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At least 19 recordsLinked to original sources
PubMed1976

Leucocyte migration inhibitory activity (LMIA) on concanavalin A (Con-A) stimulated human lymphocytes. Comparison of leucocyte migration capillary technique (LMCT), leucocyte migration agarose technique (LMAT), and leucocyte migration fibrinolysis technique (LMFT).

Leucocyte migration and migration inhibition in fibrin medium may reveal new aspects of lymphokine activity associated with immunological inflammation. Leucocyte migration fibrinolysis technique is compared with the leucocyte migration capillary technique and the leucocyte migration agarose technique. In the present model experiment the three methods gave comparable results. The leucocyte migration fibrinolysis technique involves a new principle for detection of lymphokines and can probably be developed to give more exact information about the interrelationship between thrombosis, fibrinolysis and lymphokines.

Adult↗
PubMed1991

Differential expression of migration inhibitory and migration stimulatory factors in two lines of mice genetically selected for high or low responsiveness to phytohemagglutinin. 1. Migration stimulatory factor(s) from T and B cells of immune spleen.

Expression of the lymphokine migration inhibition factor in two lines of mice genetically selected for the high (Hi/PHA) or low (Lo/PHA) response of their lymph node cells to phytohemagglutinin was found to be modulated by concomitant expression of migration stimulation factor(s) [MStF(s)]. The expression of both lymphokines was dependent on genetic character and the immunizing dose of antigen. In mice immunized 5 days earlier with 50 micrograms ovalbumin in Freund's complete adjuvant (Ova in FCA immune), migration inhibition factor, assessed with a sensitive photoelectric method, was well expressed by male spleen or lymph node 24-hour culture supernatants of Lo/PHA but Hi/PHA, especially female, expressed marked MStF(s) instead. Immunization with 500 micrograms Ova in FCA markedly enhanced expression of MStF(s) in Lo/PHA but inhibited it in Hi/PHA. MStF(s) of Ova in FCA immune spleens of the two lines were found to derive from both T and B cells, B cell activity being greater. Lo/PHA were by far better expressors of both T- and B-cell-derived MStF(s) as compared to Hi/PHA (p less than 0.01). Spleen cells of mice immunized with FCA alone also expressed MStF(s) but to lesser extent than Ova in FCA immune spleens, expression by Lo/PHA B cells being significantly higher than in Hi/PHA (p less than 0.05). The MStF(s) of Ova in FCA immune spleens was found to be non-immunoglobulin in nature.

Animals↗
PubMed1989

Mechanism of fibronectin-mediated cell migration: dependence or independence of cell migration susceptibility on RGDS-directed receptor (integrin).

Cell migration on fibronectin (FN)-coated substrata was studied using 10 cell lines, of which only 2 showed clear enhancement and 1 showed marginal enhancement of cell migration. The migration of the other 7 cell lines was not affected on FN-coated substrata, although they all showed FN-dependent cell adhesion. The migration-enhancing activity of FN was found in the fragment including the cell-adhesion and Hep-2 domains, but not other domains (Hep-1/Fib-1, Gel, Fib-2). No difference in the migration-enhancing effect was seen among FNs from plasma, fibroblasts, or transformed cells. FN-dependent cell migration was inhibited by polyclonal antibodies directed to the C-terminal half region including the cell binding domain, but not by antibodies directed to five other domains. Since these results indicated that FN-mediated cell migration could be controlled by the cell-adhesion domain of FN and its receptor, studies were then focused on the effect of antibodies directed to receptors for FN and collagen, and on the effect of tetrapeptide sequences recognized by these receptors. It was found that (i) cell migration on FN-coated surfaces was specifically inhibited by anti-FN receptor antibody P1F8 but not by anticollagen receptor antibody P1H5; (ii) the migration was strongly inhibited by Arg-Gly-Asp-Ser but not by other oligopeptide sequences. However, the majority of those cell lines not susceptible to FN-dependent cell migration were characterized by having FN receptors and the ability to adhere on FN-coated matrix. Based on these findings, it was concluded that FN-dependent cell migration shares the same recognition mechanism as FN-dependent cell adhesion, but that the majority of cell lines not exhibiting FN-dependent migration still show FN-dependent cell adhesion and express the FN receptor (integrin); i.e., cell migration and adhesion involve the same receptor and the same FN loci, but migration is controlled by still-unidentified cellular factors which determine the susceptibility of the cell to the dynamic function of the FN receptor (integrin) unit.

Animals↗
PubMed1990

An in vitro model of cell migration: evaluation of vascular endothelial cell migration.

In vivo vascular endothelial cell (VEC) migration is thought to play a central role in the development of new capillaries as well as the resurfacing of large vessels. Recently, we have developed an in vitro VEC migration assay system based on the ability of VEC to migrate off of tissue culture microcarrier beads. For these studies, bovine pulmonary artery VEC were grown to confluence on Cytodex 3 microcarrier beads (MCB). Next, the confluent VEC covered microcarrier beads were pipetted into 4-cm2 wells of a tissue culture plate and incubated at 37 degrees C/5% CO2. At various time intervals, the movement of the VEC off of the MCB onto the tissue culture surface was evaluated microscopically. Using this assay, we have studied the effect of endothelial cell growth supplement and various matrices (i.e., fibronectin, gelatin, and Matrigel) on VEC migration. These studies demonstrated that: (i) gelatin had no effect on normal or mitomycin C-pretreated VEC migration; (ii) fibronectin had no effect on normal VEC migration, but stimulated the relative migration of mitomycin pretreated VEC; and (iii) Matrigel significantly suppressed both normal and mitomycin C-pretreated VEC migration. Endothelial cell growth supplement (ECGS) stimulated both normal and mitomycin C-pretreated VEC migration on fibronectin at concentrations of 10 micrograms/ml ECGS. Pretreatment with ECGS had no effect of normal or mitomycin C VEC migration on gelatin. Finally, ECGS stimulated a statistically significant increase in the migration of normal and mitomycin C-pretreated VEC migration on Matrigel.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Migrating endothelial cells are distinctly hyperglycosylated and express specific migration-associated cell surface glycoproteins.

Migration of endothelial cells is one of the first cellular responses in the cascade of events that leads to re-endothelialization of an injured vessel and neovascularization of growing tissues and tumors. To examine the hypothesis that endothelial cells express a specific migration-associated phenotype, we analyzed the cell surface glycoprotein expression of migrating bovine aortic endothelial cell (BAECs). Light microscopic analysis revealed an upregulation of binding sites for the lectins Concanavalin A (Con A), wheat germ agglutinin (WGA), and peanut agglutinin after neuraminidase treatment (N-PNA) on migrating endothelial cells relative to contact-inhibited cells. These findings were confirmed and quantitated with an enzyme-linked lectin assay (ELLA) of circularly scraped BAEC monolayers. The expression of migration-associated cell surface glycoproteins was also analyzed by SDS-PAGE. The overall expression of cell surface glycoproteins was upregulated on migrating BAECs. Migrating BAECs expressed Con A- and WGA-binding glycoproteins with apparent molecular masses of 25 and 48 kD that were not expressed by contact-inhibited BAEC monolayers and, accordingly, disappeared as circularly scraped monolayers reached confluence. Subconfluent BAEC monolayers expressed the same cell surface glycoconjugate pattern as migrating endothelial cells. FACS analysis of circularly scraped BAEC monolayers showed that the phenotypic changes of cell surface glycoprotein expression after release from growth arrest occurred before the recruitment of the cells into the cell cycle (3 vs. 12 h). Suramin, which inhibits endothelial cell migration, abrogated the expression of the migration-associated phenotype and induced the expression of a prominent 28-kD Con A- and WGA-binding cell surface glycoprotein. These results indicate that endothelial cells express a specific migration-associated phenotype, which is characterized by the upregulation of distinct cellular glycoconjugates and the expression of specific migration-associated cell surface glycoproteins.

Animals↗
PubMed1989

Timing in the regulation of neural crest cell migration: retarded "maturation" of regional extracellular matrix inhibits pigment cell migration in embryos of the white axolotl mutant.

In larvae of the white axolotl mutant (Ambystoma mexicanum), contrary to normal dark ones, trunk pigmentation is restricted because the epidermis is unable to support subepidermal migration of pigment cells from the neural crest (NC). This study examines whether the subepidermal extracellular matrix (ECM) is the defective component which prevents pigment cell migration in the white embryo. We transplanted subepidermal ECM, adsorbed in vivo on membrane microcarriers, from and to white and dark embryos in various combinations. White embryos have demonstrated normal NC cell migration along the medioventral pathway, and in order to test the effects of medial ECM on subepidermal migration, this ECM was similarly transplanted. Carriers with ECM attached were inserted subepidermally in host embryos at a premigratory NC stage. Control carriers without ECM and carriers with subepidermal ECM from white donors did not affect NC cell migration in white or dark embryos. In contrast, subepidermal ECM from dark donors triggered NC cell migration in the subepidermal space of both white and dark hosts. Remarkably, subepidermal ECM from white donors which were older than those normally used also stimulated migration in embryos of both strains. Likewise, medial ECM from white donors elicited migration in white as well as dark hosts. Pigment cells occurred among those NC cells that were stimulated to migrate in response to contact with ECM on carriers. These results indicate that the subepidermal ECM of the white embryo is transiently defective as a substrate for pigment cell migration, implying that "maturation" of the ECM is retarded beyond the times during which pigment cells are able to respond. In contrast, the medial ECM of the white embryo appears to mature normally. These findings suggest that the effect of the d gene is expressed regionally through the subepidermal ECM during a limited period of development. Hence, the action of the d gene seems to retard ECM maturation, bringing it out of phase with the migratory capability of the pigment cells. We propose that such a shift in relative timing of the developmental phenomena involved inhibits pigment cell migration in embryos of the white axolotl mutant and, accordingly, that the restricted pigmentation of the mutant larva is generated through heterochrony.

Ambystoma mexicanum↗
PubMed1988

Macrophage migration in fibrin gel matrices. II. Effects of clotting factor XIII, fibronectin, and glycosaminoglycan content on cell migration.

We investigated the migration of oil-induced, guinea pig peritoneal macrophages in three-dimensional fibrin matrices, with particular attention to variables which modified fibrin gel structure and/or its adhesive properties for cells. The variables studied were fibrin concentration, gel cross-linking, and fibronectin and glycosaminoglycan content. Macrophage migration was an inverse linear function of fibrinogen concentration. Little or no fibrinolysis accompanied macrophage migration; rather, macrophages migrated through fibrin gels by an active process associated with marked distortions of cell shape and specialized plasma membrane contacts with fibrin strands. Fibrin matrices prepared from fibrinogen that had been depleted of clotting factor XIII and/or fibronectin provided a superior matrix for macrophage migration. Both the number of migrating cells and distance of migration were reduced when the gel matrix included fibronectin and was cross-linked by factor XIII. A hexapeptide containing the fibronectin cell-binding RGDS sequence reversed this migration inhibition, suggesting that fibronectin immobilized by cross-linking to fibrin may have bound macrophages and restricted cell migration. Hyaluronic acid, heparin, and heparan sulfate inhibited macrophage migration in cross-linked fibrin-fibronectin gels over a range of concentrations. These data are relevant to an understanding of macrophage migration in vivo where cross-linked fibrin-fibronectin gels containing variable amounts of glycosaminoglycans are deposited in tissues in immunologic reactions and in many other types of pathology.

Animals↗
PubMed1976

[Migration inhibition of mononuclear cells in idiopathic adrenal insufficiency. Inhibition of migration of mononuclear cells with adrenal microsomes and blocking of the reaction by adrenal antibodies (author's transl)].

In 19 patients with idiopathic adrenal insufficiency and in 19 controls, cellular (as measured by the migration inhibition test) and humoral (by means of immunoflourescence) immune reaction to adrenal antigens were investigated. Significant inhibition of migration was observed in 12 patients with adrenal microsomes; migration of mononuclear cells was however within normal range in 18 out of 19 controls. Adrenal antibodies could be detected in 11 (53%) of the patients. In a further series of investigations adrenal microsomes have been preincubated with specific antibody and used in migration inhibition tests. The migration indices observed with microsomes were compared to those obtained with microsomes preincubated with adrenal antibody. Migration inhibition with microsomes could be blocked by antibody in almost all antibody-positive patients. No uniform trend on the migration of mononuclear cells was found in the antibody-negative patients. A blocking of the cellular immune reaction by specific antibody seems likely. Possible mechanisms which could lead to such phenomena as well as the biologic significance of adrenal antibodies are discussed.

Adrenal Glands↗
PubMed1977

Leukocyte migration agarose test for the assessment of human neutrophil chemotaxis. I. Effects of environmental factors on neutrophil migration under agarose.

To apply the leukocyte migration agarose test (LMAT) to the in vitro assessment of human neutrophil chemotaxis, effects of different culture conditions on neutrophil migration under agarose were studied. Presence of either serum or human serum albumin (HSA) in the culture medium was necessary for detectable neutrophil migration. HSA was preferred since heat-stabile chemotactic agents were found to be generated from fresh serum in the presence of agarose. Additional CO2 in the assay milieu could be replaced by decreasing the NaHCO3 concentration of the culture medium. Both the directed and the spontaneous migration rates of neutrophil leukocytes increased when the concentration of agarose was decreased. Area and distance of migration and cumulative cell count of migrated neutrophil leukocytes were suitable for quantitating the neutrophil migration rate.

Adult↗
PubMed1976

The sealed capillary migration technique and thymocyte migration in vitro.

The in vitro migration of thymocytes in sealed capillary tubes was influenced by cell number, temperature, cell viability and oxygen supply. Migration was successively slower over a 24 h period. There was no major influence of gravity or the degree of initial packing of the cells by centrifugation. Migration was inhibited by cytochalasin B, although the cells escaped from this effect after 8 h. A transient stimulatory effect on migration was seen after addition of serum or supernatants from cultured thymocytes. There was no effect of isoproterenol, theophylline or carbacholine. A paradoxic effect was obtained with high doses of some metabolic inhibitors, which produced increased migration in spite of cell death. The technique may be used for studies on lymphocyte migration in vitro, but care must be taken to exclude a toxic influence of added substances, and expected effects should preferably be looked for early after onset of migration, since cell viability is gradually decreased.

Animals↗
PubMed1987

Macrophage migration inhibition induced by MDP, LPS, PMA, and MIF/MAF: reversal by macrophage migration enhancement factor (MEF), L-fucose, L-fucosyl BSA, D-mannose, and D-mannosyl BSA.

Our data establish that migration inhibition factor (MIF) and migration enhancement factor (MEF) mutually neutralize the effect of each other in a concentration-dependent manner. The monosaccharides L-fucose and D-mannose were also shown to reverse MIF and additionally to stimulate alveolar macrophage (AM) migration in the absence of MIF. The specific activity of these sugars was increased 200-fold when conjugated to bovine serum albumin (BSA). Macrophage activation is usually observed concurrently with migration inhibition when macrophages are incubated with MIF preparations. Migration inhibition occurred also when AM were incubated in the presence of known metabolic activators (MDP, PMA, and LPS). It was found that L-fucose, D-mannose, L-fucosyl BSA, and D-mannosyl BSA could reverse migration inhibition caused by MIF as well as by these metabolic activators. These observations suggest that reversal of MIF by L-fucose is unexplained solely on the basis that L-fucose is functioning as a competitive inhibitor; instead, they suggest that MEF and the above sugars and their conjugates stimulate AM through a receptor system different from the MIF receptor. These observations support the concept that MEF is an important macrophage modulator in CMI responses.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1976

Assay of human lymphokines in vitro. Evidence for a migration stimulation factor (MStF) which interferes with the macrophage migration inhibition assay.

When cultured in vitro, human lymphocytes produced a range of materials which were able to reduce the migration inhibitory effect of human macrophage migration inhibition factor (MIF) and in some cases stimulated macrophage migration to greater than control levels. In addition, lymphocytes stimulated with antigen or mitogen produced a lymphokine-like migration stimulation "factor". Detectable production of this factor occurred 24--48 h after antigen stimulation. The migration stimulation factor (MStF) (MW 50-250,000; pI 6-5) was not chemotactic and could be separated from migration inhibition and chemotactic factors by chromatography and iso-electric focussing.

Cell Migration Inhibition↗
PubMed1992

Lymphocyte migration in the mouse. II. Differential B and T-lymphocyte migration into a site of chronic inflammation.

Different patterns of B and T-lymphocyte migration were observed in normal mice and in animals with a site of chronic inflammation. The early migration of lymphocytes into a site of chronic inflammation, induced by sensitisation and challenge to Bordetella pertussis vaccine (BPV), comprised mainly B-cells. Subsequently, a greater influx of T-cells occurred as the inflammation progressed. The lymphocyte population in the inflammatory exudate was composed of equal numbers of B and T-cells throughout the 30 day time course. Preferential migration of B-cells to Peyer's patches (PP) and T-cells to peripheral lymph nodes (PLN) occurred in both normal mice and animals with a site of chronic inflammation. In contrast, B-cells migrated preferentially to the spleen in normal mice while in mice with chronic inflammation a greater migration of T-cell was observed. These findings indicate the presence of homing receptors for PP on B-cells and of PLN homing receptors on T-cells, with their distribution unaffected during the development of the inflammatory response. In contrast, the inflammatory process did alter the type of cell migrating into the spleen which may reflect an increase in antigen presentation in the mice challenged with BPV.

Animals↗
PubMed1975

Studies on leukocyte migration inhibiton: the role of E rosette-forming cells in specific antigen-induced inhibition of migration.

The role of E rosette-forming cells in leukocyte migration inhibition was investigated with human buffy coat cells fractionated by combined E rosette formation and Ficoll-Hypaque (FH) density gradient centrifugation. The migration of unfractionated dextran-sedimented leukocytes and FH-separated mononuclear cells (MN) were equally inhibited in the presence of Escherichia coli somatic antigen (E. coli), purified protein derivative of tuberculin (PPD) and influenza virus antigen (Flu). Polymorphonuclear leukocytes (PMN) separated from whole leukocytes by one FH density gradient fractionation contained greater than 1.0% E rosette-forming cells and were inhibited by E. coli and PPD. PMN submitted to three transits of FH (DF III) contained less than or equal to 0.02% E rosette forming cells and were unaffected by each of the three antigens. The migration of mixtures of 10% MN and 90DF III cells were inhibited in the presence of specific antigen, while MN depleted of E rosette-forming cells (less than or equal to 0.5%) pooled with equal numbers of DF III cells did not respond to any antigen by migration inhibition. These results show that PMN purified by three transits of FH are unable to respond to specific antigen by inhibition of migration from microcapillary tubes, and specific antigen-induced inhibition of migration of peripheral blood leukocytes does not occur in the absence of D rosette-forming cells in normal subjects.

Adolescent↗
PubMedDate not supplied

Migration from plasticized films into foods. 5. Identification of individual species in a polymeric plasticizer and their migration into foods.

To assess the significance of migration of polymeric plasticizers into foods, chemical characterization and quantification of individual oligomeric species is required. This paper reports the identification of seven individual oligomers isolated from a poly(butylene adipate) plasticizer. Based on mass spectrometry, NMR and chemical degradation, the oligomers were identified as a series of diol-terminated units ranging from a trimer up to an 11-monomer unit, along with a cyclic tetramer, all in the molecular weight range of 300-1100. A study of the migration of polymeric plasticizer from PVC film into olive oil indicated preferential migration of low molecular weight species. These oligomers which comprised 24% of the parent plasticizer contributed more than 90% of the plasticizer migration with the smallest oligomers migrating 90-fold more readily than the bulk of the plasticizer. From a knowledge of total polymeric plasticizer migration from PVC films under actual conditions of food-use, the abundance of individual oligomers in the foods has been estimated.

Adipates↗
PubMedDate not supplied

Japanese migration in contemporary Japan: economic segmentation and interprefectural migration.

This paper examines the economic segmentation model in explaining 1985-86 Japanese interregional migration. The analysis takes advantage of statistical graphic techniques to illustrate the following substantive issues of interregional migration: (1) to examine whether economic segmentation significantly influences Japanese regional migration and (2) to explain socioeconomic characteristics of prefectures for both in- and out-migration. Analytic techniques include a latent structural equation (LISREL) methodology and statistical residual mapping. The residual dispersion patterns, for instance, suggest the extent to which socioeconomic and geopolitical variables explain migration differences by showing unique clusters of unexplained residuals. The analysis further points out that extraneous factors such as high residential land values, significant commuting populations, and regional-specific cultures and traditions need to be incorporated in the economic segmentation model in order to assess the extent of the model's reliability in explaining the pattern of interprefectural migration.

Adolescent↗
PubMed1992

Eosinophil transendothelial migration induced by cytokines. I. Role of endothelial and eosinophil adhesion molecules in IL-1 beta-induced transendothelial migration.

IL-1 beta promotes adhesiveness in human umbilical vein endothelial cells (HuVEC) for eosinophils through expression of adhesion molecules including intercellular adhesion molecules-1 (ICAM-1), E-selectin, and vascular cell adhesion molecule-1 (VCAM-1). Using an in vitro endothelial monolayer system, we examined whether IL-1 beta or TNF-alpha can promote eosinophil transendothelial migration. We also evaluated the contributions of ICAM-1, E-selectin, VCAM-1, leukocyte adhesion complex (CD11/18), and very late Ag-4 (CD11b/18) (VLA-4) in this process using blocking mAb, and determined the changes in expression of CD11b and L-selectin on eosinophils that had undergone transmigration. IL-1 beta and TNF-alpha treatment of HuVEC (4 h, 5 ng/ml) induced significant transendothelial migration of eosinophils (a 4.1 +/- 0.4-fold (IL-1 beta) and 2.0 +/- 0.9-fold (TNF-alpha) increase from the spontaneous value of 3.2 +/- 0.3%). Increased CD11b expression and shedding of L-selectin were observed on eosinophils following IL-1 beta-induced eosinophil transendothelial migration. Studies with mAb revealed that blockade of either ICAM-1 or CD11/18 inhibited transmigration, while antibodies against VCAM-1 and VLA-4 had no inhibitory effect. Among antibodies which block beta 2 integrins, anti-CD18 mAb had the best inhibitory effect (88% inhibition). The combined inhibitory effect of anti-CD11a mAb and anti-CD11b mAb was roughly equal to that of anti-CD18, although anti-CD11a (31% inhibition) and anti-CD11b (52% inhibition) were less effective individually. Anti-ICAM-1 by itself inhibited IL-1 beta-induced eosinophil transendothelial migration (24% inhibition) whereas neither anti-E-selectin nor anti-VCAM-1 were effective inhibitors. Interestingly, the combination of anti-E-selectin and anti-VCAM-1 with anti-ICAM-1 inhibited IL-1 beta-induced eosinophil transendothelial migration significantly better (53% inhibition) than anti-ICAM-1 alone. These results suggest that although the initial attachment of eosinophils to IL-1 beta-activated endothelial cells involves VCAM-1, E-selectin, and ICAM-1, the subsequent transendothelial migration process relies heavily on ICAM-1 and CD11/18. Finally, the changes that eosinophils have been observed to undergo during infiltration in vivo, namely increased expression of CD11/18 and shedding of L-selectin, appear to take place as a direct result of the interaction between eosinophils and endothelial cells.

Antibodies, Monoclonal↗