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PubMed1989

Dextran sulfate prevents LTB4-induced permeability increase, but not neutrophil emigration, in the hamster cheek pouch.

Leukotriene B4 (LTB4) is known to induce neutrophil-dependent macromolecular leakage in the hamster cheek pouch. LTB4 was superfused over cheek pouches dissected for intravital microscopy; and leukocyte rolling and firm adhesion in venules, neutrophil emigration, and macromolecular permeability as leakage of fluorescent dextran was quantified. Dextran sulfate (MW 500,000; 17.5 mg/kg iv bolus), but not uncharged dextran, reduced the LTB4-induced venular leakage of macromolecules by 85%. Histamine-induced leakage, which is neutrophil independent, was left unaffected. Dextran sulfate had no effect on leukocyte adhesion in postcapillary venules induced by LTB4, nor on their subsequent emigration to the surrounding tissue. Dextran sulfate significantly inhibited leukocyte rolling during nonstimulated conditions along the walls of collecting venules, but not postcapillary venules. Consequently, neutrophil-induced macromolecular leakage and neutrophil emigration appear to be independent, separable events. As an explanation of the present results it is proposed that the dextran sulfate complexes neutrophil granule cationic proteins, thus preventing neutrophil-mediated permeability increase.

Animals↗
PubMed1985

Effect of a fibrin(ogen)-derived vasoactive peptide on polymorphonuclear leukocyte emigration.

A vasoactive peptide known to increase vascular permeability and corresponding to residues 30-43 of the human fibrinogen B beta-chain induced polymorphonuclear leukocyte emigration in rabbit skin in vivo. The leukocyte emigration was much stronger after 2 h than after 0.5 h. Addition of prostaglandin E2 (PGE2) did not influence the chemotactic activity, which might possibly be explained by a known PGI2 releasing capacity of this peptide. PGE2 enhanced the leukocyte emigration due to leukotriene B4.

Animals↗
PubMed1992

Endothelial cell binding of NAP-1/IL-8: role in neutrophil emigration.

In this article Antal Rot calls into question the generally accepted notion that gradients of soluble chemotactic factors are responsible for leukocyte emigration from the circulation into sites of inflammation. He presents an alternative model in which chemoattractants bound to the surface of endothelial cells promote neutrophil adhesion and emigration, while soluble blood-borne attractants inhibit adhesion and emigration.

Animals↗
PubMed2004

A protocol for quantifying the birth, death and emigration rates of produce-associated bacteria, illustrated by its application to Salmonella enterica serovar Typhimurium on cultivated mushrooms.

Colony counts, counts of immunostained cells, fluorescent assays for cell viability and titration of a superinfecting bacteriophage were incorporated into a protocol for studying the growth kinetics of produce-associated bacteria in vivo. A set of equations was assembled for measuring the true rates of birth, death and emigration of the bacteria within the frame of a "transit growth" model, thus allowing the independent measurement of the carrying capacity of the substrate and of the overall productivity of the system. Implementation of the protocol on two species of cultivated mushrooms inoculated with Salmonella enterica serovar Typhimurium showed that large bacterial populations developed on Agaricus bisporus A15 but emigration was not detected, whereas resident populations on Agrocybe aegerita FAR142 amounted to 79.7%, 65.1% and 80.7% of the cultivable, dead and total bacterial cells produced, owing to emigration.

Agaricales↗
PubMed1999

Lymphocyte migration in the intestinal mucosa: entry, transit and emigration of lymphoid cells and the influence of antigen.

Lymphocyte migration is important to transport immunological information between the different compartments of the intestinal immune system. Large numbers of lymphocytes emigrate from the Peyer's patches and reach the blood circulation after expansion and maturation within the mesenteric lymph nodes. So far the frequency of antigen specific lymphocytes emigrating from the Peyer's patches after oral stimulation is not known. After mesenteric lymph node resection those cells emigrating from the intestinal wall are accessible by calculating the major intestinal lymph duct. The first antigen specific cells draining from the intestines are obviously not lymphocytes but dendritic cells, thus the antigen is rapidly trapped in the parenchyma of the lymph nodes in vivo. When lymphocytes were taken from intestinal lymph, labeled in vitro and retransfused, marked numbers of B-cells were re-detected in intestinal lymph. Later preferentially T-cells recirculated through the gut wall. After immigration into the intestinal lamina propria the lymphocytes may enter the space between epithelial cells, where they are present as intraepithelial lymphocytes. Lymphoid cells in the S-phase of the cell cycle have been detected in all compartments of the intestinal wall. Apoptosis is probably a further important mechanism for the regulation of intestinal immunity in removing cells reacting against harmless dietary antigens to maintain oral tolerance.

Animals↗
PubMed2003

Ventrally emigrating neural tube cells contribute to the normal development of heart and great vessels.

We investigated the contributions of a recently described population of neural tube cells, which participates in the development of a variety of tissues, to the development of the heart and great vessels. These cells, termed as the ventrally emigrating neural tube (VENT) cells, originate in the ventral part of the hindbrain neural tube, emigrate at the site of attachment of the cranial nerves, and populate their respective target tissues. VENT cells of the caudal hindbrain neural tube at the level of the vagus nerve, which were previously reported to migrate into the heart, were tagged with replication-deficient retroviruses containing the LacZ gene in chick embryos, after the emigration of neural crest from this region. In older embryos, VENT cells were detected in a variety of locations including the ventricles, atria, their septa, aorticopulmonary septum, and great vessels of the heart. Immunostaining with a specific marker revealed that VENT cells differentiated into smooth muscle cells of great vessels. Differentiation of VENT cells into cardiac muscle cells was reported previously. Extirpation of the VENT cells prior to their departure from the neural tube resulted in some common cardiovascular malformations: thin-walled ventricles and atria, ventricular and atrial septal defects, persistent truncus arteriosus, and stenosis of the great vessels. These results suggest that a novel population of neural tube cells also contributes to the normal development of the heart and great vessels. Thus, the heart and great vessels develop from three sources of cells: mesoderm, neural crest, and VENT cells.

Animals↗
PubMed2004

Continued maturation of thymic emigrants in the periphery.

Developing thymocytes are selected for recognition of molecules encoded by the major histocompatibility complex, purged of self-reactive cells and committed to either the CD4 or CD8 lineage. The 1% of thymocytes that complete these tasks emigrate and join the population of peripheral lymphocytes. Whether T cell maturation is complete at the time of thymic exit has been a subject of debate. Using mice transgenic for green fluorescent protein driven by the recombination activating gene 2 promoter to identify recent thymic emigrants, we now show that T cell differentiation continues post-thymically, with progressive maturation of both surface phenotype and immune function. In addition, the relative contribution of CD4 and CD8 recent thymic emigrants was modulated as they entered the peripheral T cell pool. Thus, T cell maturation and subset contribution are both finalized in the lymphoid periphery.

Animals↗
PubMed1997

Differential effect of L-NAME and S-methyl-isothiourea on leukocyte emigration in carrageenin-soaked sponge implants in rat.

1. The role of nitric oxide (NO) in leukocyte (polymorphonuclear cells, monocytes and lymphocytes) emigration was studied in a model of carrageenin-sponge implants in rats. 2. The subcutaneous implantation of 1% (w/v) of lambda-carrageenin-soaked sponges elicited an inflammatory response that was characterized by a time-related increase in leukocyte infiltration in the sponges and increased levels of nitrite in the exudate. Total leukocyte infiltration and nitrite production were maximal at 24 h and decreased after 48 and 96 h. The mononuclear cell influx was maximal at 48 h (21% of the total leukocytes). Therefore, this time point was used in the successive experiments. 3. Polymorphonuclear cell (PMN) and lymphocyte infiltration in the sponges significantly increased when rats were treated with the non-specific NO-synthase (NOS) inhibitor, NG-nitro-L-arginine methylester (L-NAME) (1 mg ml-1) in drinking water ad libitum). Monocyte emigration was not affected by L-NAME treatment. The nitrite levels in the exudate of L-NAME-treated rats were significantly reduced. The concomitant ingestion of L-arginine (30 mg ml-1) resulted in a reversion of the L-NAME effect, while D-arginine (30 mg ml-1) had no effect, indicating the involvement of the L-arginine: NO pathway. 4. Administration of L-NAME resulted also in an increased release of tumour necrosis factor-alpha (TNF-alpha) and prostacyclin (measured as the stable metabolite, 6-keto-PGF 1 alpha). L-NAME had no effect on monocyte chemoattractant protein-1 (MCP-1) release in the exudate. 5. Since L-NAME may have effects on the local blood flow, phenylephrine (0.034 mg ml-2) in drinking water) was used as it has an effect on the local blood flow similar to L-NAME. Phenylephrine had no effect on either leukocyte emigration, or on nitrite, TNF-alpha, prostacyclin or MCP-1 accumulation in the exudate. 6. In contrast, the more selective iNOS inhibitor S-methyl-isothiourea (SMT) (10 micrograms ml-1) in drinking water) significantly reduced PMNs and lymphocyte influx in the sponge having no effect on monocyte influx. Moreover, SMT decreased nitrite production in the exudate to a comparable extent as L-NAME. 7. Administration of SMT significantly reduced MCP-1 release in the exudate, without an effect on TNF-alpha or prostacyclin production. Moreover SMT did not produce any changes in local blood flow. 8. Our results show that a different outcome of the inflammatory process can be obtained depending on the types of NOS inhibitor used.

Animals↗
PubMed1998

Presence of miniature inverted-repeat transposable elements (MITEs) in the genome of Arabidopsis thaliana: characterisation of the Emigrant family of elements.

Although the genome of Arabidopsis thaliana has a small amount of repetitive DNA, it contains representatives of most classes of mobile elements. However, to date, no miniature inverted-repeat transposable element (MITE) has been described in this plant. Here, we describe a new family of repeated sequences that we have named Emigrant, which are dispersed in the genome of Arabidopsis and fulfil all the requirements of MITEs. These sequences are short, AT-rich, have terminal inverted repeats (TIRs), and do not seem to have any coding capacity. Evidence for the mobility of Emigrant elements has been obtained from the absence of one of these elements in a specific Arabidopsis ecotype. Emigrant is also present in the genome of different Brassicae and its TIRs are 74% identical to those of Wujin elements, a recently described family of MITEs from the yellow fever mosquito Aedes aegypti.

Arabidopsis↗
PubMed2004

Emigration of monocyte-derived cells from atherosclerotic lesions characterizes regressive, but not progressive, plaques.

Some monocytes normally take up residence in tissues as sessile macrophages, but others differentiate into migratory cells resembling dendritic cells that emigrate to lymph nodes. In an in vitro model of a vessel wall, lipid mediators lysophosphatidic acid and platelet-activating factor, whose signals are implicated in promoting atherosclerosis, blocked conversion of monocytes into migratory cells and favored their retention in the subendothelium. In vivo studies revealed trafficking of monocyte-derived cells from atherosclerotic plaques during lesion regression, but little emigration was detected from progressive plaques. Thus, progression of atherosclerotic plaques may result not only from robust monocyte recruitment into arterial walls but also from reduced emigration of these cells from lesions.

Animals↗
PubMed1996

Selectins and neutrophil traffic: margination and Streptococcus pneumoniae-induced emigration in murine lungs.

The roles of selectins in the pulmonary margination and emigration of neutrophils were investigated by using mice genetically deficient in both E- and P-selectins (E/P mutants) and/or by intravenous injections of fucoidin (inhibiting both L- and P-selectins). E/P mutants were neutrophilic (14.7 +/- 4.9 x 10(6) vs. 0.8 +/- 0.1 x 10(6) neutrophils/ml). This neutrophilia was associated with increased margination of neutrophils within pulmonary capillaries (39.7 +/- 9.4 vs. 4.6 +/- 1.1 neutrophil profiles per 100 red blood cell profiles) but no change in margination within noncapillary pulmonary microvessels. After intratracheal instillation of Streptococcus pneumoniae, lungs of E/P mutants displayed increased neutrophil emigration (564 +/- 92 vs. 116 +/- 19 neutrophils per 100 alveolar profiles), edema (5.3 +/- 1.5 vs. 1.5 +/- 0.4 microliter/g body weight), and histologic evidence of lung injury compared with those in wild-type (WT). Fucoidin treatment did not affect neutrophil emigration during streptococcal pneumonia in WT or E/P mice. During pneumonia, the number of white blood cells (WBC) tethered to or spread upon the noncapillary vessel endothelium increased in both WT and E/P lungs. These are the first data demonstrating that neutrophil margination in uninfected pulmonary capillaries does not require E- and P-selectins; that streptococcal pneumonia induces an E- and P-selectin-independent increase in WBC interactions with noncapillary endothelium; and that migration of neutrophils to alveoli can occur despite deficiency or inhibition of all of the known selectins.

Animals↗
PubMed2006

Intraluminal crawling of neutrophils to emigration sites: a molecularly distinct process from adhesion in the recruitment cascade.

The prevailing view is that the beta2-integrins Mac-1 (alphaMbeta2, CD11b/CD18) and LFA-1 (alphaLbeta2, CD11a/CD18) serve similar biological functions, namely adhesion, in the leukocyte recruitment cascade. Using real-time and time-lapse intravital video-microscopy and confocal microscopy within inflamed microvessels, we systematically evaluated the function of Mac-1 and LFA-1 in the recruitment paradigm. The chemokine macrophage inflammatory protein-2 induced equivalent amounts of adhesion in wild-type and Mac-1-/- mice but very little adhesion in LFA-1-/- mice. Time-lapse video-microscopy within the postcapillary venules revealed that immediately upon adhesion, there is significant intraluminal crawling of all neutrophils to distant emigration sites in wild-type mice. In dramatic contrast, very few Mac-1-/- neutrophils crawled with a 10-fold decrease in displacement and a 95% reduction in velocity. Therefore, Mac-1-/- neutrophils initiated transmigration closer to the initial site of adhesion, which in turn led to delayed transmigration due to movement through nonoptimal emigration sites. Interestingly, the few LFA-1-/- cells that did adhere crawled similarly to wild-type neutrophils. Intercellular adhesion molecule-1 but not intercellular adhesion molecule-2 mediated the Mac-1-dependent crawling. These in vivo results clearly delineate two fundamentally different molecular mechanisms for LFA-1 and Mac-1 in vivo, i.e., LFA-1-dependent adhesion followed by Mac-1-dependent crawling, and both steps ultimately contribute to efficient emigration out of the vasculature.

Animals↗
PubMed2002

Sodium nitroprusside decreases leukocyte adhesion and emigration after hemorrhagic shock.

UNLABELLED: The adhesion of polymorphonuclear leukocytes to the capillary endothelium is one of the key events in the pathophysiology of hemorrhagic shock. We studied sodium nitroprusside (SNP) for its ability to modulate leukocyte-endothelial cell interactions induced by hemorrhagic shock and reinfusion of blood by using intravital microscopy of the rat mesentery. Administration of SNP at a dose of 0.1 microg x kg(-1) x min(-1) infusion neither significantly decreased mean arterial blood pressure nor significantly altered bleedout volumes in hemorrhagic rats, indicating that SNP at this dose did not modify the severity of the shock protocol. Resuscitation from 1 h of hemorrhagic shock (mean arterial blood pressure approximately 45 mm Hg) significantly increased the number of adherent and emigrated leukocytes in the rat mesenteric microcirculation. However, infusion of SNP, started 15 min before hemorrhage, and continued over the entire experimental period, markedly reduced the leukocyte adhesion after reinfusion and emigration during hemorrhagic shock and after reinfusion. We concluded that the nitric oxide donor SNP is effective at reducing the leukocyte-endothelial interaction after blood reinfusion after hemorrhagic shock in rats. IMPLICATIONS: The i.v. infusion of 0.1 microg x kg(-1) x min(-1) of sodium nitroprusside, a dose that does not exert a significant vasodilator effect, reduces leukocyte adhesion and emigration after hemorrhagic shock.

Animals↗
PubMed1992

Reduction of leukocyte adherence and emigration by cyclosporine and L683,590 (FK506) in postcapillary venules.

Although the actions of immunosuppressive agents on lymphocytes are well characterized, their influence on leukocyte-endothelial cell adhesive interactions has not been defined. The objective of this study was to determine whether cyclosporine and L-683,590 (FK520) could modify the adhesion and emigration of leukocytes in postcapillary venules that are exposed to inflammatory mediators such as platelet activating factor (PAF) and leukotriene B4 (LTB4). The rat mesentery was prepared for in vivo microscopic observation. Venules with internal diameters ranging between 25 microns and 35 microns were selected for study. Erythrocyte velocity, vessel diameter, leukocyte rolling velocity, and the number of adherent (stationary for > 30 sec) and emigrated leukocytes were measured during superfusion of the mesentery with bicarbonate-buffered saline. Repeat measurements of adhesive and hemodynamic parameters were obtained between 50 and 60 min of superfusion with either 100 nM PAF or 20 nM LTB4 added to bicarbonate-buffered saline. In some experiments, animals were treated with either cyclosporine or L-683,590. Both PAF and LTB4 caused increases in leukocyte adherence and emigration, and reductions in leukocyte rolling velocity and venular shear rate. Cyclosporine prevented all of the adhesive and hemodynamic alterations induced by PAF, but not LTB4. L-683,590 was effective in preventing the responses elicited by both PAF and LTB4. These results indicate that modulation of leukocyte-endothelial cell adhesive interactions may represent a novel mechanism of action for cyclosporine and L-683,590.

Animals↗
PubMed1999

Neutrophil emigration in the lungs, peritoneum, and skin does not require gelatinase B.

Polymorphonuclear leukocytes (PMN) release gelatinase B in response to variable stimuli. Gelatinase B degrades basement membrane components in vitro, and inhibition of matrix metalloproteinase activity blunts PMN migration through a prototype basement membrane (Matrigel) and amnionic membranes. Accordingly, it has been speculated that gelatinase B is necessary for PMN emigration. To test this hypothesis we induced acute inflammation in the lungs, peritoneum, and skin in mice with a null mutation of the gelatinase B gene (gelatinase B-/-) and littermate controls (gelatinase B+/+). At 3, 6, 12, and 24 h after intratracheal instillation of LPS, the emigration of PMN in the lung, as determined by PMN in bronchoalveolar lavage fluid, was similar in gelatinase B-/- and gelatinase B+/+ mice. The number of PMN in the peritoneal cavity 4 h after thioglycollate-induced peritonitis was also comparable in gelatinase B-/- and gelatinase B+/+ mice. At 4 h after an intradermal injection of interleukin-8, numerous PMN were present extravascularly in the dermis in both gelatinase B-/- and gelatinase B+/+ mice and the myeloperoxidase activities of the skin at the injection sites were indistinguishable between the two types of mice. PMN from gelatinase B-/- mice migrated through Matrigel in response to zymosan-activated serum with the same efficiency as did PMN from gelatinase B+/+ mice. In vitro, gelatinase B-/- PMN killed Staphylococcus aureus and Klebsiella pneumoniae as effectively as did PMN from gelatinase B+/+ mice. These findings indicate that gelatinase B is not required for PMN emigration, and suggest that the antibacterial function of PMN is preserved despite gelatinase B deficiency.

Animals↗
PubMed1992

Lamella formation and emigration from the water by a laboratory colony of Biomphalaria glabrata (Say) in a flow-through system.

Lamella formation and emigration from the water were investigated in juvenile Biomphalaria glabrata reared at two temperatures in aquaria with a constant water flow. Most snails (97.4%) reared at the lower temperature (21 degrees C) formed lamella at the shell aperture and emigrated from the water, whereas only 10.1% did so at 25 degrees C. Eighty percent of emigrations at 21 degrees C occurred within a period of 15 days, 70-85 days after hatching. A comparison of the studies done so far indicates that the phenomenon may be affected by the ageing of snail colonies kept in the laboratory and their geographic origin, rather than the rearing conditions. This hypothesis, however, requires experimental confirmation.

Age Factors↗
PubMed1999

Cutting edge: secondary lymphoid-tissue chemokine (SLC) and CC chemokine receptor 7 (CCR7) participate in the emigration pathway of mature dendritic cells from the skin to regional lymph nodes.

Dendritic cells (DCs) emigrate to regional lymph nodes (LNs) during immune responses via afferent lymphatic channels. Secondary lymphoid-tissue chemokine (SLC), a CC chemokine, is expressed in secondary lymphoid organs and mediates the chemotaxis of lymphocytes and DCs via its receptor, CC chemokine receptor 7 (CCR7). By dual-label fluorescence confocal microscopy, we showed MHC class II-positive cells within SLC-staining lymphatic channels in the mouse dermis. SLC was a potent in vitro chemoattractant for cultured, migratory skin DCs, and it enhanced the emigration of MHC class II-positive DCs from mouse skin explants by an average of 2.5-fold. Mature or cytokine-activated, but not resting, Langerhans cells expressed CCR7 mRNA by RT-PCR. Anti-SLC Abs, but not control or anti-eotaxin Abs, blocked the in vivo migration of 51Cr-labeled, skin-derived DCs from footpads to draining LNs by 50% (n = 9, p < 0. 005). Thus, we provide direct evidence that SLC and CCR7 participate in the emigration of DCs from peripheral tissue to LNs via lymphatics.

Animals↗
PubMed2005

Relationship between changes in thymic emigrants and cell-associated HIV-1 DNA in HIV-1-infected children initiating antiretroviral therapy.

OBJECTIVES AND METHODS: To investigate the relationship between cell-associated HIV-1 dynamics and recent thymic T-cell emigrants, HIV-1 DNA and T-cell receptor rearrangement excision circles (TREC, a marker of recent thymic emigrants) were measured in peripheral blood mononuclear cells in 181 samples from 33 HIV-1-infected children followed for 96 weeks after antiretroviral therapy (ART) initiation. RESULTS: At baseline, HIV-1 DNA was higher in children with higher TREC (P=0.02) and was not related to age, CD4 or HIV-1 RNA in multivariate analyses (P>0.3). Overall, TREC increased and HIV-1 DNA decreased significantly after ART initiation, with faster HIV-1 DNA declines in children with higher baseline TREC (P=0.009). The greatest decreases in HIV-1 DNA occurred in children with the smallest increases in TREC levels during ART (P=0.002). However, this inverse relationship between changes in HIV-1 DNA and TREC tended to vary according to the phase of HIV-1 RNA decline (P=0.13); for the same increase in TREC, HIV-1 DNA decline was much smaller during persistent or transient viraemia compared with stable HIV-1 RNA suppression. CONCLUSIONS: Overall, these findings indicate that TREC levels predict HIV-1 DNA response to ART and suggest that immune repopulation by thymic emigrants adversely affects HIV-1 DNA decline in the absence of persistent viral suppression, possibly by providing a cellular source for viral infection and replication.

Adolescent↗