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PubMed1998

Emigration of mature T cells from the thymus is inhibited by the imidazole-based compound 2-acetyl-4-tetrahydroxybutylimidazole.

The primary role of the thymus is to provide mature T cells for the peripheral immune system. The mechanisms involved in the cellular export processes are as yet unknown. In this study, we examined the ability of 2-acetyl-4-tetrahydroxybutylimidazole (THI), an agent widely used as a component of ammonia caramel food colouring, to inhibit T-cell export from the thymus. BALB/c mice were maintained on drinking water containing THI for 5 days. The mice showed a twofold increase in the total number of mature medullary thymocytes (CD4+CD8- and CD4-CD8+) as well as a slight decrease in the total number of immature double-positive cells (CD4+CD8+). The mature single-positive thymocytes were found to express high levels of the homing molecule L-selectin, suggesting that these potential emigrants were prevented from leaving the thymus. To confirm this, THI-treated mice were injected intrathymically with fluorescein isothiocyanate and the number of labelled T cells appearing in the lymph nodes and spleen was determined 16 hr later. A 10-fold decrease in the number of CD4+ and CD8+ recent thymic emigrants in the lymph nodes and spleen of THI-treated mice was observed. Previous studies have shown that THI does not affect other aspects of thymocyte development, such as proliferation and differentiation. Taken together, these results suggest that the immunosuppressive effects of THI may be due, in part, to preventing of the final step of T-cell export out of the thymus.

Animals↗
PubMed2006

A unique lymphotoxin {alpha}beta-dependent pathway regulates thymic emigration of V{alpha}14 invariant natural killer T cells.

Natural killer (NK) T cells using an invariant Valpha14 (Valpha14i) T cell receptor rearrangement form a distinct immunoregulatory T cell lineage. Several studies indicated that a NK1.1(-) Valpha14i NKT precursor cell differentiates and expands within the thymus before export to the peripheral tissues occurs. However, little is known about the signals that cause the emigration of Valpha14i NKT cells from the thymus to the periphery. Here we show that signaling of lymphotoxin (LT) alphabeta through the LTbeta receptor (LTbetaR) is indispensable for regulating peripheral but not thymic Valpha14i NKT cell numbers. Homing to and homeostatic proliferation of thymic Valpha14i NKT cells in peripheral organs, however, was not dependent on LTbetaR. Instead, our data indicate that a LTbetaR-expressing thymic stromal cell regulates the thymic emigration of Valpha14i NKT cells but not conventional T cell receptor alphabeta cells.

Animals↗
PubMed2001

Oxygen radical generation by emigrated, intra-abdominal, and circulating PMNLs during human secondary peritonitis.

The purpose of the study was to characterize oxygen radical generation by emigrated, intraabdominal and circulating polymorphonuclear leukocytes (ePMNLs and cPMNLs) during peritonitis, as well as to assess any differences between oxygen radical production in patients with low Mannheim peritonitis index (MPI < 26, group 1) or high Mannheim peritonitis index (MPI > or = 26, group 2). Lucigenin-enhanced chemiluminescence was used to determine spontaneous and stimulated (FMLP, PMA, and A23 187) oxygen radical generation by ePMNLs and cPMNLs. In group 1 spontaneous and stimulated oxygen radical generation by emigrated PMNLs was markedly enhanced compared to circulating PMNLs (e.g., spontaneous oxygen radical generation: 30.3 +/- 11.8 cpm/cPMNLs versus 107 +/- 46 cpm/ePMNLs, P < 0.05) . In group 2 oxygen radical generation by cPMNLs markedly increased within 48 h after diagnosis of peritonitis and surgery, contrary to radical generation by ePMNLs (e.g., A23 187-stimulated oxygen radical generation 993.7 +/- 350 cpm/cPMNLs versus 285.6 +/- 77 cpm/ePMNLs, P < 0.05. In conclusion, cPMNLs and ePMNLs exhibit marked polymorphism in their capacity to generate oxygen radicals in response to secondary peritonitis. Severe peritonitis (MPI - 26) was associated with a strong increase in oxygen radical generation by cPMNLs without a parallel activity being manifest by ePMNLs.

Abdomen↗
PubMed1990

Increased vascular permeability, erythema, and leukocyte emigration induced in rabbit skin by streptococcal erythrogenic toxin type A.

A highly purified streptococcal erythrogenic toxin type-A (SET-A) caused increased vascular permeability, erythema, and leukocyte emigration when injected into the skin of rabbits. A blueing reaction indicating increased vascular permeability appeared at 1 h, reaching the highest intensity between 4 and 5 h, decreasing thereafter and completely disappearing at 12 h after toxin injection. The intensity of the increase in permeability was found to be dose dependent. The erythematous reaction began later and persisted longer than the blueing. The time course of leukocyte emigration was found roughly to parallel that of the blueing reaction. The skin reaction to SET-A in rabbits can be characterized as having an acute non-specific exudative inflammatory nature.

Animals↗
PubMed2005

Levels of recent thymic emigrant cells decrease in children undergoing partial thymectomy during cardiac surgery.

The human thymus is required for establishment of a T-cell pool in fetal life, but postnatal thymectomy is not known to cause immunodeficiency. T-cell emigration from thymus (thymic recent emigrants [TRECs]) is a continuous thymic-dependent process. We studied TREC levels pre- and post-partial thymectomy in children undergoing cardiac surgery. TRECs were quantitated by real-time PCR in peripheral blood lymphocytes of 24 children (0 to 12 years). TREC values were 47916 +/- 9271 pre-partial thymectomy and 33157 +/- 8479 post-partial thymectomy in 11 paired patients (P = 0.014). Interval between pre- and post-partial thymectomy was 8.8 days +/- 5.8 days. Another group of 8 children had 30384 +/- 9748 TRECs 16 days to 6 years post-partial thymectomy. There was a significant drop in TREC values post-partial thymectomy in the immediate postoperative period compared to prethymectomy TREC levels. While decreased thymic output may persist, the long-term implications were not evaluated in this patient population.

Cardiac Surgical Procedures↗
PubMed2000

Systemic hypoxia increases leukocyte emigration and vascular permeability in conscious rats.

We recently observed that acute systemic hypoxia produces rapid increases in leukocyte adherence in the mesenteric microcirculation of the anesthetized rat Wood JG, Johnson JS, Mattioli LF, and Gonzalez NC. J Appl Physiol 87: 1734-1740, 1999; Wood JG, Mattioli LF, and Gonzalez NC. J Appl Physiol 87: 873-881, 1999. Hypoxia-induced leukocyte adherence is associated with an increase in reactive oxygen species (ROS) generation and is attenuated by antioxidants or interventions that increase tissue levels of nitric oxide (NO). These results suggest that the acute effects of hypoxia on leukocyte-endothelial interactions are caused by a change in the ROS-NO balance. The present experiments were designed to extend our observations of the initial microcirculatory response to hypoxia; specifically, we wanted to determine whether the response to systemic hypoxia involves increased microvascular permeability and leukocyte emigration and whether ROS generation and decreased NO levels contribute to these responses. At this time, there is conflicting evidence, from in vitro studies, regarding the effect of hypoxia on these indexes of vascular function. Our studies were carried out in the physiological setting of the conscious animal, in which a prolonged hypoxic exposure is possible without the adverse effects that may develop under anesthesia. The central observation of these studies is that conscious animals exposed for 4 h to environmental hypoxia show increased microvascular permeability and emigration of leukocytes into the extravascular space of the mesenteric circulation. Furthermore, these events are dependent on increased ROS generation and, possibly, a subsequent decrease in tissue NO levels during systemic hypoxia. Our results show that systemic hypoxia profoundly affects vascular endothelial function through changes in the ROS-NO balance in the conscious animal.

Animals↗
PubMed2002

Molecular pathways of monocyte emigration into the alveolar air space of intact mice.

The adhesive interactions involved in monocyte recruitment to the alveolar space in vivo are only poorly defined. To study these interactions, we used a recently developed mouse model that allowed the separation and quantification of freshly recruited monocytes, resident alveolar macrophages (rAM), neutrophils, and lymphocytes in the bronchoalveolar compartment by fluorescence activated cell sorting technology. In these mice, the combined intratracheal administration of the monocyte chemoattractant JE/monocyte chemotactic protein (MCP)-1 and low dose Escherichia coli lipopolysaccharide (LPS) induces a self-limiting pulmonary inflammatory response, characterized by well-controlled sequelae of both neutrophil and monocyte emigration into the alveolar space. In contrast, challenge with JE/MCP-1 provokes the emigration only of monocytes in the absence of lung inflammation. Using an array of function-blocking monoclonal antibodies (mAb) (anti-CD11a, -CD11b, -CD18, -CD49d, -CD54, and -CD106), we characterized the adhesive interactions underlying the transendothelial and transepithelial leukocyte traffic in intact animals. Alveolar monocyte recruitment elicited by JE/MCP-1 alone was strictly dependent on CD11b/CD18, CD54, and CD49d, and partly dependent on CD11a, but not dependent on CD106. In response to JE/MCP-1 plus E. coli LPS, we observed additional engagement of CD11a and CD106 for enhanced alveolar monocyte transmigration. Comigrating neutrophils were found to primarily utilize CD11b, CD18, and CD54, but not CD49d, CD106, or, surprisingly, CD11a. This contrasted with the effect of CD11a on alveolar challenge with macrophage inflammatory protein (MIP)-1alpha instead of JE/MCP-1. In conclusion, we found that in an intact mouse model allowing detailed phenotyping of leukocyte traffic into the alveolar space, the molecular pathways involved in JE/MCP-1-driven monocyte efflux differed under noninflammatory and inflammatory (presence of LPS) conditions. Moreover, the profile of adhesive interactions underlying the monocyte efflux differed from that characterizing neutrophil trafficking.

Animals↗
PubMed1997

Neutrophil margination, sequestration, and emigration in the lungs of L-selectin-deficient mice.

These studies tested the hypothesis that L-selectin plays a role in neutrophil traffic in the lungs, particularly in neutrophil margination, sequestration, and emigration, using L-selectin-deficient mice. No defect in neutrophil margination within either capillaries or arterioles and venules was observed in uninflamed lungs of L-selectin-deficient mice. The initial rapid sequestration of neutrophils within the pulmonary capillaries 1 min after intravascular injection of complement fragments was not prevented. In contrast, L-selectin did contribute to the prolonged neutrophil sequestration (> or = 5 min). Interestingly, neutrophil accumulation within noncapillary microvessels required L-selectin at both 1 and 5 min after complement injection. During bacterial pneumonias, L-selectin played a role in neutrophil accumulation within noncapillary microvessels in response to either Escherichia coli or Streptococcus pneumoniae and within capillaries in response to E. coli but not S. pneumoniae. However, L-selectin was not required for emigration of neutrophils or edema in response to either organism. These studies demonstrate a role for L-selectin in the prolonged sequestration of neutrophils in response to intravascular complement fragments, in the intracapillary accumulation of neutrophils during E. coli-induced pneumonia, and in the accumulation of neutrophils within noncapillary microvessels when induced by either intravascular complement fragments or

Animals↗
PubMed1997

LFA-1 is sufficient in mediating neutrophil emigration in Mac-1-deficient mice.

To better define the specific function of Mac-1 (CD11b) versus LFA-1 (CD11a) and the other CD11 integrins in vivo, we have disrupted murine CD11b by targeted homologous recombination in embryonic stem cells and generated mice which are homozygous for a mutation in CD11b. A null mutation was confirmed by Southern blotting, RNase protection assay, immunohistochemistry, and flow cytometry. Neutrophils isolated from mice deficient in Mac-1 were defective in adherence to keyhole limpet hemocyanin-coated glass, iC3b-mediated phagocytosis, and homotypic aggregation. When challenged by thioglycollate intraperitoneally, Mac-1-deficient mice had similar levels of neutrophil accumulation in the peritoneal cavity at 1, 2, and 4 h. Treatment with mAb to LFA-1 blocked 78% of neutrophil accumulation in Mac-1-deficient mice and 58% in wild-type mice. Neutrophil emigration into the peritoneal cavity 16 h after the implantation of fibrinogen-coated disks was not reduced in Mac-1-deficient mice whereas neutrophil adhesion to the fibrinogen-coated disks was reduced by > 90%. Neutrophils from Mac-1-deficient mice also showed reduced degranulation. Our results demonstrate that Mac-1 plays a critical role in mediating binding of neutrophils to fibrinogen and neutrophil degranulation, but is not necessary for effective neutrophil emigration, which is more dependent upon LFA-1.

Animals↗
PubMed1995

Correlation of CSF 5-HIAA concentration with sociality and the timing of emigration in free-ranging primates.

OBJECTIVE: The purpose of this study was to examine the relationship between behavior and serotonin in nonhuman primates. METHOD: During a routine capture and medical examination, 26 adolescent male rhesus macaques (Macaca mulatta) were selected as subjects from a free-ranging population of 4,500 rhesus monkeys inhabiting a 475-acre sea island. Blood samples (N = 23) and CSF samples (N = 22) were obtained, and each subject was fitted with a radio transmitter collar for rapid location. The subjects were released into their social groups, and quantitative behavioral observations were made over a 3-month period. RESULTS: CSF 5-hydroxyindoleacetic acid (5-HIAA) concentration was positively correlated with three measures of sociality: 1) total time spent grooming others, 2) total time spent in close proximity to other group members, and 3) mean number of neighbors within a 5-m radius. In addition, CSF 5-HIAA concentration was positively correlated with age at emigration from the natal group (in months). CONCLUSIONS: In adolescent male rhesus macaques living in naturalistic settings, CSF 5-HIAA concentration is positively correlated with affiliative sociality. Rhesus males with low CSF 5-HIAA concentrations exhibit less social competence and emigrate from their social groups at a younger age than do males with higher concentrations of CSF 5-HIAA.

Age Factors↗
PubMed2000

Inhibition of noggin expression in the dorsal neural tube by somitogenesis: a mechanism for coordinating the timing of neural crest emigration.

We have previously shown that axial-dependent delamination of specified neural crest cells is triggered by BMP4 and negatively regulated by noggin. Increasing activity of BMP4 towards the rostral part of the axis is achieved by graded expression of noggin in the dorsal neural tube, the latter being high opposite unsegmented mesoderm, and progressively downregulated facing epithelial and dissociating somites, coinciding in time and axial level with initial delamination of neural crest cells (Sela-Donenfeld, D. and Kalcheim, C. (1999) Development 126, 4749-4762). Here we report that this gradient-like expression of noggin in the neuroepithelium is controlled by the paraxial mesoderm. Deletion of epithelial somites prevented normal downregulation of noggin in the neural tube. Furthermore, partial ablation of either the dorsal half or only the dorsomedial portion of epithelial somites was sufficient to maintain high noggin expression. In contrast, deletion of the segmental plate had no effect. These data suggest that the dorsomedial region of developing somites produces an inhibitor of noggin transcription in the dorsal neural tube. Consistent with this notion, grafting dissociating somites in the place of the unsegmented mesoderm precociously downregulated the expression of noggin and triggered premature emigration of neural crest progenitors from the caudal neural tube. Thus, opposite the unsegmented mesoderm, where noggin expression is high in the neural tube, BMP4 is inactive and neural crest cells fail to delaminate. Upon somitogenesis and further dissociation, the dorsomedial portion of the somite inhibits noggin transcription. Progressive loss of noggin activity releases BMP4 from inhibition, resulting in crest cell emigration. We propose that this inhibitory crosstalk between paraxial mesoderm and neural primordium controls the timing of neural crest delamination to match the development of a suitable mesodermal substrate for subsequent crest migration.

Animals↗
PubMed1991

Chemical communication of emigration behavior of Drosophila melanogaster. II. Identification of chemical substances.

Two chemical substances isolated from adult flies of Drosophila melanogaster differently affected the emigration activity of genetically different strains. These substances were identified as palmitic acid and oleic acid, respectively. Chemical and biological comparisons of the natural and authentic compounds showed them to be identical. The behavior response was dependent on the concentration of these fatty acids. The two chemical substances are excreted by adult flies, both male and female, but the emigration activity of one strain was affected by only palmitic acid and that of the other strain, by only oleic acid.

Animals↗
PubMed2001

Black cutworm (Lepidoptera: Noctuidae) larval emigration and biomass in mixtures of endophytic perennial ryegrass and Kentucky bluegrass.

Studies examined the possibility that mixtures of endophytic perennial ryegrass and Kentucky bluegrass provide resistance against larvae of the black cutworm, Agrotis ipsilon (Hufnagel). We hypothesized that resistance against A. ipsilon in such stands would stem from the influence of Kentucky bluegrass on A. ipsilon growth and behavior rather than the influence of endophytic perennial rvegrass. In replicated greenhouse experiments, black cutworm larvae initially emigrated more quickly from pots containing monocultures of endophytic perennial ryegrass than from Kentucky bluegrass monocultures or polycultures of Kentucky bluegrass and endophytic perennial ryegrass. However, biomass of emigrating larvae decreased linearly as the proportion of Kentucky bluegrass increased. Turfgrass mixtures containing endophytic perennial ryegrass and Kentucky bluegrass may provide resistance against A. ipsilon mainly through the physiological effects of Kentucky bluegrass on A. ipsilon growth and development, but possibly through the influence of endophytic perennial ryegrass on A. ipsilon movement and foraging behavior as well.

Animal Migration↗
PubMed2004

Schistosoma mansoni: antigen-presenting cells emigrating from skin exposed to attenuated cercariae activate lymphoid cells and transfer protection in C57B1/6 mice.

C57B1/6 mice develop significant levels of protection to a challenge infection after percutaneous exposure to irradiated Schistosoma mansoni cercariae. Although some circumstantial evidence has suggested that antigen-presenting cells (APCs) within the skin play a role in priming anti-schistosomula effector mechanisms, no direct evidence has been presented. In this study, we describe efforts to directly test whether skin-resident APCs exposed to irradiated cercariae are capable of mediating responses consistent with previously proposed mechanisms associated with delayed-type hypersensitivity reactions. We demonstrate that a population of APCs emigrates from the skin after percutaneous vaccination and that these cells are able to induce proliferation of S. mansoni-specific lymphocytes. We describe our experiments conducted to confirm that proliferation is dependent on major histocompatibility complex (MHC) Class-II interactions and cell-to-cell contact between APCs and lymphocytes. Immunohistological staining of emigrating cells revealed a population of large MHC Class-II+ cells with a morphology characteristic of mature dendritic cells. On recovery and adoptive transfer into naive mice, these cells demonstrated the ability to mediate protection to a challenge infection at levels similar to those in percutaneously vaccinated controls. This confirms that cutaneous APCs can initiate anti-schistosomula effector mechanisms in C57B1/6 mice after percutaneous vaccination.

Adoptive Transfer↗
PubMed2004

Platelet endothelial cell adhesion molecule deficiency or blockade significantly reduces leukocyte emigration in a majority of mouse strains.

PECAM is a molecule used specifically during the diapedesis step when neutrophils and monocytes leave the blood compartment. Anti-PECAM reagents, such as Abs and soluble fusion proteins, block diapedesis both in vivo and in vitro. However, the PECAM knockout mouse in C57BL/6 strain has no serious defects in most models of inflammation. We show in this study that the same PECAM knockout backcrossed into the FVB/n strain clearly has reduced leukocyte emigration in two models of inflammation. Furthermore, we show that anti-PECAM reagents can block leukocyte emigration in several other wild-type strains of mice like FVB/n, SJL, and the outbred strain Swiss Webster. This clearly shows that the C57BL/6 strain is uniquely able to compensate for the loss of PECAM function. Murine models of inflammatory disease that have been studied using C57BL/6 mice should be re-evaluated using FVB/n or other mouse strains to determine whether PECAM plays a role in those models.

Animals↗
PubMed2006

Intradermal delivery of adenoviral type-35 vectors leads to high efficiency transduction of mature, CD8+ T cell-stimulating skin-emigrated dendritic cells.

Recombinant adenovirus (Ad) type 35 (rAd35) shows great promise as vaccine carrier with the advantage of low pre-existing immunity in human populations, in contrast to the more commonly used rAd5 vector. The rAd35 vector uses CD46 as a high-affinity receptor, which, unlike the rAd5 receptor, is expressed on human dendritic cells (DC), the most powerful APCs identified to date. In this study, we show that in contrast to rAd5, rAd35 infects migrated and mature CD83+ cutaneous DC with high efficiency (up to 80%), when delivered intradermally in an established human skin explant model. The high transduction efficiency is in line with high expression levels of CD46 detected on migratory cutaneous DC, which proved to be further increased upon intradermal administration of GM-CSF and IL-4. As compared with Ad5, these Ad35 infection characteristics translate into higher absolute numbers of skin-emigrated DC per explant that both express the transgene and are phenotypically mature. Finally, we demonstrate that upon intracutaneous delivery of a rAd35 vaccine encoding the circumsporozoite (CS) protein of Plasmodium falciparum, emigrated DC functionally express and process CS-derived epitopes and are capable of activating specific CD8+ effector T cells, as evidenced by activation of an HLA-A2-restricted CS-specific CD8+ T cell clone. Collectively, these data demonstrate the utility of rAd35 vectors for efficient in vivo human DC transduction.

Adenoviruses, Human↗
PubMed1986

The role of interleukin-1 in neutrophil leukocyte emigration induced by endotoxin.

Chemotactic factors induce neutrophil emigration into tissues. Interleukin-1 (IL-1) was found to be several log times more potent in this respect than C5a des Arg, leukotriene B4, and f-Met-Leu-Phe and of comparable potency to endotoxin. Kinetic studies revealed a rapid and transient neutrophil influx, with the peak rate at 30-90 minutes. Cross tachyphylaxis was observed between IL-1 and endotoxin; and this, together with its high potency and rapid onset of action, suggest that IL-1 mediates endotoxin-induced neutrophil emigration.

Animals↗
PubMed1996

In vivo fate of the inflammatory macrophage during the resolution of inflammation: inflammatory macrophages do not die locally, but emigrate to the draining lymph nodes.

The resolution of acute inflammation requires bulk clearance of extravasated inflammatory cells in an ordered manner. Neutrophils undergo apoptosis and are ingested by macrophages (M psi) via a novel recognition mechanism that fails to provoke proinflammatory responses. Thereafter, the fate of inflammatory M psi themselves remains unclear. We investigated this in vivo, developing a semiallogeneic adoptive transfer system to track the fate of inflammatory M psi in a murine model of resolving peritonitis. Fluorescently labeled M psi from H-2k/d mice were transferred into the peritoneal cavity of H-2k mice at the same stage of resolving inflammation as the donor mice. Dual color flow cytometry permitted discrimination among donor cells, recipient cells, and donor cells that had been phagocytosed by recipient M psi. Despite the absence of significant local phagocytosis, the number of transferred M psi free in the peritoneum of recipient mice declined rapidly, being undetectable by 96 h. These data suggest that inflammatory M psi normally emigrate rapidly from the peritoneal cavity during the resolution of inflammation, contrasting with resident M psi, which persist in the noninflamed peritoneum for weeks. Accordingly, labeled nonphagocytosed cells were detected in the draining lymph nodes, but not in a variety of other tissues. Thus, unlike the polymorphonuclear leukocyte, which dies by apoptosis and is ingested by M psi, the inflammatory M psi itself does not die locally. Having performed its acute inflammatory and scavenging roles, it emigrates in a nonrandom fashion to the draining lymph node, where it may play an important part in the presentation of Ags from the inflamed site.

Adoptive Transfer↗