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PubMed1992

Phalloidin prevents leukocyte emigration induced by proinflammatory stimuli in rat mesentery.

The objective of this study was to determine whether phalloidin, a potent microfilament stabilizer, can modify inflammatory mediator-induced leukocyte adhesion and extravasation in postcapillary venules of the rat mesentery. To address this issue, the rat mesentery was prepared for in vivo microscopic observation. Venules with initial diameters ranging between 25 and 35 microns were selected for study. Erythrocyte velocity, vessel diameter, leukocyte rolling velocity, and the number of adherent (stationary for 30 s) and emigrated leukocytes were initially determined during superfusion of the mesentery with phosphate-buffered saline. After these variables were recorded during the control period, either 100 nM platelet-activating factor (PAF), 20 nM leukotriene B4 (LTB4), or 1 microM N-formyl-methionyl-leucyl-phenylalanine (FMLP) was added to the superfusate. Repeat measurements were obtained between 50 and 60 min after initial exposure to the inflammatory mediator. In some experiments, rats were given phalloidin (25 or 500 micrograms/kg iv) 30 min before superfusion with the inflammatory mediators. Superfusion of the mesentery with either PAF, LTB4, or FMLP enhanced leukocyte adherence and emigration and reduced leukocyte rolling velocity. Pretreatment with the low dose of phalloidin effectively prevented leukocyte emigration but had no effect on the increased leukocyte adherence elicited by the three inflammatory mediators. However, when administered at the higher dose, phalloidin prevented both leukocyte adherence and emigration. Neither dose of phalloidin altered the upregulation of neutrophil membrane CD11/CD18 glycoprotein adherence complex induced by PAF or LTB4. These results are consistent with the concept that PAF, LTB4, and FMLP increase leukocyte extravasation by a process that may involve alterations in the endothelial cell cytoskeleton.

Animals↗
PubMed1994

Molecular determinants of lipid mediator-induced leukocyte adherence and emigration in rat mesenteric venules.

The objective of this study was to identify the molecular determinants of leukocyte rolling, adherence, and emigration elicited in postcapillary venules by the lipid mediators leukotriene B4 (LTB4) or platelet-activating factor (PAF). Leukocyte-endothelial cell adhesion and shear rate were monitored in rat mesenteric venules during superfusion with either LTB4 or PAF in the presence or absence of monoclonal antibodies (MAbs) directed against either leukocyte (CD18, CD11b) or endothelial cell [intercellular adhesion molecule 1 (ICAM-1), E-selectin, P-selectin] adhesion glycoproteins. In untreated animals and in animals receiving a nonbinding control MAb, LTB4 and PAF increased the number of both adherent (8- and 4-fold, respectively) and emigrated (14- and 8-fold, respectively) leukocytes, while reducing leukocyte rolling velocity (36 and 33%, respectively). The LTB4- and PAF-induced leukocyte adherence and emigration were significantly attenuated by pretreatment with MAbs directed against CD18, CD11b, ICAM-1, and E-selectin, but not P-selectin. The reduction in leukocyte rolling velocity induced by LTB4 was not affected by any of the MAbs; however, both P- and E-selectin MAbs significantly attenuated the reduction in leukocyte rolling velocity elicited by PAF. The results of this study indicate that the leukocyte adherence and emigration induced by both LTB4 and PAF are mediated by CD11b/CD18 on leukocytes and by ICAM-1 and E-selectin on endothelial cells. The molecular determinant of leukocyte rolling appears to be mediator specific, with the selectins mediating the rolling elicited by PAF.

Animals↗
PubMed1996

Ischemic preconditioning attenuates postischemic leukocyte adhesion and emigration.

Intravital microscopy was used to determine whether ischemic preconditioning (IPC; 5 min ischemia and 10 min reperfusion) would attenuate leukocyte adhesion and emigration induced by subsequent prolonged ischemia (60 min) and reperfusion (60 min) (I/R) in murine cremaster muscle and whether adenosine produced during IPC and/or reperfusion contributed to these beneficial effects. I/R elicited a marked increase in the number of adherent and emigrated leukocytes compared with the nonischemic control muscles, an effect that was largely prevented by IPC. Superfusion of the cremaster with adenosine deaminase only during IPC or only during 60-min reperfusion attenuated the inhibitory effect of IPC on postischemic leukocyte adhesion and emigration. However, the beneficial effects of IPC were mimicked in cremaster muscles preconditioned with adenosine (topical application for 10 min beginning 20 min before the onset of prolonged ischemia). Similar results were obtained in experiments in which adenosine was topically applied to the cremaster only during the 60-min reperfusion period. Our findings suggest that the ability of IPC to attenuate postischemic leukocyte adhesion and emigration may be mediated by adenosine released during IPC and during reperfusion after prolonged ischemia.

Adenosine↗
PubMed1995

Effect of pentoxifylline on changes in neutrophil sequestration and emigration in the lungs.

The response of neutrophils to inflammatory stimuli includes sequestration, adhesion, and migration. Pentoxifylline protects against many neutrophil-mediated lung injuries. This study investigated whether pentoxifylline prevented changes in neutrophil kinetics induced by infusion of complement fragments or neutrophil emigration induced by Streptococcus pneumoniae. Complement fragments were infused in New Zealand White rabbits treated with pentoxifylline or saline, and the circulating neutrophil counts in the arterial and venous blood samples were measured. Neutrophil emigration was induced by intrabronchial instillation of S. pneumoniae and quantitated morphometrically. The results show that, at doses achievable in vivo, pentoxifylline did not prevent either the CD18-dependent or -independent phase of complement-mediated neutrophil sequestration within the pulmonary microvasculature or the release of neutrophils from the bone marrow. Pentoxifylline also did not alter either the deformability of unstimulated leukocytes or stimulus-induced decreases in deformability. Finally, neutrophil emigration into the alveolar space was neither attenuated nor accentuated by pentoxifylline. These data suggest that, in vivo, pentoxifylline does not protect against lung injury by inhibiting neutrophil sequestration or emigration and may act to alter the generation of mediators that affect neutrophil behavior, rather than acting directly on neutrophils.

Animals↗
PubMed1995

Intratracheal injection of endotoxin and cytokines. IX. Contribution of CD11a/ICAM-1 to neutrophil emigration.

Intratracheal injection of endotoxin [lipopolysaccharide (LPS)] in rats causes acute inflammation characterized by the emigration of neutrophils (PMNs) into the bronchoalveolar airspace. Antibody to PMN adhesion molecule CD11a inhibited LPS-initiated PMN accumulation in bronchoalveolar lavage (BAL) fluid by 32% (P < 0.001). Antibody to the endothelial CD11a counterreceptor intercellular adhesion molecule-1 (ICAM-1) inhibited LPS-initiated PMN accumulation in BAL fluid by 66% (P < 0.0001). Combined antibody blockade of ICAM-1 and the C-X-C chemokine cytokine-induced neutrophil chemoattractant (CINC) inhibited LPS-initiated PMN emigration by 80%, significantly more than antibody against either ICAM-1 or CINC alone. To study the relative contribution of alveolar macrophages and PMNs to intra-alveolar tumor necrosis factor (TNF), the LPS-induced TNF in BAL fluid was measured after depletion of circulating PMNs with a cytolytic antibody to CD18. Although the anti-CD18 antibody completely abrogated LPS-initiated PMN emigration into BAL fluid, TNF levels in BAL fluid were unaffected, suggesting that alveolar macrophages are the predominant cellular source of LPS-induced TNF production. In conclusion, 1) CD11a, ICAM-1, and CINC play major roles in the LPS-initiated emigration of PMNs into the bronchoalveolar space, and 2) the TNF that drives ICAM-1 and CINC expression is derived largely from alveolar macrophages rather than PMNs.

Animals↗
PubMed1995

Antigen-independent maturation of CD2, CD11a/CD18, CD44, and CD58 expression on thymic emigrants in fetal and postnatal sheep.

We have compared the expression of CD2, CD11a/CD18, CD44, and CD58 and alpha beta and gamma delta T cells emigrating from the fetal and postnatal thymus. We report that both gamma delta and the CD4+CD8- and CD4-CD8+ subsets of alpha beta T cells express mature levels of the adhesion molecules CD11a/CD18, CD44, and CD58 upon emigration from the thymus. Whereas CD44 is up-regulated on gamma delta + thymocytes prior to export, down-regulation of both CD11a/CD18 and CD58 occurs prior to emigration from the thymus, suggesting that down-regulation of these molecules may be a final maturational step taken by developing gamma delta T cells before their export from the thymus. In contrast, there is continued up-regulation of CD2 on gamma delta and alpha beta T cells upon emigration from the thymus and as they move into the mature peripheral T-cell pool. There was also a marked reduction in the number of CD2+ gamma delta T cells exported during fetal development that was associated with a marked reduction in the percentage of CD2+ gamma delta thymocytes exported. The postthymic maturation of CD2 and the other changes in adhesion-molecule expression appear to be independent of extrinsic antigen, as the same changes were observed in the antigen-free environment of the fetus as in the postnatal lamb, which has been exposed to extrinsic antigen. It thus appears that these changes in adhesion-molecule expression are as a result of the normal maturation pathway from a developing thymocyte to a mature peripheral T cell.

Animals↗
PubMed1994

The role of cytoskeletal proteins in neutrophil emigration during pneumonia in rabbits.

The cytoskeletal proteins, actin and tubulin, are critical in modulating many aspects of the structural, mechanical, and biochemical properties of cells. This study determined if rearrangements of microtubules or filamentous actin were necessary for neutrophil margination within the pulmonary microvasculature or emigration into the alveolar spaces in response to Streptococcus pneumoniae. Microtubule assembly was inhibited using colchicine, and F-actin depolymerization was inhabited using phalloidin. Anesthetized rabbits received an intrabronchial instillation of S. pneumoniae either after intravenous pretreatment with colchicine (1 mg/kg every 2 h) or combined with TRITC-phalloidin (2 microM in instillate). Four hours later, the lungs were fixed and removed. The results show that the intravenous injection of colchicine caused a rapid decrease in circulating neutrophil counts, most likely caused by sequestration within the pulmonary microvasculature, that gradually recovered. In the pneumonic region, colchicine inhibited neutrophil emigration by 74 +/- 5%, but it did not prevent the stimulus-induced increase in margination. Phalloidin inhibited neutrophil emigration by 83 +/- 4%. These studies suggested that microtubule reassembly occurs during neutrophil transit through the normal pulmonary microvasculature and that it is required for migration but not sequestration during pneumonia. Rearrangement of actin filaments in lung cells but not neutrophils are required for neutrophil emigration induced by S. pneumoniae.

Actins↗
PubMed2002

Thymocyte emigration is mediated by active movement away from stroma-derived factors.

T cells leave the thymus at a specific time during differentiation and do not return despite elaboration of known T cell chemoattractants by thymic stroma. We observed differentiation stage-restricted egress of thymocytes from an artificial thymus in which vascular structures or hemodynamics could not have been playing a role. Hypothesizing that active movement of cells away from a thymic product may be responsible, we demonstrated selective reduction in emigration from primary thymus by inhibitors of active movement down a concentration gradient (chemofugetaxis). Immature intrathymic precursors were insensitive to an emigration signal, whereas mature thymocytes and peripheral blood T cells were sensitive. Thymic stroma was noted to elaborate at least two proteins capable of inducing emigration, one of which was stromal cell-derived factor-1. Thymic emigration is mediated, at least in part, by specific fugetaxis-inducing factors to which only mature cells respond.

Animals↗
PubMed1999

Accelerated emigration of B lymphocytes in the Xid mouse.

The B cell receptor is required for the emigration of newly generated B lymphocytes and for their maintenance in the periphery. A specific maintenance defect was noted in fraction I (IgDhighIgMlow) B cells in Xid mice (which harbor a mutation in Btk). Although Bcl-2 levels in fractions I and II (IgDhighIgMhigh) are equivalent in normal and Xid B cells, a novel peak of Bcl-2low fraction III (IgDlowIgMhigh) B cells was noted in the Xid mouse. Since this B cell population resembled bone marrow immature B cells, we examined the emigration of newly formed B cells in normal and Xid mice. These studies revealed the accelerated emigration of newly formed Xid B cells. We conclude that distinct Btk-independent and Btk-dependent signals mediate emigration and maintenance events during peripheral B cell maturation.

Agammaglobulinaemia Tyrosine Kinase↗
PubMed1988

["It is a new kind of diaspora ..." Some notes on the politics of psychanalysts emigration, according to E. Jones's correspondence with Anna Freud].

This paper is an attempt to describe the forced emigration of the Jewish and non Jewish German and Austrian psychoanalysts, to Great Britain and to America and other countries, during the nazi persecution started in Germany in 1933. The paper is mainly based on the unpublished correspondence between A. Freud and E. Jones and other documents. The paper deals with the two major waves of forced emigration from Berlin in 1933-1934 and from Vienna in 1938 and illustrates E. Jones's and A. Freud's attempts to organize and direct the emigration and all the problems, difficulties and political decisions connected with it. There were objective difficulties due to the economical and social situation of Great Britain and America at that time. Yet there were also the difficulties related to the internal conflicts of schools and personalities of the various national Societies belonging to the International Psychoanalytical Association chaired by Jones. Using some details of the correspondence, the paper tries to show the differences in tactics to deal with very delicate and complex issues, adopted by E. Jones and A. Freud at times, especially for what concerned the attempt to save psychoanalysis as an Institution in Germany. To illustrate the difficulties related to the acceptance of some psychoanalysts coming from Berlin or from Vienna, the paper focuses on W. Reich's episode as it was dealt with in the correspondence between A. Freud and E. Jones, and finally on the problems created in the British Psychoanalytical Society, by the emigration of S. Freud and his daughter to Great Britain.

Germany↗
PubMedDate not supplied

Emigration of activated leukocytes augments transvascular permeability in mesenteric venules of rat.

Effects of leukocyte adhesion and emigration on the microvascular permeability were analyzed by the combined use of high resolution transilluminated intravital microscopy and the epiilluminated fluorescent tracer imaging. After stimulating leukocytes by topical application of PAF-LPS or fMLP solution on the mesentery of a rat, a dynamic process of leukocyte emigration was visualized under high resolution transilluminated microscopic observation. When considerable emigration of leukocytes was observed, the same microvasculature was subjected to a permeability study to visualize the diffusional process of the FITC-labeled macromolecules under an epiilluminated fluorescent microscope. Dye diffusion was accelerated in the PAF-LPS or fMLP-treated group, and also a distinctly spotty leakage was observed in venules where successive adhesion and emigration of leukocytes were observed.

Animals↗
PubMed1990

Characterization of lymphatic and venous emigrants from the thymus.

Lymphocytes leaving the thymus via two different pathways were examined as to their morphology and phenotype. Cells leaving the thymus via lymphatics were obtained by a direct cannulation of thymic lymphatics and those leaving via the thymic vein were labelled within the thymus using an extracorporeal perfusion system and identified subsequently as fluorescent cells in the draining vein. In both cases the cervical thymus in lambs was used, since it is located in the neck region and ensures easy access to both blood and lymphatic vessels of the thymus without subjecting the animal to a major trauma or stress. Cells obtained from the thymic lymphatics or lymphatic emigrants were found to have distinct features different from peripheral T cells in terms of their surface morphology and expression of the MHC antigens. Venous emigrants were also slightly different from peripheral T cells in MHC expression. Estimation on the rate of thymocyte emigration into the periphery suggested that neither venous nor lymphatic emigrants represent a major fraction of de novo synthesized cells in the thymus of this animal species, as has been suggested in the mouse.

Animals↗
PubMed1988

Synergistic effects of LTB4 and LTD4 on leukocyte emigration into the guinea pig conjunctiva.

Leukotrienes (LT) B4 and D4, alone and in combination, were topically applied to the eyes of guinea pigs, and their effects on conjunctival leukocyte infiltration studied. LTD4 potentiated the neutrophil response to LTB4, even though no neutrophil emigration was evoked by LTD4 itself over a dose range of 10-1000 ng. LTB4 alone at the 1-ng and 10-ng doses failed to evoke any leukocyte emigration, but significant numbers of neutrophils were observed at these concentrations when LTD4 (1-1000 ng) was present. Although a dose-dependent increase in neutrophil infiltration was observed for the 100-ng and 1000-ng doses of LTB4, cell counts were substantially higher with these doses in the presence of LTD4. Eosinophil numbers increased in a dose-related manner in response to LTB4 and LTD4 alone, with a greater response to LTD4. The addition of either 10 ng or 100 ng of LTB4 to graded doses of LTD4 (10-1000 ng) caused increased eosinophil numbers, the lower dose of LTB4 potentiating the response to LTD4 and the higher LTB4 dose showing no significant effect. The effects on leukocyte infiltration that were evoked by the LT combinations could not be explained simply on the basis of an increase in vascular permeability. Bradykinin (BK), a potent conjunctival microvascular permeability factor that does not elicit any leukocyte infiltration, did not significantly potentiate LTB4-induced eosinophil or neutrophil emigration. The synergistic effects of LTs on leukocyte emigration are also difficult to ascribe to hyperemia (ie, increased blood volume in the conjunctiva), because both LTB4 and LTD4 caused only very modest increases in conjunctival blood content, and BK, which did not potentiate the leukocytic responses to LTB4, caused marked increases in tissue blood content. High-dose LT combinations caused eosinophils, but not neutrophils, to migrate into the conjunctival epithelium and fragment, resulting in overt tissue damage. These results further suggest a synergistic interaction between LTB4 and LTD4 that directly alters leukocyte function. The relevance of these observations to a number of disease and trauma states is discussed.

Animals↗
PubMed1988

T lymphocytes emigrating from the thymus to the spleen during postpartum regulate serum immunoglobulin levels in mice.

We noted an increase of a splenic T-cell population in early postpartum normal mice, but not in thymectomized (Tx) postpartum mice. The T-cell population consisted mainly of Lyt-1+2- cells and exerted suppressive activity in in vitro assays. To determine the in vivo function of these emigrant T lymphocytes during postpartum, we investigated the effect on immunoglobulin levels in the sera of mice, from pregnancy through the postpartum stages. A reduction in serum IgG1 levels in the late postpartum period was subsequent to the transitory elevation of IgG1 levels in early postpartum. However, this reduction of IgG1 was not seen in Tx mice at the late postpartum stage. To confirm the relationship between emigrant T cells and the immunoglobulin level, an adoptive transfer experiment was done. The level of IgG1 was reduced in the sera of recipients to which enriched splenic T cells from 3-day postpartum mice had been transferred. The data from the adoptive transfer experiment provided evidence that the increased T-cell population in mice in the early postpartum period regulates the IgG1 level in the serum. It was also recognized that T lymphocytes with the Lyt-1+2-phenotype, which emigrated from the thymus to the spleen after delivery, were able to suppress the IgG1, IgG2a,IgG2b levels in the serum. In addition, the appearance of the suppressive function of the Lyt-1+2- cells in these IgG subclasses required co-operation with the Lyt-1-2+ cells. Therefore, the thymus-dependent emigrant cells in the periphery in early postpartum mice may play a significant role in controlling immunoglobulin levels in the serum.

Animals↗
PubMed1986

Emigration of polymorphonuclear leucocytes into the intestinal lumen of the neonatal piglet in response to challenge with K88-positive Escherichia coli.

The emigration of neutrophils from the blood of neonatal piglets into the intestinal lumen in response to a K88-positive strain of Escherichia coli was investigated. The pig herd used was of known genetic susceptibility to K88-positive E coli and had recently experienced an outbreak of neonatal diarrhoea. Neutrophil emigration depended on certain factors. Neutrophils emigrated into ligated loops in susceptible piglets sucking immune colostrum from susceptible dams but not into loops in colostrum deprived resistant piglets or piglets sucking non-immune colostrum from resistant dams. In susceptible, colostrum deprived piglets neutrophils in intestinal contents were only associated with severe lesions. Large numbers of neutrophils which appeared at several foci on the villi were observed in three of six resistant piglets that sucked immune colostrum from susceptible dams. It was concluded that neutrophil emigration into the intestinal lumen of piglets could occur in response to K88-positive E coli and resulted not from the presence or absence of the intestinal K88-receptor but from the ingestion of immune colostrum.

Animals↗
PubMed1996

Defect of thymocyte emigration in a T cell deficiency strain (CTS) of the mouse.

As bone marrow progenitors migrate to the thymus, differentiate into immunologically competent T cells, then leave the thymus and home to the peripheral lymphoid organs, each migration or homing is an essentially critical process for T cell differentiation. Homing of thymocytes into peripheral lymphoid organs has been extensively analyzed. On the contrary, little is known about the mechanism whereby mature thymocytes emigrate from the thymus to peripheral lymphoid organs. In this work, we show that the mutant T cell deficiency strain (CTS) of mouse, previously described as a peripheral T cell deficiency strain, has a novel defect of mature thymocyte emigration process. Flow-cytometric analysis demonstrated a marked decrease in T lymphocytes in peripheral lymphoid organs and an accumulation of mature thymocytes in the thymus. Histologic study revealed the high concentration of thymocytes within the giant perivascular space at thymic corticomedullary junction. These accumulating cells closely resemble normal peripheral T lymphocytes in terms of cell surface phenotype and responsiveness to mitogens or allogeneic cells. They were found to express the Mel-14 Ag, the homing receptor to lymph nodes, and had a high capability of homing to peripheral lymphoid organs when explanted thymocytes were injected i.v. The intrathymic labeling methods detected hardly any emigrating CTS thymocytes from the thymus. These results indicate that emigration defect lies in the thymus of CTS mice, and suggest that this mutation is due to abnormal releasing mechanisms occurring between the thymus and the bloodstream. Complete delineation of the precise mechanisms of this defect, however, requires further studies.

Animals↗
PubMed1997

Absence of mast cell involvement in leukocyte adhesion and emigration induced by inhibition of nitric oxide synthase.

Leukocyte adhesion on venules and their emigration to extravascular connective tissue are induced by administration of a nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester. In the present study, the involvement of mast cells in the process was examined in genetically mast cell-deficient and normal rats by intravital microscopy. Superfusion of the NOS inhibitor into the mesentery induced partial degranulation of mast cells in normal rats. However, leukocyte adhesion on mesenteric venules and emigration to extravascular connective tissue occurred even in mast cell-deficient rats, with no significant difference from the normal rats. When the reverse-passive Arthus reaction, characterized by generalized antigen-antibody complex formation, was induced in the rat mesentery, the immune complex increased both the adhesion and emigration in normal rats but not in mast cell-deficient rats. These results show that mast cells are not involved in the leukocyte adhesion and emigration induced by NOS inhibition, but are in the reverse-passive Arthus reaction.

Animals↗
PubMed1994

International migration in China: a survey of emigrants from Shanghai.

"Migration trends have been largely unexamined in China, due to restrictive government policies and lack of data. This article presents the results of two surveys on emigrants from Shanghai, the largest source of emigrants and the only province with official migration records since 1958. Using information from the 1990 census, passport applications, and a survey of emigrant families in one city ward, the study concludes that migration policies, structural economic and social factors, and individual characteristics and needs shape migration patterns in Shanghai."

Asia↗