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PubMed1977

[Leucocyte migration inhibition test in diabetes mellitus (author's transl)].

The leucocyte migration inhibition test (LMT) using the agarose plate method introduced by Clausen is simple and highly reproducible. Using human pancreas extract and beef insulin as antigen, LMT was performed on ten patients with insulin dependent diabetes, twenty patients with insulin independent diabetes, and twelve healthy controls. The migration index was expressed as a percentage of migration calculated from the following formula. Migration index (MI) = average areas of migration in test suspension/average areas of migration in control suspension. Using human pancreas extract, the mean migration index for the insulin dependent diabetics (87.6 +/- 11.1) was significantly lower than in the normal subjects (99.3 +/- 6.3) (p less than 0.05). Using beef insulin as antigen for the insulin dependent diabetics and insulin independent diabetics, the mean migration indices (+/- SD) were 95.8 +/- 14.9 and 98.7 +/- 12.3 respectively. The corresponding values for the control group were 98.9 +/- 7.8. Cellular hypersensitivity to human pancreas extract was shown in the leucocyte migration inhibition test with insulin dependent diabetics, but a negative result was obtained with beef insulin.

Adult↗

PubMed1992

Inhibition of lymphocyte endothelial adhesion and in vivo lymphocyte migration to cutaneous inflammation by TA-3, a new monoclonal antibody to rat LFA-1.

Lymphocyte function-associated Ag-1 (LFA-1) or CD11a/CD18 mediates lymphocyte adhesion to cultured vascular endothelial cells (EC). Thus, LFA-1 likely plays a major role in lymphocyte migration out of the blood, but there is little information on this in vivo. Small peritoneal exudate lymphocytes (sPEL) and lymph node (LN) lymphoblasts adhere to cytokine-activated EC and preferentially migrate to cutaneous inflammatory sites. The role of LFA-1 in the adherence and in vivo migration of these T cells was determined. Because of a lack of anti-rat LFA-1, mAb were prepared to rat T cells. One mAb, TA-3, inhibited homotypic aggregation; T cell proliferation to Ag, alloantigens, and mitogens; stained all leukocytes; and immunoprecipitated 170- and 95-kDa polypeptides from lymphocytes and neutrophils. TA-3 binding to lymphocytes also required Ca2+, but not Mg2+. Thus, TA-3 appears to react with rat LFA-1. TA-3 inhibited spleen T cell adhesion to unstimulated EC by 30% and to IFN-gamma, TNF-alpha, IL-1 alpha, and LPS stimulated EC by 50 to 60% but inhibited sPEL EC adhesion by only 10%. TA-3 also strongly inhibited anti-CD3-stimulated LN T cell adherence. The migration of spleen T cells to delayed-type hypersensitivity and skin sites injected with LPS, poly I:C, IFN-gamma, IFN-alpha/beta, and TNF was inhibited by 72 to 88% by TA-3, and was decreased by 50% to peripheral LN. TA-3 caused less but still 50 to 60% inhibition of sPEL migration to inflamed skin. Lymphoblast migration to skin was inhibited 40 to 80% and to PLN by 30%. Migration of lymphocytes from all sources to mesenteric LN was inhibited by 32 to 60%. In conclusion, LFA-1 mediates much of the adherence of spleen T cells and lymphoblasts to EC in vitro, most of the migration of these cells to dermal inflammation and about 50% of the homing of LN and spleen T cells to peripheral and mesenteric LN. sPEL are less dependent on LFA-1 for adhesion to EC in vitro and for migration to inflamed skin and LN in vivo.

Animals↗

PubMed1977

Inhibition of leukocyte migration by the agarose plate technique. Application to antigen from Candida albicans and Fusobacterium nucleatum.

Leukocyte migration inhibition by antigen from Candida albicans and Fusobacterium nucleatum was studied in man by means of the direct leukocyte migration agarose technique (LMAT). Antigens were prepared by prolonged ultrasonication and were added to the leukocyte cultures in the original as well as in the concentrated solutions. Significant inhibition of migration with a 10-fold concentrated solution of candida antigen was demonstrated in subjects showing apositive intracutaneous reaction to candida. With the fusobacterial antigen, inhibition of migration or stimulation of migration were demonstrated in subjects with slight peridontal inflammation. A 5-fold increase in the concentration of fusobacterial antigen resulted in increased stimulation of migration or inhibition of migration. Preincubation of the leukocytes with puromycin abolished both inhibition and stimulation of migration by candidal or fusobacterial antigen. The study confirms that it is important to study dose-related effects when applying the LMAT to test cell-mediated immunity. The study is in support of stimulation of migration being an immunologic reaction.

Antigens, Fungal↗

PubMed1992

Platelet-derived growth factor in combination with collagen promotes the migration of human skin fibroblasts into a denuded area of a cell monolayer.

Since we have found previously that adult donor skin fibroblasts (TIG-114) migrated more slowly in serum-depleted medium than in medium supplemented with 10% FBS, we tried to identify a factor(s) which promotes fibroblast migration from the edge of a denuded area in a monolayer. In medium supplemented with 10% FBS, the effects of both suramin, a competitor of growth factors at the receptor level, and monensin, an inhibitor of the secretion of extracellular matrix, were examined. Both substances suppressed cell migration, suggesting that growth factors and matrix substances are important for cell migration. Then, we examined the effects of growth factors and extracellular matrix on fibroblast migration in serum-free medium. Platelet-derived growth factor (PDGF), basic fibroblast growth factor, acidic fibroblast growth factor, and transforming growth factor-beta did not stimulate cell migration. Type I collagen, plasma fibronectin, and heparin also did not promote cell migration. However, the combination of PDGF and type I collagen did promote cell migration. Addition of anti-PDGF antibody reduced the stimulatory effect induced by the combination of PDGF and type I collagen. These results suggest that the copresence of growth factors and extracellular matrix regulates fibroblast migration into a denuded area in a monolayer.

Adult↗

PubMed1992

Lymphocyte migration into the CNS modelled in vitro.

We report on a series of experiments which examines the factors controlling lymphocyte adhesion to brain endothelium in vitro and the factors which control cell migration across the endothelium, using a new migration assay. Although lymphocyte adhesion preceded migration across the brain endothelium, the two processes are not identical. We noted that activated CD4+ T cells were particularly good at migrating across endothelia. CD8+ T cells and B cells did not migrate but adhered well to endothelia. Moreover, the endothelium maintained high levels of cell traffic without being disrupted and without exhausting the molecular systems which allowed migration. From the viewpoint of migration of dividing cells, the state of lymphocyte activation appeared to be the most important controlling factor--these cells migrated equally well across endothelium activated with cytokines or untreated endothelium. The kinetics of adhesion suggested that the LFA-1/ICAM-1 and VLA-4/VCAM combinations of adhesion molecules were important in controlling migration. With antibody blocking studies, the role of the LFA-1/ICAM-1 system was equivocal. While anti-LFA-1 blocked lymphocyte adhesion, anti-ICAM-1 did not, suggesting that the level of ICAM-1 was not critical.

Animals↗

PubMed1992

Comparative effects of pollen and seed migration on the cytonuclear structure of plant populations. II. Paternal cytoplasmic inheritance.

We continue our study of the effects of pollen and seed migration on the cytonuclear structure of mixed-mating plant populations by analyzing two deterministic continent-island models under the critical assumption of paternal cytoplasmic inheritance. The major results of this study that contrast with our previous conclusions based on maternal cytoplasmic inheritance are (i) pollen gene flow can significantly affect the cytonuclear structure of the island population, and in particular can help to generate cytonuclear disequilibria that greatly exceed the magnitude of those that would be produced by seed migration or mixed mating alone; (ii) with simultaneous pollen and seed migration, nonzero cytonuclear disequilibria will be maintained not only when there is disequilibrium in the immigrant pollen or seeds, but also through a variety of intermigrant admixture effects when the two pools of immigrants differ appropriately in their cytonuclear compositions; (iii) either immigrant pollen or immigrant seeds can generate disequilibria de novo in populations with initially random cytonuclear associations, but pollen migration alone generally produces lower levels of disequilibrium than does comparable seed migration, especially at high levels of self-fertilization when the overall fraction of immigrant pollen is low; (iv) the equilibrium state of the island population will be influenced by the rate of pollen gene flow whenever there is either allelic disequilibrium in the immigrant pollen or simultaneous seed migration coupled with different cytoplasmic or nuclear allele frequencies in immigrant pollen and seeds or nonzero allelic disequilibrium in either immigrant pool. The estimation of pollen migration should therefore be facilitated with paternal cytoplasmic inheritance relative to the case of maternal cytoplasmic inheritance. These basic conclusions hold whether the population is censused as seeds or as adults, but with simultaneous pollen and seed migration, the relationship between census time and the ability to detect nonrandom cytonuclear associations is complex. When migration is through pollen alone, however, the cytonuclear structure of the island population is independent of the life stage censused.

Alleles↗

PubMed1979

The effect of hyperoxia on migration of alveolar macrophages in vitro.

There is in vitro evidence to support the notion that directed migration (chemotaxis) is involved in the recruitment of alveolar macrophages in vivo. Because O2 is widely used in the treatment of pulmonary diseases, we examined the effect of hyperoxia on migration of guinea pig alveolar macrophages in vitro. Migration was measured in blind-well chambers incubated in either room air or hyperoxia. N-formyl-methionyl-phenylalanine was used to stimulate random migration and to produce directed migration. Migration was quantified by counting the number of mononuclear cells per oil immersion field that had migrated completely through a polycarbonate filter with 5-micrometer pores. The average PO2 in the cell suspensions incubated in room air was 100 mm Hg. In the hyperoxic environments, the average PO2 at 1 h was 260 mm Hg, whereas at 2 and 3 h, it was 410 and 425 mm Hg, respectively. In 6 separate experiments, there was no significant difference between the mean response to N-formyl-methionyl phenylalanine in hyperoxia and in room air after 1 h of incubation. After 2 and 3h of incubation, however, the response in hyperoxia was significantly (P less than 0.002) lower than that in room air. The decreased response in hyperoxia did not appear to result from loss of viability of responding cells, diminished adherence of cells to the filters, loss of activity of N-formyl-methionyl phenylalanine exposed to high PO2, or failure of the cells to exhibit directed migration. Instead, it appeared that hyperoxia decreased the response of alveolar macrophages primarily by impairing random migration.

Animals↗

PubMed1992

Antagonistic effects of TGF-beta 1 and MSF on fibroblast migration and hyaluronic acid synthesis. Possible implications for dermal wound healing.

The migration of adult skin fibroblasts into three-dimensional collagen gel matrices is differentially affected by cell density, with subconfluent cells displaying a significantly elevated level of migration compared to confluent ones. Fetal fibroblasts differ from adult cells in that they display an elevated level of migration at both subconfluent and confluent cell densities. We have previously reported that this difference in behaviour results from the secretion by fetal fibroblasts of a 'migration stimulating factor' (MSF) which is not made by their normal adult counterparts, and that MSF appears to act by stimulating the synthesis of hyaluronic acid (HA). Data presented in this communication indicate that (a) MSF specifically stimulates the synthesis of high molecular weight species of HA, (b) TGF-beta 1 inhibits the elevated migration of adult fibroblasts plated at subconfluent cell density, (c) under these conditions, TGF-beta 1 induces a parallel decrease in the synthesis of high molecular weight HA and increase in the synthesis of low molecular weight HA, (d) TGF-beta 1 is a potent antagonist of MSF, effectively blocking its stimulation of cell migration and synthesis of high molecular weight HA, and (e) the inhibition of fibroblast migration by TGF-beta 1 does not appear to be a chemotactic response dependent upon the existence of a concentration gradient of the cytokine. Our observations regarding the inhibitory effects of TGF-beta 1 on fibroblast migration into 3D collagen gels stand in marked contrast to various published reports indicating that this cytokine stimulates the migration of human skin fibroblasts through the pores of polycarbonate filters as used in modified Boyden chamber assays; this discrepancy underscores the importance of the substratum in modulating cellular response to cytokines. Our results are discussed in terms of the possible combined contribution of MSF and TGF-beta 1 to wound healing.

Cell Movement↗

PubMed1975

An explanation of the apparent reversal of the circadian migration by Hymenolepis diminuta (Cestoda) in the rat.

Hymenolepis diminuta exhibits 2 concurrent migrations: an age-dependent, forward migration and a circadian migration. In experiments where the age of worms was assumed to be uniform throughout the test-day, 2 patterns (7-day-old and 16-day-old) of circadian migration were seen and an apparent reversal in circadian pattern suggested. In experiments where the age of worms became progressively older during the test-day, only the 16-day-old pattern was seen and no reversal was observed. The 7-day-old pattern and hence the apparent reversal in circadian migration is postulated to be an artifact of the method whereby both the age and size of worms were presumed to be uniform throughout the test-day. The 7-day-old pattern results from comparing worms of unequal size and thus at different positions in their forward migration. Data on the daily variation of stomach contents of rats and the results from protein determinations of 6-day-old worms support this hypothesis. Therefore H. diminuta is believed to exhibit only the 16-day-old pattern of circadian migration: an anterior migration between 12 midnight and 6 AM, and a posterior migration between 12 noon and 6 PM.

Age Factors↗

PubMed1992

Involvement of beta 2-integrins in the migration of human natural killer cells.

Human large granular lymphocytes with the NK cell phenotype (CD16+ or CD56+CD3-) were greatly enriched among the cells which migrated spontaneously through untreated or albumin-coated, 3-microns pore size polycarbonate filters for 1 to 8 h. Three days of rIL-2 treatment (300 IU/ml) and 3 to 5 wk of rIL-2 treatment (100 IU/ml) generated a 2.7 +/- 0.9-fold and 5.6 +/- 0.8-fold increase in cell migration, respectively. The adhesion and subsequent migration of freshly isolated NK cells was mainly mediated by CD11b/CD18, because migration could be inhibited by 80 +/- 8% anti-CD11b (Mac-1) antibodies but not with antibodies against CD11a (LFA-1) or CD11c (p150,95), the other alpha-chains of the beta 2-integrins. After rIL-2 activation, however, CD11a/CD18 was the major receptor utilized in migration, inasmuch as anti-CD11a antibody caused a 69 +/- 8% reduction in the number of migrated cells. Anti-CD11b antibody decreased migration by 43 +/- 12%, and together these antibodies inhibited migration by 82 +/- 7%. Anti-CD11a alone did not have any effect on adhesion, but CD11a/CD18 cooperated in the adhesion because anti-CD11b decreased adhesion by 40 +/- 11% and together these antibodies inhibited adhesion by 74 +/- 6%. The ability of large granular lymphocytes to rapidly utilize beta 2-integrins and unidentified ubiquitous ligands for binding and migration may be significant for their capacity to function in the first line of immune defense under highly variable conditions.

Antibodies, Monoclonal↗

PubMed1977

Factors which influence blood platelet migration.

Migration of human blood platelets in vitro was investigated by a modification of the capillary-tube migration chamber technique used to study the migration inhibition factor of macrophages. Platelets were packed in capillary tubes and incubated in autologous platelet-free plasma (PFP). The extent of migration was quantified by planimetry (measurement of the area of platelet migration visible by stereomicroscopy). Among the various anticoagulants employed, sodium citrate was most suitable for studying platelet migration. Optimal migration occured at 22 degrees to 37 degrees C and pH 7.2 to 7.4. Migration was inhibited by metabolic inhibitors such as iodoacetic acid, sodium fluoride, and 2,4-dinitrophenol, and inhibition was proportional to the dose of the agent added to the incubation medium. Mobility was also inhibited by cytochalasin B, which disrupts cellular microfilaments, at 1 microgram/ml PFP, but not by colchicine, a microtubule inhibitor, even at 40 microgram/ml of PFP. Light and electron microscopy showed that this inhibition was not ascribable to platelet clumping. These observations suggest that platelet mobility is an active process. The possible significance of platelet migration in hemostasis is discussed.

Anticoagulants↗

PubMed1976

Studies on delayed hypersensitivity pleural exudates in guinea-pigs. II. The interrelationship of monocytic and lymphocytic cells with respect to migration activity.

The in vitro migration activity of monocytic cells and the effect of lymphocytes in the delayed hypersensitivity (DH) reaction induced by intrapleural injection of PPD into FCA-sensitized guinea-pigs was investigated. The in vitro migration of exudate mononuclear cells was lower than that of comparable blood cells, and continued to decrease as the reaction progressed. An inverse relaationship was observed between the migration area and cell volume of mononuclear cells from both blood and exudate. Similar experiments were performed on the reversed passive Arthus (RPA) reaction in the pleural cavity of guinea-pigs. For 6-h exudate, the mononuclear cell migration exceeded that for blood mononuclear cells. However, the migration of mononuclear cells from 18-h exudates was markedly reduced. As with DH, an inverse relationship between the migration area and cell volume was observed with the mononuclear cells of RPA exudates. Following the addition of antigen, the migration of DH exudate mononuclear cells was inhibited whereas the exudate mononuclear cells of the RPA reaction remained unaffected. For DH, the inhibition of migration induced by antigen appeared to be related to the non-adherent cells of 6-h exudates, and both the adherent and non-adherent cells of 18-h exudates.

Animals↗

PubMed1978

Migration inhibition of T lymphocytes from human peripheral blood by specific antigen and lymphokines.

The inhibition of migration of human peripheral blood cells in the presence of PPD was studied. It was found that migration inhibition of peripheral blood mononuclear cells (MN) from Mantoux-positive donors was far greater than the migration inhibition of peripheral blood leucocytes (PBL). Moreover, MN cells and T lymphocytes showed larger and more uniform areas of migration. In contrast, the migration of B lymphocytes and monocytes was poor. Further analysis using purified subpopulations of MN cells showed that PPD inhibited the migration of T lymphocytes but not of B lymphocytes and monocytes. Corresponding to these findings, lymphokine-containing supernatants also inhibited the migration of purified T cells from Matoux-negative donors. It was concluded that the T lymphocyte was the predominant cell in the MN cell population, which migrated, and was subject to inhibition by PPD or lymphokines. These results imply that the movement of human T lymphocytes may be influenced by soluble factors from antigen-activated sensitized cells.

Adult↗

PubMed1992

Platelet endothelial cell adhesion molecule, PECAM-1, modulates cell migration.

Cell migration is an important process in such phenomena as growth, development, and wound healing. The control of cell migration is orchestrated in part by cell surface adhesion molecules. These molecules fall into two major categories: those that bind to extracellular matrix and those that bind to adjacent cells. Here, we report on the role of a cell-cell adhesion molecule, platelet-endothelial cell adhesion molecule-1, (PECAM-1), a member of the lg superfamily, in the modulation of cell migration and cell-cell adhesion. PECAM-1 is a 120-130 kDa integral membrane protein that resides on endothelial cells and localizes at sites of cell-cell contact. Since endothelial cells express PECAM-1 constitutively, we studied the effects of PECAM-1 on cell-cell adhesion and migration in a null-cell population. Specifically, we transfected NIH/3T3 cells with the full length PECAM-1 molecule (two independent clones). Transfected cells containing only the neomycin resistance gene, cells expressing a construct coding for the extracellular domain of the molecule, and cells expressing the neu oncogene were used as controls. The PECAM-1 transfectants appeared smaller and more polygonal and tended to grow in clusters. Indirect immunofluorescence of PECAM-1 transfectants showed peripheral staining at sites of cell-cell contact, while the extracellular domain transfectants and the control cells did not. In two quantitative migration assays, the full-length PECAM-1 transfectants migrated more slowly than control cells. Thus, PECAM-1 transfected into a null cell appears to localize to sites of cell-cell contact, promote cell-cell adhesion, and diminish the rate of migration. These findings suggest a role for this cell-cell adhesion molecule in the process of endothelial cell migration.

Animals↗

PubMed1992

Requirement for VLA-4 and VLA-5 integrins in lymphoma cells binding to and migration beneath stromal cells in culture.

Physical interaction between human lymphomas and murine bone marrow derived stromal cells were studied. Nalm-6 pre-B cells adhered to BMS2 stromal cells and subsequently migrated beneath them, while Ramos Burkitt lymphoma cells, adhered but did not migrate. Four mAbs were established against Nalm-6 cells, which were able to block initial adhesion of Nalm-6 cells. Two of them were directed against the alpha 4 chain of VLA-4, and other two recognized the beta 1 chain of VLA integrins. Therefore, the initial adhesion of Ramos and Nalm-6 cells to BMS2 was largely mediated by the VLA-4 integrin expressed on lymphocytes. The corresponding ligand on stromal cells appears to be VCAM-1, because antibodies against murine VCAM-1 blocked the adhesion. However, antibodies against the alpha chain of VLA-4 were not capable of blocking subsequent migration beneath stromal cells. In contrast, antibodies against the beta chain of VLA integrins blocked the migration beneath stromal cells as well as the initial adhesion. Because a common beta chain can be shared among integrins, the role of other VLA integrins in Nalm-6 cells migration was investigated. VLA-5 and VLA-6 as well as VLA-4 were expressed on Nalm-6 cells, but not on Ramos cells. Additional blocking experiments revealed that VLA-4 and VLA-5 are likely to work in concert to mediate the migration of Nalm-6 cells beneath stromal cells. Thus, particular VLA integrins appear to be responsible not only for lymphocyte adhesion but also for migration with respect to stromal cells. These findings may have implications for cell-cell interactions and directed migration of lymphocytes in bone marrow and other tissues.

Animals↗

PubMed1976

Migration of Baroda medical graduates, 1949--72.

1. The migration of doctors from Medical College, Baroda, is studied in detail. 2. From 1949 to 1972, 584 doctors migrated to other countries and only twenty-nine doctors have returned so far. The incidence of migration is to the extent of 39-75%. 3. Among those who migrated 77-7% have gone to U.S.A. and 11-7% have gone to the U.K. 4. Ninety-four women graduates out of 241 passed prior to 1971 are abroad.. 5. The majority migrate for better and more comfortable living conditions. A small number migrate for better research facilities and encouragement. Those who are denied the opportunity of a post-graduate training also migrate. 6. Migration of doctors, though universal, is disturbingly high in India and a major cause of concern to the government and the educationist.

Africa↗

PubMed1992

Independent modulation of enterocyte migration and proliferation by growth factors, matrix proteins, and pharmacologic agents in an in vitro model of mucosal healing.

BACKGROUND: Gastrointestinal mucosa heals by restitution and proliferation. These are difficult to distinguish in vivo. METHODS: Human Caco-2 enterocytes were cultured on matrix proteins (collagen I, laminin, fibronectin) with growth factors (epidermal growth factor [EGF] and transforming growth factor-beta 1 [TGF-beta 1]) and the tyrosine kinase and prostaglandin inhibitors genistein and indomethacin. Healing was modeled by means of monolayer expansion, proliferation by means of 3H-thymidine uptake, and restitution by means of mitomycin-blocked migration. RESULTS: Changing matrix composition failed to alter proliferation, but collagen I stimulated migration more than laminin or fibronectin (laminin/collagen, 68% +/- 2%; p less than 0.05). EGF (30 ng/ml) increased proliferation on both collagen (225% +/- 11% of basal) and laminin (206% +/- 26%) but increased migration only over laminin (210% +/- 17%) (all, p less than 0.05). TGF-beta 1 (200 pg/ml) stimulated migration over laminin (187% +/- 18%, p less than 0.005) but inhibited migration over collagen (89% +/- 3%, p less than 0.01) and did not affect 3H-thymidine uptake. When cultured on laminin, EGF but not TGF-beta 1 altered organization of the alpha 2 integrin subunit. Genistein (100 mumol/L) inhibited basal and EGF-stimulated 3H-thymidine uptake. In addition, it prevented EGF stimulation of replication-blocked migration (81% +/- 10% vs 190% +/- 20% of basal, p less than 0.0001) without altering basal replication-blocked migration. Indomethacin (10(-5) mol/L) did not alter migration but inhibited basal and EGF-stimulated proliferation by 7% +/- 1% (each, p less than 0.005). CONCLUSIONS: Restitution and proliferation appear independently regulated by matrix and growth factors. It may be possible to individually target specific phases of mucosal healing by means of pharmacologic agents.

Cell Division↗

PubMed1975

[A simplified macrophage migration inhibition test to measure T-cell derived immunity in man].

A macrophage migration inhibition test using heterologous cells (DMMTH) is performed in an agarose-droplet technique. A suspension consisting of peritoneal exsudate cells from Guinea pig and human lymphocytes, mixed with 0,2 percent agarose is dispensed in droplets with a dispenser into culture chambers used for the leukocyte migration inhibition test. Macrophages migrate out of the gelified droplets. Migration areas can be measured by planimetry. Migration areas are exact to 8.6 percent. A significant migration inhibition, caused by migration inhibitory factors is observed after the reaction of the specific antigen with sensitized lymphocytes in the agarose droplet. The sensitivity of the test has been demonstrated in Mantoux positive persons.

Cell Migration Inhibition↗