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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↗

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↗

PubMed1977

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↗

PubMed1978

[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↗

PubMed1978

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↗

PubMed1979

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↗

PubMed1975

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↗

PubMed1975

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↗

PubMed1979

A blocking factor in amniotic fluid causing leukocyte migration enhancement.

Amniotic fluid was found to cause significant leukocyte migration enhancement during the second and third trimester of pregnancy and in the early postpartum period when compared to the migration area obtained with an ovarian tumor homogenate antigen (p less than 0.01), choriocarcinoma spent medium (p less than 0.01), and placental pool homogenate (p less than 0.01). Only borderline significance (p less than 0.1) was obtained when migration enhancement with AF was compared between pregnant and nonpregnant female control patients, indicating minimal unspecific activity of AF. Migration enhancement with autologous amniotic fluid was slightly larger than with homologous amniotic fluid, but the difference did not reach significance (p less than 0.4). None of the control antigens caused migration enhancement; placental pool homogenate in concentrations above 4 mg. per cent caused migration inhibition but did not in lower concentrations. The enhancing effect of AF could be abolished by dilution but not by addition of excessive antibody to estrogen of HCG. It is suggested that a blocking factor is present in AF preventing recognition of fetoplacental antigen by the maternal immune system. Thus in vitro leukocyte migration enhancement may correlate to in vivo graft enhancement.

Amniotic Fluid↗

PubMed1977

Interactions between salmonellae and macrophages of guinea pigs. IV. Relationship between migration inhibition and antibacterial action of macrophages.

The in vitro macrophage migration inhibition test was used to detect the development of delayed-type hypersensitivity in guinea pigs infected with Salmonella typhimurium. Four different preparations from supernatants of S. typhimurium cultures were used as the antigens in this test. They included the concentrated bacterial antigens, the high-molecular-weight (>50,000) antigens, the ammonium sulfate-precipitated antigens, and the ribonuclease-treated antigens. All four antigen preparations were shown to inhibit the migration of peritoneal macrophages of salmonella-infected (immune) guinea pigs from capillary tubes, in comparison with cells of normal control animals. By use of the high-molecular-weight antigens and the ammonium sulfate-precipitated antigens, the production of the migration inhibition factor(s) was elicited from cultures of lymphocytes obtained from the peripheral blood of immune guinea pigs. The activity of the migration inhibition factor(s) was demonstrated by its ability to inhibit the migration of peritoneal macrophages of normal guinea pigs from capillary tubes. In contrast, normal peritoneal macrophages exposed to products of antigen-stimulated immune lymphocytes did not exhibit an enhanced phagocytic or bactericidal action against virulent S. typhimurium as compared with those of the normal control. The present study indicated that the bacterial antigens responsible for the elicitation of the production of the migration inhibition factor from lymphocytes of immune guinea pigs are inactivated by proteolytic enzymes, but not by ribonuclease, and have molecular weights of >50,000.

Animals↗

PubMed1976

[Effect of synovial fluid from rheumatoid arthritis patients on leukocyte migration].

By means of the migration inhibition test, the influence of the synovial fluid of rheumatoid arthritis patients on normal blood lymphocytes was investigated. There was the hypothesis that the migration inhibitory factor is already formed in the synovial membrane of rheumatoid arthritis patients. In 35 cases a migration inhibition could be demonstrated, in 3 cases the migration of normal lymphocytes remained uninfluenced, in 6 cases a migration enhancement occurred. The demonstration of the rheumatic factor in the synovial fluids used was partly positive, partly negative. Especially the demonstration of a migration enhancement--this phenomenon could be reproduced repeatedly--cannot yet be interpreted unequivocally and requires further investigations.

Arthritis, Rheumatoid↗

PubMed1976

Leucocyte capillary migration: an adherence dependent phenomenon.

To determine the mode of action of leucocyte inhibitory factor (LIF) on polymorphonuclear leucocyte (PMN) migration out of capillary tubes, this phenomenon has been compared with PMN adhesion to cotton wool columns. Colchicine and vinblastine sulphate had no effect on either of these processes but cytochalasin B caused marked inhibition of PMN migration and increased PMN adhesion. The cytochalasin B effect could be reversed in the presence of drugs known to increase intracellular levels of cyclic AMP. For inhibition of PMN migration by LIF, Mg2+ but not Ca2+ was essential. LIF not only inhibited PMN migration but also increased PMN adhesion to cotton wool columns. LIF inhibitory activity on PMN migration was not affected by colchicine or vinblastine. Leucocyte migration and adhesion depend on similar mechanisms, and are both influenced by LIF which probably acts by affecting micro-filament function.

Calcium↗

PubMed1979

Delayed hypersensitivity to human encephalitogenic protein as assayed by agarose leucocyte migration in multiple sclerosis patients.

Using a leucocyte migration test (Clausen's direct agarose gel migration method) hypersensitivity to human encephalitogenic protein has been examined in 50 multiple sclerosis patients (group 1), 50 healthy persons (group 2) and 25 patients with other neurological diseases (group 3). In group 1, 30 MS patients (60%) show an abnormal migration index, manifested either as inhibition or stimulation of migration; 29 controls in group 2 (58%), 11 O.N.D. patients in group 3 (44%) show an abnormal migration index. These results mean that lymphocyte hypersensitivity to myelin basic protein appears neither to be constant nor specific to multiple sclerosis. Three migration index curve types at different antigen concentration are obtained: monophasic curves within the normal index zones; monophasic curves staying in the inhibition or stimulation zone and biphasic curves with dose-effect relationship. Whatever the antigen used, this dose-effect relationship implies that the test must be carried out at different concentrations. The meaning of spontaneous sensitisation in healthy controls is discussed.

Adolescent↗

PubMed1979

Regulation of macrophage migration by products of the complement system.

Agents formerly shown to induce rapid macrophage spreading were examined for their ability to modify the migration of macrophages in the capillary tube assay. Products of the activation of the contact phase of blood coagulation as well as the purified component Bb, the large cleavage fragment of factor B of the alternative complement pathway produced a dose-dependent inhibition of migration. In addition, inflammatory macrophages elicited with either a lipopolysaccharide endotoxin or thioglycollate medium exhibited rapid spreading and inhibited migration, whereas resident cells did not. A close correlation existed, therefore, between enhanced spreading and inhibited migration under both in vitro induced and in vivo situations. Cleavage products of component C5 of the classical complement pathway enhanced macrophage migration and did not alter spreading. In mixtures of C5 cleavage products and Bb, the predominant peptide determined the outcome of the reaction. Factor B, a normal secretory product of macrophages, may represent a common substrate for several of the proteases that induce spreading, inhibit migration, and lead to the generation of the enzymatically active fragment Bb.

Ascitic Fluid↗

PubMed1978

Human leucocyte response to migration inhibitory activity from lymphocytes. Modification by aprotinin, Tranexamic acid and phenylmethyl sulfonylfluoride.

Human lymphokines can elicit several effects associated with inflammation, e.g. leucocyte migration inhibition and fibrinolysis. These effects can be assessed in vitro by the leucocyte migration agarose technique (LMAT) and the leucocyte migration fibrinolysis technique (LMFT). The present study shows that preincubation of normal leucocytes with aprotinin, tranexamic acid and phenyl-methyl-sulfonylfluoride (PMSF) reduces or abolishes their migration inhibition response to leucocyte migration inhibition factor. The compounds exert this effect at non-toxic concentrations, which do not otherwise interfere with migration or fibrinolysis, and are non-toxic as estimated by PHA stimulation of lymphocytes. The LMFT is more sensitive to the modifying effect than the LMAT. The effect of aprotinin and tranexamic acid is reversible, the effect of PMSF is irreversible.

Aprotinin↗

PubMed1975

Leukocyte migration in agarose, a study on multiple sclerosis.

The effect of low concentrations of bovine encephalitogenic protein on the migration of human peripheral leukocytes in agarose was studied. A concentration of 0.3 mug/ml of the protein stimulated the migration of cells from many donors, including some healthy subjects. An indirect technique suggested that the migration enhancement is due to the production of soluble factor, possibly corresponding to the leukocyte migration enhancement factor described by others. The frequency of subjects whose cells could be stimulated and the recorded degree of stimulation tended to be higher in a group of patients with multiple sclerosis than in a group of healthy subjects. When the effect of some of the main peptide fragments of the protein was studied on cells that were stimulated by the intact protein, one or more of these peptides sometimes induced the opposite effect: a migration inhibition. There is, apparently, a complex balance between enhancing and inhibiting factors acting on leukocyte migration in vitro; and the character of the antigen seems to be one important factor.

Amyotrophic Lateral Sclerosis↗