The aim of our study was to examine the effect of amoxycillin/clavulanic acid (co-amoxiclav) on leucocyte migration through endothelial cell monolayers (ECMs). Human umbilical endothelial cells were cultured on microporous membranes, achieving a monolayer. Polymorphonuclear neutrophil leucocytes (PMNLs) were used in a migration assay. The numbers of untreated PMNLs migrating through untreated ECMs were used as control and set as 100%. PMNLs and/or ECMs were pretreated with co-amoxiclav using clinically relevant as well as higher and lower concentrations. Co-amoxiclav was able to increase PMNL migration through ECMs significantly (P<0.05) when both cell types were treated (291+/-18.7%). When PMNLs or ECMs were treated alone, it could be shown that ECMs were more affected than PMNLs. The greatest effect was shown when both cell types, PMNLs and ECMs, were treated. In conclusion, co-amoxiclav was identified as a potent drug to increase leucocyte transmigration through ECMs. ECMs were also critically involved. Co-amoxiclav also affects endothelial cells.

Amoxicillin-Potassium Clavulanate Combination↗
PubMed2001

Selection of phage-displayed llama single-domain antibodies that transmigrate across human blood-brain barrier endothelium.

Delivery to the brain of drugs, peptides, and genes depends on the availability of brain-specific delivery vectors. We used a phage-displayed library of llama single-domain antibodies (sdAbs) to enrich for species that selectively bind to and are internalized by human cerebromicrovascular endothelial cells (HCEC). Two sdAbs (FC5 and FC44) were selected, sequenced, subcloned, and expressed as fusion proteins with c-Myc-His5 tags. Similar to phage-displayed sdAbs, soluble FC5 and FC44 were shown to selectively bind HCEC and to transmigrate across an in vitro human blood-brain barrier (BBB) model. Both FC5 and FC44, in contrast to an unrelated llama sdAb, were also detected in the brain after i.v. injection into mice. These small (approximately 14 kDa) antibodies have characteristics essential for a carrier-vector and can be used to facilitate drug transport across the BBB.

Amino Acid Sequence↗
PubMed2003

Hypertonic saline resuscitation attenuates neutrophil lung sequestration and transmigration by diminishing leukocyte-endothelial interactions in a two-hit model of hemorrhagic shock and infection.

BACKGROUND: Hypertonic saline (HTS) attenuates polymorphonuclear neutrophil (PMN)-mediated tissue injury after hemorrhagic shock. We hypothesized that HTS resuscitation reduces early in vivo endothelial cell (EC)-PMN interactions and late lung PMN sequestration in a two-hit model of hemorrhagic shock followed by mimicked infection. METHODS: Thirty-two mice were hemorrhaged (40 mm Hg) for 60 minutes and then given intratracheal lipopolysaccharide (10 microg) 1 hour after resuscitation with shed blood and either HTS (4 mL/kg 7.5% NaCl) or Ringer's lactate (RL) (twice shed blood volume). Eleven controls were not manipulated. Cremaster intravital microscopy quantified 5-hour EC-PMN adherence, myeloperoxidase assay assessed lung PMN content (2 1/2 and 24 hours), and lung histology determined 24-hour PMN transmigration. RESULTS: Compared with RL, HTS animals displayed 55% less 5-hour EC-PMN adherence (p = 0.01), 61% lower 24-hour lung myeloperoxidase ( p= 0.007), and 57% lower mean 24-hour lung histologic score ( p= 0.027). CONCLUSION: Compared with RL, HTS resuscitation attenuates early EC-PMN adhesion and late lung PMN accumulation in hemorrhagic shock followed by inflammation. HTS resuscitation may attenuate PMN-mediated organ damage.

Animals↗
PubMed2006

Pertussis toxin transiently affects barrier integrity, organelle organization and transmigration of monocytes in a human brain microvascular endothelial cell barrier model.

Encephalopathies and neurological disorders are sometimes associated with respiratory tract infections caused by Bordetella pertussis. For these complications to occur cerebral barriers have to be compromised. Therefore, the influence of pertussis toxin (PT), a decisive virulence determinant of B. pertussis, on endothelial barrier integrity was investigated. Human brain microvascular endothelial cells cultured on Transwell filter devices were used as model for the blood brain barrier. PT, but not its B-oligomer, induced a reduction of the transendothelial resistance and enhanced the permeability for the protein marker horseradish peroxidase. Moreover, transmigration of human monocytes was also elevated suggesting a PT-associated enhancement of the diapedesis of blood leucocytes. Uptake and trafficking of PT was followed by electron microscopy via clathrin-coated pits and accumulation in lysosomes and microvesicular bodies. The breach in barrier integrity was accompanied by a transient disintegration of Golgi structures. Interestingly, PT-induced effects were only transient and restoration of barrier function was observed after 24 h. In summary, intoxication by PT causes a transient destruction of the cellular organization in human brain-derived endothelial cells resulting in a transient disruption of barrier functions. We suggest that these findings reflect early steps in the development of neurological disorders associated with pertussis disease.

Blood-Brain Barrier↗
PubMed1988

The Indonesian transmigration program in historical perspective.

"The purpose of this paper is to look at what has been achieved by the transmigration program [in Indonesia], to examine the major problems that have arisen and to consider the present constraints which now cast some doubt upon the future of the program." A historical overview of government policies from 1905 to 1988 is provided, and problems of land supply, land use, and lack of funds are discussed. Data are from the 1961 and 1980 Indonesian censuses. (SUMMARY IN FRE AND SPA)

Agriculture↗
PubMed2005

The blood-brain barrier transmigrating single domain antibody: mechanisms of transport and antigenic epitopes in human brain endothelial cells.

Antibodies against receptors that undergo transcytosis across the blood-brain barrier (BBB) have been used as vectors to target drugs or therapeutic peptides into the brain. We have recently discovered a novel single domain antibody, FC5, which transmigrates across human cerebral endothelial cells in vitro and the BBB in vivo. The purpose of this study was to characterize mechanisms of FC5 endocytosis and transcytosis across the BBB and its putative receptor on human brain endothelial cells. The transport of FC5 across human brain endothelial cells was polarized, charge independent and temperature dependent, suggesting a receptor-mediated process. FC5 taken up by human brain endothelial cells co-localized with clathrin but not with caveolin-1 by immunochemistry and was detected in clathrin-enriched subcellular fractions by western blot. The transendothelial migration of FC5 was reduced by inhibitors of clathrin-mediated endocytosis, K+ depletion and chlorpromazine, but was insensitive to caveolae inhibitors, filipin, nystatin or methyl-beta-cyclodextrin. Following internalization, FC5 was targeted to early endosomes, bypassed late endosomes/lysosomes and remained intact after transcytosis. The transcytosis process was inhibited by agents that affect actin cytoskeleton or intracellular signaling through PI3-kinase. Pretreatment of human brain endothelial cells with wheatgerm agglutinin, sialic acid, alpha(2,3)-neuraminidase or Maackia amurensis agglutinin that recognizes alpha(2,3)-, but not with Sambucus nigra agglutinin that recognizes alpha(2,6) sialylgalactosyl residues, significantly reduced FC5 transcytosis. FC5 failed to recognize brain endothelial cells-derived lipids, suggesting that it binds luminal alpha(2,3)-sialoglycoprotein receptor which triggers clathrin-mediated endocytosis. This putative receptor may be a new target for developing brain-targeting drug delivery vectors.

Amiloride↗
PubMed2006

Endothelial signalling events during leukocyte transmigration.

The notion that it takes two to tango is certainly true for leukocyte transendothelial migration. A growing pallet of leukocyte adhesion-induced signaling events in endothelial cells have been identified, mediating both short-term (i.e. permeability) as well as long-term (i.e. regulation of transcription) effects. Efficient paracellular migration (i.e. through endothelial cell-cell junctions) requires both intracellular calcium and the actin cytoskeleton, but also involves small GTPases, reactive oxygen species and protein kinases. The alternative route of transcellular migration appears to depend on components such as caveolae and intermediate filaments. This minireview discusses our current knowledge on the regulation of leukocyte transmigration through endothelial signalling.

Animals↗
PubMed1992

The belief in the transmigration of souls: psychotherapy of a Druze patient with severe anxiety reaction.

In this paper the culture-sensitive psychotherapy of a 19-year-old Druze patient with severe anxiety reaction is described. The patient explained his anxiety and his symptoms as stemming from violent death in his former life and subsequent transmigration. The therapists joined the patient's explanatory model and previous traditional healing, adding hypnotic suggestion which relieved the symptoms. The relationship of patient symptomatology to cultural background, multiple personality disorder, possession and dissociation is discussed. The strategic combination of culture-specific and modern psychiatric approaches is advocated in similar cases.

Adult↗
PubMed1998

Escherichia coli cytotoxic necrotizing factor 1 effaces microvilli and decreases transmigration of polymorphonuclear leukocytes in intestinal T84 epithelial cell monolayers.

Cytotoxic necrotizing factor type 1 (CNF1), a 110-kDa toxin-like protein from pathogenic Escherichia coli strains, induces an actin cytoskeleton reorganization consisting of the formation of prominent stress fibers by permanent activation of the small GTP-binding protein Rho. Since p21Rho regulates tight-junction permeability and perijunctional actin reorganization in epithelial intestinal cells (A. Nusrat, M. Giry, J. R. Turner, S. P. Colgan, C. A. Parkos, E. Lemichez, P. Boquet, and J. L. Madara, Proc. Natl. Acad. Sci. USA 92:10629-10633, 1995), we used polarized T84 epithelial intestinal cell monolayers to examine whether CNF1 could affect microvillus structure, transepithelial resistance, and polymorphonuclear leukocyte (PMN) transmigration. Incubation of T84 cells with CNF1 did not influence transepithelial resistance, suggesting that barrier function and surface polarity were not affected by the toxin. However, CNF1 effaced intestinal cell microvilli and induced a strong decrease of PMN transepithelial migration in either the luminal-to-basolateral or the basolateral-to-luminal direction. CNF1 could thus be a virulence factor exhibiting a new type of combined activity consisting of effacing of microvilli and occlusion of the epithelial barrier to PMNs. Attenuated transepithelial migration of PMNs could result in the enhanced growth and protection of luminal bacteria.

Bacterial Toxins↗
PubMed2001

Activation of endothelium by Borrelia burgdorferi in vitro enhances transmigration of specific subsets of T lymphocytes.

Lyme disease, caused by Borrelia burgdorferi, is characterized by the accumulation of lymphocytes and monocytes in the affected tissue. Endothelial cells line the blood vessel walls and control the trafficking of inflammatory leukocytes from the blood into the surrounding tissues. A model of the blood vessel wall, consisting of human umbilical vein endothelial cells (HUVEC) grown on amniotic connective tissue, was utilized to examine the effects of B. burgdorferi on the transendothelial migration of T lymphocytes. Maximal migration occurred when the HUVEC-amnion cultures were preincubated with B. burgdorferi for 24 h and T lymphocytes were added for an additional 4 h, yielding a two- to fourfold increase compared to migration across unstimulated cultures. The number of T lymphocytes that migrated was proportional to the number added. The anti-inflammatory cytokine interleukin 10 (IL-10), added during activation of the HUVEC, significantly diminished (by an average of 70% +/- 21%) the migration of T lymphocytes across endothelium stimulated for 8 or 24 h with B. burgdorferi, but not IL-1. Compared to the initially added population of T lymphocytes, the population that migrated across untreated endothelium or HUVEC activated with B. burgdorferi or IL-1 contained a significantly smaller percentage of CD45RA+RO- (naïve) cells and a greater proportion of CD45RA+RO+ cells. The migratory population was also enriched for CD8+ T lymphocytes when the endothelium was incubated with either control medium or B. burgdorferi, but not IL-1. B. burgdorferi thus activates endothelium in a manner that promotes the transmigration of T lymphocytes, and IL-10 inhibits this activation. These data further suggest that endothelium plays an active role in promoting the recruitment of specific subpopulations of T lymphocytes.

Borrelia burgdorferi Group↗
PubMed1996

Glucose-induced transmigration of monocytes is linked to phosphorylation of PECAM-1 in cultured endothelial cells.

The adherence of circulating monocytes to the endothelium, their migration into the subendothelium, and the subsequent formation of foam cells are initial events in the pathogenesis of atherosclerosis. However, the effect of hyperglycemia on the transendothelial migration of monocytes is not known. Exposure of human umbilical vein endothelial cells (HUVEC) cultured in a Transwell chamber to 25 mM D-glucose (a concentration representing a hyperglycemic state) for 2 h resulted in a twofold increase in the migration of vitamin D3-differentiated monocyte-like HL-60 cells. The migration was inhibited by addition of either an antibody to platelet-endothelial cell adhesion molecule-1 (PECAM-1) or a protein kinase C inhibitor, GF-109203X. In HUVEC, high concentrations of D-glucose (25 mM), but not of other sugars such as L-glucose, 2-deoxyglucose, D-galactose, or D-mannitol, caused a sevenfold increase in the phosphorylation of PECAM-1 as a result of activation of protein kinase C. The 25 mM D-glucose-induced PECAM-1 phosphorylation and transmigration of monocyte-like HL-60 cells were further increased by treatment of HUVEC with the phosphatase inhibitor calyculin A. These results suggest that direct phosphorylation of PECAM-1 in response to elevated glucose promotes transendothelial migration of monocytes, contributing to accelerated atherogenesis in diabetics.

Cell Movement↗
PubMed1997

Cell adhesion and migration. III. Leukocyte adhesion and transmigration in the liver vasculature.

Leukocytes, i.e., neutrophils, monocytes, and lymphocytes, can accumulate in the hepatic vasculature and contribute to the pathophysiology of various liver diseases. Recently, significant progress has been made in the understanding of the basic mechanisms of neutrophil infiltration and cytotoxicity in the liver. However, there are a substantial number of unresolved issues. This article describes the current knowledge and the gaps in our understanding of mechanisms of neutrophil sequestration in sinusoids and venules, adhesion to endothelial cells, and transmigration and adherence to parenchymal cells. From these data, it is clear that assumptions regarding the roles of adhesion molecules in the liver may be misleading if drawn from studies of peripheral vascular beds. Greater insight into these mechanisms is critical for the development of selective therapeutic strategies that attenuate excessive inflammatory responses without compromising the vital host defense.

Animals↗
PubMed2004

Regulation of polymorphonuclear leukocyte apoptosis: role of lung endothelium-epithelium bilayer transmigration.

Delayed polymorphonuclear leukocyte (PMN) apoptosis exacerbates acute lung injury. To reach the alveolar spaces, PMNs must migrate across both pulmonary endothelial and epithelial cell layers. We hypothesized that transmigration across the endothelium-epithelium bilayer suppresses PMN apoptosis and sought to elucidate the underlying mechanisms. PMNs freshly isolated from normal volunteers were allowed to migrate across polycarbonate membranes alone or membranes coated with a bilayer of human lung endothelial and epithelial cells. After migration toward different chemoattractants (IL-8, formyl-Met-Leu-Phe, or leukotriene B(4)), PMN apoptosis and caspase activities were assessed by annexin V, histology, and enzymatic assays, respectively. Messenger RNA and specific protein expression in three receptor ligand-mediated, apoptosis-inducing pathways (Fas, TNF-alpha, and TNF-related apoptosis-inducing ligand) were further examined by gene array, RT-PCR, flow cytometry, and Western blot analyses. The data demonstrated that transbilayer migration suppressed PMN apoptosis, and this effect was not chemoattractant type specific. Kinetic analyses further showed that the delay of apoptosis was sustained to at least 18 h. Transbilayer migration caused significant decreases in caspase (-3, -8, and -9) activities. The changes in apoptosis-related gene expression support the survival role of transbilayer migration. Furthermore, the reduced apoptosis was correlated with downregulation of Fas ligand and TNF receptor 1 expression. Our data reveal that migration across a lung endothelium-epithelium bilayer suppresses PMN apoptosis. The decreased activity and/or expression of proapoptotic proteins may provide possible targets for the regulation of inappropriate delay in PMN apoptosis during lung inflammation and injury.

Antibodies, Monoclonal↗
PubMedDate not supplied

Smooth muscle cells influence monocyte response to LDL as well as their adhesion and transmigration in a coculture model of the arterial wall.

We investigated the possible interference of smooth muscle cells with monocyte response to LDL as well as with their adhesion and transmigration in a coculture of porcine endothelial and smooth muscle cells. Lysophosphatidylcholine (LPC), a component of oxidized LDL (oxLDL), stimulated the adhesion of THP-1 cells to endothelial cells both in mono- and in coculture with smooth muscle cells. When THP-1 cells were incubated with endothelial cells in the presence of copper oxLDL, their adhesion was increased, but only in coculture. The addition of sodium nitroprusside (SNP) together with oxLDL markedly increased the adhesion of THP-1 cells in coculture. Close proximity between endothelial and smooth muscle cells was necessary to observe that effect. Furthermore, this increase in adhesion of THP-1 cells can, at least in part, be attributed to the augmented production of monocyte chemoattractant protein-1 (MCP-1) observed in coculture under the influence of oxLDL and SNP. The passage of THP-1 cells through the coculture was stimulated by MCP-1 and LPC. These results show that physical contacts or close proximity between endothelial and smooth muscle cells play a key role in the adhesion of monocytes and their infiltration into the intima in response to oxLDL.

Animals↗
PubMed2004

Neutrophil transmigration in renal proximal tubular LLC-PK1 cells.

BACKGROUND/AIMS: Adhesion of intratubular leukocytes to proximal tubules in biopsies of patients with rapidly progressive glomerulonephritis and the appearance of leukocytes in the urine in interstitial nephritis suggest interactions between leukocytes and tubular epithelia in renal disease. The present study was performed to investigate whether incubation of tubular epithelia with cytokines or endotoxin (LPS) does stimulate adhesion and migration of leukocytes through these epithelia in vitro. METHODS: Experiments determined adhesion of PMN to LLC-PK cells cultured on tissue culture plates and transepithelial migration (TEM) through LLC-PK monolayers cultured on microporous membranes. Measurements of transepithelial electrical resistance (TER), cytokine release into apical or basolateral compartments and chemotactic activities of apical and basolateral supernatants were performed. RESULTS: Preincubation of LLC-PK cells with either TNFalpha or LPS resulted in stimulation of PMN adhesion and consequently PMN migration through LLC-PK monolayers in both apical-to-basolateral and basolateral-to-apical direction. TEM was not associated with a reduction of TER. Although largely apical IL-8 secretion by LLC-PK cells was found, apical-to-basolateral migration occurred against a concentration gradient of IL-8 and could not be inhibited by IL-8 antibodies. Chemotactic activities of supernatants were slightly increased by TEM but did not show any significant differences between apical and basolateral compartments independent of the direction of PMN migration. TEM in basolateral-to-apical direction was about twice as efficient as in apical-to-basolateral direction (Transmigration Index = 3,92 +/- 0,55 and 2,28 +/-,21, respectively). Only basolateral-to-apical TEM could be partly inhibited by preincubation of basolateral membrane with IL-8 antibodies. CONCLUSION: Inflammatory mediators stimulate PMN adherence to LLC-PK cells and subsequently TEM. The mechanisms involved in TEM stimulated by cytokines or endotoxin appear to be rather changes in surface receptor properties of LLC-PK cells than chemotactic stimuli. Basolateral-to-apical TEM appears to be the favored direction most likely augmented by IL-8 associated haptotactic PMN stimulation.

Animals↗
PubMed2000

Neutrophil transmigration across human airway epithelial monolayers: mechanisms and dependence on electrical resistance.

To examine neutrophil transepithelial migration in the basolateral-to-luminal direction, bronchial epithelial cells (16HBE) were grown at an air-medium interface on the lower face of permeable supports, and resistance across each membrane was recorded before measuring neutrophil transmigration over 2 h. Subconfluent monolayers (resistance < 250 Omega) permitted high spontaneous migration of neutrophils (7.4+/-1%), which was further enhanced (29.7+/-3%) in response to interleukin (IL)-8 (100 ng/ml). Confluent monolayers (250 to 700 Omega) showed low spontaneous migration (2+/- 0.5%) but responded markedly to IL-8 (12.4+/-1.3%). Left in culture, 16HBE resistances continued to increase and were associated with minimal spontaneous migration (< 0.5%) or responses to IL-8. Using cells in the 250 to 700 Omega range, neutrophil migration to IL-8 was dose-dependent and was enhanced when epithelial cells were incubated with a combination of tumor necrosis factor-alpha and interferon-gamma. Neutrophil migration was stimulus-specific and was reduced by preincubation of epithelial cells with a F(ab')(2) anti-intercellular adhesion molecule (ICAM)-1, or by preincubation of neutrophils with anti-CD18, anti-CD11a, anti-CD11b, or anti-CD11c, but not by anti-CD11d, indicating a role for beta(2)-integrin-ICAM-1 interaction in the migration process.

Antibodies↗