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PubMed1984

Mechanisms of decreased leucocyte adhesiveness and migration in plasma from patients with IgG myelomatosis.

The adhesiveness of leucocytes in human plasma was decreased by the addition of IgG M-protein, commercial IgG, F(ab)2-fragments, or bovine serum albumin (BSA). Leucocyte migration was inhibited by IgG M-protein and commercial IgG, but not by reduced and alkylated IgG, F(ab)2-fragments or BSA. Guinea pig serum (GPS) strongly enhanced leucocyte migration in Hanks' balanced salt solution. This effect was abolished by hydrazine treatment or heating, and reduced, but not abolished, by zymosan treatment. C4-deficient guinea pig serum (C4-def-GPS), but not zymosan treated C4-def-GPS stimulated migration. In IgG myeloma sera migration was enhanced by the addition of C4-def-GPS and by untreated or heated, but not hydrazine treated GPS, and inhibited by zymosan treated GPS. IgG M-protein inhibits leucocyte adhesiveness and migration. Migration is specifically inhibited by the intact IgG, probably through complement activation with consumption of heat stable chemokinetic factor(s) and production of migration inhibitors.

Animals↗
PubMed1991

Dual effects of vasoactive intestinal peptide (VIP) on leucocyte migration.

Vasoactive intestinal peptide, at different concentrations, was tested on the migration of leucocytes by using the sealed capillary migration test. Vasoactive intestinal peptide, at 10(-7)-10(-9)M, inhibited, while at 10(-12)-10(-14)M, stimulated mononuclear leucocyte migration. The migration of polymorphonuclear leucocytes was inhibited by vasoactive intestinal peptide at 10(-6)-10(-9)M, a stimulation was found at 10(-13)-10(-14)M. The inhibiting effect of vasoactive intestinal peptide on leucocyte migration was abolished when vasoactive intestinal peptide was split into C- and N-terminal fragments, while a stimulating effect was retained in the N-terminal fragment, at 10(-14)M, for mononuclear cells. Helodermin and peptide T, as well as two other members of the secretin-glucagon family, secretin and gastric inhibitory peptide, had no effect on the migration. When VIP antiserum was tested, it had an inhibiting effect, which was not seen with control serum, supporting a physiological effect of the lower vasoactive intestinal peptide concentrations. Vasoactive intestinal peptide seems to have dual effects on mononuclear and polymorphonuclear leucocyte migration and, generally, intact vasoactive intestinal peptide seems to be needed for these effects.

Cell Migration Inhibition↗
PubMed1985

The effect of chemotherapeutic agents on chemotaxis and random migration of human leukocytes.

Chemotherapeutic agents (CTAs) used for treatment of neoplastic and other diseases may influence defense mechanisms of the patient, altering various humoral and cellular immunologic functions. Herein we report the influence of 16 CTAs on random migration and chemotaxis of human polymorphonuclear cells (PMNCs), using two methods, under-agarose migration and double-filter Boyden chambers with 51Cr-PMNCs. Random migration was inhibited by vinblastine only (P less than .01). BCNU and daunorubicin inhibited random migration only when used in high concentrations. In under-agarose migration, only BCNU and vinblastine inhibited chemotaxis (P less than .01) in therapeutic concentrations. Inhibition was also observed when higher concentrations of vincristine were tested. In the Boyden method, marked inhibition of chemotaxis (P less than .01) was caused by BCNU, vinblastine, vincristine, daunorubicin, and doxorubicin. Inhibition of chemotaxis could not be reversed by washing the cells after preincubation. CTAs per se did not have chemoattractant activity. This study shows that some chemotherapeutic agents inhibit random and directed migration of human PMNCs. It also supports the evidence that Boyden chamber method may detect chemotactic abnormalities that escape recognition by the under-agarose migration method. Suppression of locomotion of PMNCs should be taken into consideration in patients treated with CTAs.

Antineoplastic Agents↗
PubMed2004

Control of planula migration by LWamide and RFamide neuropeptides in Hydractinia echinata.

Planula larvae of Hydractinia echinata (Cnidaria) settled on a substratum migrate toward light. We observed that planula migration is not a continuous process. Instead, it consists of repeating cycles of active migration (about 8 min on average) and inactive resting periods (about 26 min on average). This pattern of periodic migration is regulated by LWamide and RFamide neuropeptides. LWamide (10(-8) mol l(-1)) stimulates migration primarily by making the active periods longer, whereas RFamide (10(-7) mol l(-1)) inhibits migration by blocking the initiation and also shortening the length of the active periods. Since sensory neurons containing LWamides and RFamides are present in planula larvae, it appears likely that planula migration is regulated by the release of endogenous neuropeptides in response to environmental cues.

Animal Migration↗
PubMed2006

Concordant genetic estimators of migration reveal anthropogenically enhanced source-sink population structure in the river sculpin, Cottus gobio.

River systems are vulnerable to natural and anthropogenic habitat fragmentation and will often harbor populations deviating markedly from simplified theoretical models. We investigated fine-scale population structure in the sedentary river fish Cottus gobio using microsatellites and compared migration estimates from three FST estimators, a coalescent maximum-likelihood method and Bayesian recent migration analyses. Source-sink structure was evident via asymmetry in migration and genetic diversity with smaller upstream locations emigration biased and larger downstream subpopulations immigration biased. Patterns of isolation by distance suggested that the system was largely, but not entirely, in migration-drift equilibrium, with headwater populations harboring a signal of past colonizations and in some cases also recent population bottlenecks. Up- vs. downstream asymmetry in population structure was partly attributable to the effects of flow direction, but was enhanced by weirs prohibiting compensatory upstream migration. Estimators of migration showed strong correspondence, at least in relative terms, especially if pairwise FST was used as an indirect index of relative gene flow rather than being translated to Nm. Since true parameter values are unknown in natural systems, comparisons among estimators are important, both to determine confidence in estimates of migration and to validate the performance of different methods.

Animal Migration↗
PubMed2006

Three-dimensional visualization of suprarenal aortic stent-grafts: evaluation of migration in midterm follow-up.

PURPOSE: To investigate the midterm results of transrenal fixation of abdominal aortic stent-grafts with regard to device migration and encroachment of stent wires on the renal and visceral branches. METHODS: Imaging data from 18 patients (15 men; mean age 75 years, range 63-84) undergoing transrenal stent-graft fixation for abdominal aortic aneurysm (AAA) were included in the study. Computed tomographic angiographic data acquired within 1 week of stent-graft implantation were compared to the latest follow-up images. Postprocessing methods generated 3-dimensional (3D) maximum intensity projections (MIP) and virtual intravascular endoscopy (VIE) for evaluation of the relationship between suprarenal stents and aortic branches. Aortic neck angulation was measured in each patient for correlation with the incidence of stent migration. RESULTS: The mean follow-up period was 40 months. 3D image visualizations showed that the stent-graft moved caudally in all patients (range 2.6-14.2 mm), with migration (>10 mm) observed in 4 (22%) patients. Corresponding VIE images documented changes in stent wire encroachment on the aortic branch ostia in 11 patients, including the number and position of crossing stent wires. There was no close relationship between aortic neck angulation and stent migration. CONCLUSION: The current study demonstrated that migration occurs at midterm follow-up in transrenally deployed stent-grafts. 3D images were valuable for the assessment of stent migration, as well as its relationship with aortic branch ostia. Long-term follow-up of transrenal fixation deserves to be investigated, especially after observing stent migration relative to aortic ostial encroachment.

Aged↗
PubMed2000

Differential ability of exogenous chemotactic agents to disrupt transendothelial migration of flowing neutrophils.

Neutrophils migrate through endothelium using an ordered sequence of adhesive interactions and activating signals. To investigate the consequences of disruption of this sequence, we characterized adhesion and migration of neutrophils perfused over HUVEC that had been treated with TNF-alpha for 4 h and evaluated changes caused by exogenously added chemotactic agents. When HUVEC were treated with 2 U/ml TNF, flowing neutrophils adhered, with the majority rolling and relatively few migrating through the monolayer. If fMLP, IL-8, zymosan-activated plasma (a source of activated complement factor C5a), epithelial cell-derived neutrophil-activating peptide (ENA-78), or growth-regulating oncogene, GRO-alpha, was perfused over these neutrophils, they stopped rolling and rapidly migrated over the monolayer, but did not penetrate it. When HUVEC were treated with 100 U/ml TNF, the majority of adherent neutrophils transmigrated. If neutrophils were treated with fMLP, IL-8, C5a, ENA-78, or GRO-alpha just before perfusion over this HUVEC, transmigration, but not adhesion, was abolished. However, when platelet-activating factor was used to activate neutrophils, migration through HUVEC treated with 100 U/ml TNF was not impaired, and migration through HUVEC treated with 2 U/ml TNF was actually increased. Transmigration required ligation of CXC chemokine receptor-2 on neutrophils, and differential desensitization of this receptor (e.g., by fMLP but not platelet-activating factor) may explain the pattern of disruption of migration. Thus, transmigration may require presentation of the correct activators in the correct sequence, and inappropriate activation (e.g., by systemic activators) could cause pathological accumulation of neutrophils in the vessel lumen.

Cell Adhesion↗
PubMed2003

Determinants of human B cell migration across brain endothelial cells.

Circulating B cells enter the CNS as part of normal immune surveillance and in pathologic states, including the common and disabling illness multiple sclerosis. However, little is known about the molecular mechanisms that mediate human B cell interaction with the specialized brain endothelial cells comprising the blood-brain barrier (BBB). We studied the molecular mechanisms that regulate the migration of normal human B cells purified ex vivo, across human adult brain-derived endothelial cells (HBECs). We found that B cells migrated across HBECs more efficiently than T cells from the same individuals. B cell migration was significantly inhibited by blocking Abs to the adhesion molecules ICAM-1 and VLA-4, but not VCAM-1, similar to the results previously reported for T cells. Blockade of the chemokines monocyte chemoattractant protein-1 and IL-8, but not RANTES or IFN-gamma-inducible protein-10, significantly inhibited B cell migration, and these results were correlated with the chemokine receptor expression of B cells measured by flow cytometry and by RNase protection assay. Tissue inhibitor of metalloproteinase-1, a natural inhibitor of matrix metalloproteinases, significantly decreased B cell migration across the HBECs. A comprehensive RT-PCR comparative analysis of all known matrix metalloproteinases and tissue inhibitors of metalloproteinases in human B and T cells revealed distinct profiles of expression of these molecules in the different cell subsets. Our results provide insights into the molecular mechanisms that underlie human B cell migration across the BBB. Furthermore, they identify potential common, and unique, therapeutic targets for limiting CNS B cell infiltration and predict how therapies currently developed to target T cell migration, such as anti-VLA-4 Abs, may impact on B cell trafficking.

Adult↗
PubMed2004

Prostaglandin E2-dependent enhancement of tissue inhibitors of metalloproteinases-1 production limits dendritic cell migration through extracellular matrix.

Dendritic cell (DC) migration is crucial for the initiation of immune responses. The balance between metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) has been shown to modulate DC migration. PGE2, which is overproduced in a wide variety of human malignancies, has been implicated in MMP and TIMP regulation in various cells, including monocytes. In the present study, we hypothesized that tumor-derived PGE2 would affect DC migratory capacity through the extracellular matrix (ECM) by altering MMP and TIMP balance. Treatment of monocyte-derived immature DC with exogenous PGE2 induced TIMP-1 secretion but not MMP-9 production and was correlated with reduced DC migration through ECM. Because recombinant TIMP-1 replicated PGE2 inhibition of DC migration while anti-TIMP-1 neutralizing Ab reversed it, we conclude that PGE2-mediated induction of TIMP-1 was responsible for the reduced migration of PGE2-treated DC. Similarly, DC cultured for 48 h in supernatants from cyclooxygenase-2 overexpressing lung cancer cells that secrete high levels of PGE2, exhibited decreased migration through ECM. Finally, analysis of E prostanoid receptor expression and their selective inhibition revealed that the enhanced TIMP-1 secretion in PGE2-treated DC was mediated predominantly by the E prostanoid receptor 2. These findings indicate that PGE2-dependent enhancement of TIMP-1 production causes reduced migration of DC through ECM.

16,16-Dimethylprostaglandin E2↗
PubMed2004

Levels of fecal corticosterone in sandhill cranes during a human-led migration.

Fourteen captive-reared greater sandhill cranes (Grus canadensis tabida) were conditioned to follow ultralight aircraft to promote migration between Wisconsin and Florida (USA) after release. Fecal samples were collected throughout the training period in Wisconsin and during a l977-km human-led migration to Florida to determine fecal corticosterone (FC) concentrations by radioimmunnoassay. The mean (+/-SE) FC concentration during the training period was 109.5 +/- 7.5 ng/g and was representative of baseline levels recorded previously from sandhill cranes. Fecal corticosterone concentrations increased in early migration compared to concentrations I mo prior to departure (P < 0.01) but were not different from baseline concentrations at tile end of the 6-wk migration period. The variability of FC concentrations in individual samples was greater throughout the migration than the training period. Increases in FC during migration were modest and generally consistent with normal corticosterone elevations observed in migrating birds.

Animal Migration↗
PubMed2001

Extracellular signals that regulate the tangential migration of olfactory bulb neuronal precursors: inducers, inhibitors, and repellents.

Neuronal migration is an essential developmental step in the construction of the vertebrate nervous system, but the extracellular signals involved in initiating and regulating neuronal movement remain unclear. Here we report the identification of a novel astrocyte-derived migration-inducing activity (MIA). Using an in vitro assay, we show that MIA induces the migration of olfactory bulb interneuron precursors, increasing the number of migrating cells and the distance they move. We established quantitative criteria to distinguish between the biological effects of inducers, inhibitors, repellents, and attractants on migrating cells and used them to compare the effects of MIA with those of Slit, a putative repulsive guidance cue. Our analysis demonstrates that, by themselves, MIA induces and Slit inhibits migration from subventricular zone explants. However, when presented together with MIA, Slit acts as a repellent. This study shows that glial cells play a critical role in initiating and modulating the movement of neuronal precursors through the release of a diffusible protein. Moreover, this study provides evidence that the guidance of migrating neuronal precursors is an integrative process, resulting from the cooperation of distinct extracellular factors, and that the function of Slit is context dependent.

Animals↗
PubMed1985

Macrophage migration inhibition test of peritoneal exudate cells of Litomosoides carinii-infected cotton rats by direct method in agar plate.

The macrophage migration inhibition test (MIT) was successfully made in agar plates using peritoneal exudate cells (PEC) of cotton rats, Sigmodon hispidus, during infection with Litomosoides carinii. It was found that 1% Bacto agar plate containing heat-inactivated serum was most suitable for the migration of PEC of the cotton rat induced by liquid paraffin injection. Ten percent normal cotton rat serum mixed in agar plate was best for PEC migration as compared with the various concentrations of horse, fetal and newborn calf sera. Migration areas of PEC from normal cotton rats increased with the number of cells per well and 2 X 10(6) cells/well was optimal. With concentrations of greater than or equal to 20 micrograms/ml of adult L. carinii antigen, significant migration inhibition of PEC from infected animals was observed from 18 hours after incubation at 37 degrees C with 5% CO2 gas phase, as compared with the migration of PEC from non-infected animals. Comparative analyses of the different aspects of infection showed that there was no correlation between the degree of migration inhibition and the duration of infection or the number of live worms recovered from the pleural cavity. Cell-mediated immunity against L. carinii as indicated by MIT still existed in 18 months after infection, although adult worms had died and were absorbed in the pleural cavity of the cotton rat.

Animals↗
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↗
PubMed1984

Lactoferrin stimulates the production of leucocyte migration inhibitory factor by human peripheral mononuclear leucocytes.

The effect of lactoferrin on the migration of human polymorphonuclear cells was investigated. High concentrations of lactoferrin (greater than 250 micrograms/ml) markedly inhibited the migration of granulocytes under agarose. This migration inhibition could not be neutralized by an antibody against leucocyte migration inhibitory factor (LIF), suggesting a direct effect of lactoferrin on the granulocytes. Low concentrations of lactoferrin were, however, indirectly capable of inhibiting neutrophil migration. The overnight culture of mononuclear leucocytes with low concentrations of lactoferrin (10 micrograms/ml) resulted in the release of granulocyte migration inhibiting factors in the cell free culture supernatant. Strong evidence indicating that the migration inhibiting factors were due to LIF, was obtained in experiments whereby the inhibitory activity could be completely neutralized by anti-LIF antibodies. The lactoferrin-mediated stimulation of LIF release by mononuclear leucocytes could be neutralized by an anti-lactoferrin serum, but not by an anti-albumin serum, whereas PPD-induced LIF release was not affected by either antiserum. These findings suggest that lactoferrin besides its well known anti-microbial properties, may also play a regulatory role in the migratory response of polymorphonuclear cells during inflammatory conditions.

Cell Movement↗
PubMed1984

[Leukocyte migration inhibitory factor of synovial fluid lymphocytes in rheumatoid arthritis].

Synovial fluid lymphocytes from patients with rheumatoid arthritis were examined for the presence of leukocyte migration inhibitory factor by the agarose technique of Clausen. T and B lymphocytes were stimulated with phytohemagglutinin, concanavalin A, and pokeweed mitogen, and the culture supernatants were used for the migration inhibitory test. Migration index of the culture supernatants of T cells from rheumatoid synovial fluids was significantly greater than those of peripheral blood from rheumatoid patients and healthy controls. The results indicated that the production of leukocyte migration inhibitory factor following stimulation by mitogens was decreased in the T cells of rheumatoid synovial fluid. In the rheumatoid synovial fluid there was a positive correlation between the migration index and polymorphonuclear leukocyte counts. A similar result was also obtained in the study of B cells from rheumatoid synovial fluid. These results suggest that the rheumatoid synovial lymphocytes have been already activated in the synovial fluid. On the other hand, the supernatants of rheumatoid synovial fluid showed an elevated migration index, exceeded 1.0 and higher than those of osteoarthritic synovial fluid. This suggests that chemotactic factors play an important part in the rheumatoid synovial fluid, though the leukocyte migration inhibitory factor is present in the rheumatoid fluid.

Adult↗
PubMed1982

Characterization of the lymphokine responsible for migration-inhibitory activity against tumor cells.

Lymphokine-containing supernatants have the ability to inhibit the migration of a variety of tumor cells in vitro in the absence of cytotoxic effects. In the present study, this tumor migration inhibition activity has been characterized in order to determine whether the responsible factor is the same or different from other known migration-inhibitory lymphokines. Since no preparations purified to homogeneity are generally available for these various factors, a variety of indirect procedures is necessary to make this determination. The profile of effects of monosaccharides, protease inhibitors, and neuraminidase on tumor migration inhibition factor, taken in conjunction with previously reported studies of other physicochemical and biological properties, provides evidence that tumor migration inhibition factor is distinct from both migration inhibition and leukocyte-inhibitory factor. A lymphokine with migration-inhibitory activity against tumor cells is a good candidate for a variety of protective functions in vivo.

Animals↗
PubMed1982

[Acetaldehyde-induced leukocyte migration inhibition in alcoholic liver diseases].

Acetaldehyde in non-toxic doses (15.6 micrograms per start) causes in the inhibition test of the migration of leucocytes an inhibition of the migration in 6/13 of the patients with alcoholic hepatitis, a stimulation of the migration in 6/11 of alcohol cirrhoses. Healthy (n = 16) persons, patients with alcoholic fatty degeneration of the liver (n = 3) as well as non-alcoholic liver diseases (chronic persisting hepatitis, n = 11; chronic active hepatitis, n = 8, cirrhosis, n = 7) did not show this cellular immune reagibility. The inhibition of the migration and the stimulation of the migration, respectively, might develop by hapten autoantigen complexes (altered cytoskeleton?) with release of the factors of inhibition of migration and stimulation of migration, in which case the role of a hapten belongs to acetaldehyde. The results of the tests did not correlate with functional and histological findings of the liver, with the actual consumption of alcohol and also not with haptoglobin phaenotypes. When it is postulated that by acetaldehyde also the release of further lymphokines is mediated, origin and progression of alcoholic hepatitis and alcoholic cirrhosis might be explained immunopathogenetically.

Acetaldehyde↗