In vitro migration of Dictyocaulus viviparus larvae: migration of the infective stage inagar gel.
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Agar↗
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Application of the diffusion theory to migration of plastics components into packed goods: survey of recent migration studies.
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Acrylonitrile↗
Structural analysis of human neutrophil migration. Centriole, microtubule, and microfilament orientation and function during chemotaxis.
Orientation of nucleus, centriole, microtubules, and microfilaments within human neutrophils in a gradient of chemoattractant (5 percent Escherichia coli endotoxin-activated serum) was evaluated by electron microscopy. Purified neutropils (hypaque-Ficoll) were placed in the upper compartment of chemotactic chambers. Use of small pore (0.45 mum) micropore filters permitted pseudopod penetration, but impeded migration. Under conditions of chemotaxis with activated serum beneath the filter, the neutrophil population oriented at the filter surface with nuclei located away from the stimulus, centrioles and associated radial array of microtubules beneath the nuclei, and microfilament-rich pseudopods penetrating the filter pores. Reversal of the direction of the gradient of the stimulus (activated serum above cells) resulted in a reorientation of internal structure which preceded pseudopod formation toward the activated serum and migration off the filter. Coordinated orientation of the entire neutrophil population did not occur in buffer (random migration) or in a uniform concentration of activated serum (activated random migration). Conditions of activated random migration resulted in increased numbers of cells with locomotory morphology, i.e. cellular asymmetry with linear alignment of nucleus, centriole, microtubule array, and pseudopods. Thus, activated serum increased the number of neutrophils exhibiting locomotory morphology, and a gradient of activated serum induced the alignment of neutrophils such that this locomotory morphology was uniform in the observed neutrophil populayion. In related studies, cytochalasin B and colchicines were used to explore the role of microfilaments and microtubules in the neutrophil orientation and migration response to activated serum. Cytochalasin B (3.0 mug/ml) prevented migration and decreased the microfilaments seen, but allowed normal orientation of neutrophil structures. In an activated serum gradient, colchicines, but not lumicolchicine, decreased the orientation of nuclei and centrioles, and caused a decrease in centriole-associated microtubules in concentrations as low as 10(-8) to 10(-7) M. These colchicines effects were associated with the rounding of cells and impairment of pseudopod formation. The impaired pseudopod formation was characterized by an inability to form pseudopods in the absence of a solid substrate, a formation of narrow pseudopods within a substrate, and a defect in pseudopod orientation in an activated serum gradient. Functional studies of migration showed that colchicines, but not lumicolchicine, minimally decreased activated random migration and markedly inhibited directed migration, but had not effect on random migration. These studies show that, although functioning microfilaments are probably necessary for neutrophil migration, intact microtubules are essential for normal pseudopod formation and orientation, and maximal unidirectional migration during chemotaxis.
Blood↗
The mode of migration of neurons to the hippocampus: a Golgi and electron microscopic analysis in foetal rhesus monkey.
The mode of neuron migration from the site of their origin in the ventricular zone to area CA1 of the hippocampus was analysed with Golgi and electron microscopic methods during the first half of gestation in the foetal rhesus monkey. In the inner portion of the intermediate zone, the migrating cells have a bipolar form with one, or oaccasionally two, leading processes which do not reach the ammonic plate and with a single trailing process which usually ends within the intermediate zone. Both the nucleus and the cytoplasm of the migrating cells are relatively electron-dense and the latter contains organelles typical of young neurons as described in other brain regions. Analysis of electron micrographs from serial sections reveals that the length of the somata and of the leading and trailing processes of the migrating neurons is apposed to fascicles of radially oriented, electron-lucent, microtubule-filled fibres which are ultrastructurally similar to the radial glial fibres of the neocortex and to the Bergmann glial fibres of the cerebellum. The close (20 nm) apposition between the membranes of the migrating cell and the radial fibre is maintained even in areas where the fibres bend or curve tortuously. Migrating neurons situated at progressively more superficial levels of the intermediate zone become progressively more differentiated and complex. Thus, in the outer portion of the intermediate zone, the migrating cells acquire several additional cytoplasmic processes and occasionally a long thin axon-like process which courses into the incipient alveus. These cells have somewhat larger somata and less electron-dense nuclei and cytoplasm than the migrating neurons still situated in the inner part of the intermediate zone. Cells close to the ammonic plate usually have one to three cytoplasmic processes that enter the ammonic plate and terminate near their presumed final position. Migrating neurons situated at the lower border of the ammonic plate have a single large apical process which intermingles with neurons already in their final position and which sometimes traverses the ammonic plate. The apposition of the migrating neurons to the radial glial processes becomes less explicit as the cell soma enters the ammonic plate, reflecting the more complex three-dimensional intercellular relationships. However, the present analysis indicates that during the middle and late stages of neuronal migration to the hippocampus radial glial fibres may guide postmitotic young neurons across the intermediate zone to the ammonic plate in the same way that they guide neurons migrating to the superficial and middle layers of the neocortical plate.
Animals↗
The migration of myogenic cells from the somites into the leg region of avian embryos. An ultrastructural study.
The migration of myogenic stem cells into the leg anlagen of chick embryos between stages 16--20 of Hamburger and Hamilton was examined. SEM and TEM studies reveal that cell migration starts at stage 16 from the just-formed somites 26-28. The migrating myogenic cells are elongated and oriented in a medio-lateral direction. The leading ends branch into filopodia which contact a fibrillar network. At first, single cells migrate; later on the cells leaving the ventro-lateral edge of the dermatome migrate in strands and have specialized contacts between them. After reaction with ruthenium red and concanavalin A the migrating cells show a thick surface coat to which ruthenium red-positive particles are attached. The surface coat may be important in the interactions among the migrating cells as well as between the cells and the substrate. The migration of myogenic stem cells was found to take place in a matrix of collagenous fibrils and ruthenium red-positive particles, probably containing glycosaminoglycans. At the onset of migration the fibrillar network exhibits a preferred medio-lateral orientation. Therefore, it may be concluded that this alignment of the fibrils influences the direction of cell migration.
Animals↗
Alveolar macrophage migration. Influence of lung lining material and acute lung insult.
Migration of alveolar macrophages collected by lavage from normal rhesus monkeys was tested in an under agarose migration system. Lung lining material and serum albumin obtained from normal rhesus monkeys enhanced the random migration of alveolar macrophages. A chemotactic effect for alveolar macrophages was demonstrated in response to lung lining material. Gel filtration of lung lining material using Sephadex G-200 indicated the presence of 4 distinct fractions. Fraction IV, which had a molecular weight of less than 5,000 daltons, had the greatest ability to enhance alveolar macrophage migration. Macrophages obtained from lungs of rhesus monkeys after they breathed an oxidant gas (ozone) for 7 days demonstrated decreases in both the number of cells randomly migrating and the distance they migrated. The addition of normal lung lining material to macrophages exposed to ozone enhanced their random mobility but did not restore migration values to control values. Ozonized lung lining material or rhesus monkey serum did not significantly alter alveolar macrophage migration from that of control lung lining material or serum. These data indicate that components of the acellular lining material of the lung can produce directional migration of alveolar macrophages and may serve to direct the central flow and clearance of macrophages from alveolar regions. Intraluminal alveolar macrophage accumulation during lung insult with ozone appeared to be related more to migration inhibition of resident cells than to recruitment of additional cells by chemotaxis.
Animals↗
Scanning electron microscopy (SEM) of cranial neural crest migration in chick embryos.
This study describes migrating cranial neural crest cells and the microenvironment through which they migrate in chick embryos. Just prior to and during cell migration, an extensive fibrillar meshwork is observed, particularly on the outer surface of the neural tube and the inner surface of the ectoderm. This meshwork in general had a random orientation. This suggested to us that the meshwork does not provide a directive vector for cell migration but rather a substratum to promote or enhance crest cell filopodial attachment as the cells migrate. Much remains to be done in characterizing the composition of this meshwork. Based on other studies in which a smiliar meshwork has been observed, it is not unreasonable to consider it to be partly collagenous. Another major component in the relatively cell-free space through which avian crest cells migrate is hyaluronic acid. The migrating crest cells are characteristically bipolar and are generally oriented in the direction of migration, although little is known about the actual mechanism of motility. Alterations in the migrating cell or in the environment through which it migrates may interfere with normal craniofacial morphogenesis, as discussed elsewhere in this volume by Johnston and Sulik.
Animals↗
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↗
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↗
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↗
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↗
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↗
Canine migration inhibitory factor: effect of Corynebacterium parvum administration.
Peripheral blood lymphocytes from dogs sensitized to streptolysin O (SLO) were assayed for migration inhibitory factor (MIF) production by the indirect MIF test, using guinea pig peritoneal exudate cells as the source of macrophages. A specific direct correlation was established between the degree of inhibition of migration and the concentration of SLO-stimulated supernatants from lymphocyte cultures (SLO-S) of untreated normal dogs. Undiluted SLO-S inhibited migration by 66.8%, whereas a dilution of 1:64 elicited a 3% inhibition. In parallel tests, purified protein derivative stimulation of lymphocytes from BCG-vaccinated dogs produced 92.6% inhibition. The effect of Corynebacterium parvum on SLO-specific MIF production was evaluated in three groups of dogs administered a single intramuscular injection of C. parvum at 5 or 50 mg/m(2) or 50 mg/m(2) in suspension with 10 mg of methylprednisolone. Inhibition of migration of macrophages exposed to a 1:4 dilution of SLO-S from dogs inoculated with C. parvum (5 mg/m(2)) was 33% greater (mean inhibition, 75%) than the same SLO-S dilution from uninoculated normal dogs (mean inhibition, 42%) (P < 0.0002). Similarly, lymphocytes from dogs administered 50 mg/m(2) caused an enhancement of migration inhibition, with a mean increase of 26% over controls (P < 0.002), whereas a dose of 50 mg/m(2) with methylprednisolone produced a 16% increase in migration inhibition (P < 0.05). The administration of C. parvum resulted in a three- to fourfold increase in the SLO-S dilution, which would reduce migration by 20% (MIF titer). This increase peaked between days 20 and 30 and lasted over 50 days post-C. parvum inoculation. These findings indicate that C. parvum specifically increases MIF production by canine lymphocytes in a linear correlation with SLO concentration and suggest its use as a stimulant of canine immunity.
Animals↗
[Use of 51Cr-labelled macrophages for the objective evaluation of macrophage migration inhibition].
A possibility of using 51Cr-labeld macrophages migrating from the capillaries and lysed with sodium dodecyl sulfate for objective and quantitative assessment of the results of macrophage migration inhibition (MMI) microassay was demonstrated on the basis of correlation analysis of the experimental data. Migration area and sensitivity of 51Cr-labeled macrophages to the action of the factor of migration inhibition were found not to differ from those of unlabeled macrophages. In the assessment of the absolute macrophage migration values and its reduction under the action of the factor of migration inhibition formed in the H-2 system, and also of the specificity of this reduction there was revealed a high correlation between the migration area and the value of the migrant cell label.
Animals↗
Cellular immunity to encephalitogenic factor in man as measured by the macrophage migration inhibition test: the effects of serum.
Sensitivity to human encephalitogenic factor (EF) was measured in 70 cancer patients, in 34 patients with various non-malignant diseases and in 18 healthy volunteers, using the macrophage migration inhibition (MMI) test. Sensitization was demonstrated in 44/70 (63%) of the cancer patients, in 11/34 (32%) of the patients with non-malignant conditions and in one (5%) of the healthy individuals. No significant difference was seen in the frequency of demonstrable sensitivity with clinical stage of disease in cancer patients.Autologous serum from cancer patients had the ability to abrogate EF-mediated migration inhibition in 22/30 sensitized individuals. This blocking occurred with a similar frequency in all 3 clinical stages of cancer. Autologous serum from patients with non-malignant disease caused abrogation of EF-mediated migration inhibition in 4/11 sensitized individuals, whilst none of the healthy control individuals showed any significant change in the migration index in the presence of autologous serum. Homologous serum from patients with carcinoma of the breast or lung with and without autologous blocking activity and serum from a healthy individual were tested against lymphocytes from patients with various tumour types with the MMI test. Of 11 patients tested in the absence of serum, 8 (73%) showed significant migration inhibition with EF, whilst serum from patients with carcinoma of the lung or breast with autologous blocking activity abolished migration inhibition with EF in all 8 individuals with the former and in 6 with the latter, regardless of the tumour type from which the lymphocytes under test were derived. Homologous serum from both a carcinoma of the lung and breast without autologous blocking activity did not abolish migration inhibition with EF, except with the latter in one patient with a carcinoma of the lung.
Adolescent↗
Significance of migration stimulatory factor in human renal allotransplantation.
Seventy-four recipients of related donor renal allografts were tested for the presence of cellular immunity to specific donor lymphocyte antigens using the direct migration inhibition factor (MIF) assay. Responses on the assay fell into one of the following three statistically distinct groups: (1) greater than 20% inhibition of macrophage migration, (2) nonresponsiveness, +/- 10% of control migration, and (3) greater than 12% stimulation of macrophage migration. Migration stimulation was shown to be reproducible and to correlate well with a very benign post-transplant clinical course. The production of migration stimulatory factor appears to be an immunological response analagous to the production of migration inhibition factor.
Female↗
Modulation of human neutrophil polymorphonuclear leucocyte migration by human plasma alpha-globulin inhibitors and synthetic esterase inhibitors.
The exposure of isolated washed human neutrophils to purified human alpha1-antitrypsin resulted in a transient 2-fold enhancement of random migration and concomitant 70-90 per cent inhibition of chemotactic responsiveness to C5a or C3a, while treatment with alpha2-macroglobulin gave a less pronounced brief enhancement of random migration and prolonged 40-60 per cent suppression of chemotaxis. Peak effects occurred with concentrations of 1 mug/ml of alpha1-antitrypsin and 10 mug/ml of alpha2-macroglobulin. In contrast, the inhibitor of the activated first component of complement, at the highest concentration studied of 100/mug/ml, slightly enhanced chemotactic migration in response to C5a without influencing random migration. Preincubation of neutrophils with either L-1-tosylamide-2-phenylethyl-chloromethyl ketone (TPCK) or N-alpha-p-tosyl-L-lysine-chloromethyl ketone (TLCK) at concentrations of 10-8-10-4M suppressed chemotaxis with concomitant inhibition of random migration by TPCK and enhancement of random migration by TLCK. All agents worked directly and irreversibly on the cells but caused only slight stimulation of the activity of the hexose monophosphate shunt of layers of adherent neutrophils. The results suggest that interaction of the plasma alpha-globulins or synthetic esterase inhibitors with surface receptors on neutrophils can influence both the random migration and responsiveness to chemotactic factors of these cells.
Alpha-Globulins↗
Studies on the inhibition of macrophage migration induced by soluble antigen-antibody complexes.
Mixtures of serum of Freund's complete adjuvant (FCA) immunized guinea-pigs and tuberculin PPD consistently inhibited the in vitro migration of peritoneal exudate cells (PEC) of normal guinea-pigs. It is shown that this inhibitory effect is due to a soluble complex between an IgG2 antibody and PPD. By separation of PPD on Sephadex G-200 two peaks were obtained, corresponding respectively to molecular weights of at least 800,000 and 25,000, separated by a plateau. Material derived from both peaks and from the plateau was able to form inhibitory complexes with anti-PPD IgG2. When a mixture of small molecular weight PPD and anti-PPD IgG2 was fractionated on Sephadex G-200, the inhibitory activity was recovered in the void region only. The detection of both IgG2 and PPD in the latter was taken as evidence for the presence of a high molecular weight antigen-antibody complex. When the mechanism of complex-induced inhibition of migration was examined it was found that: (1) complexes act directly on macrophages present in the peritoneal exudate; (2) removal of the Fc fragment of IgG2 by pepsin abolishes its ability to form migration inhibitory complexes; (3) passive sensitization of macrophages with anti-PPD IgG2, followed by exposure to PPD does not result in inhibition of migration; (4) in order to obtain migration inhibition, the complexes must be present during the entire migration period. A 2-hr pulse with complexes does not induce permanent inhibition; (5) the migration inhibitory activity of antigen--antibody complexes can be abolished by certain concentrations of puromycin and aminophylline.
Aminophylline↗