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At least 19 recordsLinked to original sources
PubMed1988

The selective and superoxide-independent disruption of intestinal epithelial tight junctions during leukocyte transmigration.

Polymorphonuclear leukocyte (PMN) transmigration across cultured intestinal epithelial monolayers has been shown to be associated with a decrease in transepithelial resistance to the passive flow of ions. Using flux techniques, we show that this effect reflects selective, PMN induced alterations in paracellular, as opposed to transcellular, ion permeability. Enhancement of paracellular permeability due to PMN transmigration is not simply due to expansion of the paracellular space resulting from cell death as cytotoxicity does not occur during this process. Thus, permeability alterations accompanying PMN transmigration can be specifically attributed to altered permeability of the rate limiting barrier of the paracellular pathway, the intercellular tight junction. We have also explored the mechanism by which PMN induce transient tight junction dissolution during transmigration. Use of inhibitors of toxic oxygen metabolites or use of PMN from patients with chronic granulomatous disease show that oxygen metabolites are neither required for transmigration or for the permeability abnormality accompanying transmigration. Similarly, use of protease inhibitors suggest that release of proteases by PMN during transmigration is not the basis by which PMN are able to cross tight junctions. Structural studies show that transient intimate PMN-epithelial cell plasma membrane associations and cytoskeletal specializations preceed junctional impalement by PMN. We speculate that such putative adhesion sites serve as the foothold from which PMN may generate the mechanical force necessary to cross tight junctions during transmigration.

Biological Transport, Active↗
PubMed1991

Cytokine-activated human endothelial monolayers support enhanced neutrophil transmigration via a mechanism involving both endothelial-leukocyte adhesion molecule-1 and intercellular adhesion molecule-1.

rIL-1 beta treatment of cultured human endothelial cells (HEC) promotes polymorphonuclear leukocyte (PMN) adhesion and transmigration. Using in vitro quantitative monolayer adhesion and videomicroscopic transmigration assays, we have examined the contributions of endothelial-leukocyte adhesion molecule-1 (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and the leukocyte adhesion complex, CD11/CD18, to these processes. Maximal enhancement of PMN adhesion and transmigration were observed after 4 h of rIL-1 beta treatment, when surface expression of ELAM-1 had peaked and ICAM-1 was modestly increased. Blocking mAb directed to either ELAM-1 or ICAM-1 inhibited greater than 90% of the up-regulated PMN transmigration. Blocking mAb directed to either CD11a/CD18 (LFA-1, a ICAM-1 counter-receptor), CD11b/CD18 (Mo-1), or CD18 (common beta 2-integrin) also blocked greater than 90% of PMN transmigration. At later time points (24 or 48 h), ELAM-1 surface expression was markedly decreased, whereas ICAM-1 expression was increased over the 4-h level; PMN adhesion remained elevated (approximately 50 to 60% of 4 h level), but transmigration returned to levels seen with unactivated HEC. These data indicate that PMN interaction with at least two distinct HEC adhesion molecules is necessary for transendothelial migration and suggests that PMN adhesion and transmigration, although interrelated, are mechanistically distinct processes.

Antigens, CD↗
PubMed1991

Monocyte transmigration induced by modification of low density lipoprotein in cocultures of human aortic wall cells is due to induction of monocyte chemotactic protein 1 synthesis and is abolished by high density lipoprotein.

Incubation of cocultures of human aortic endothelial (HAEC) and smooth muscle cells (HASMC) with LDL in the presence of 5-10% human serum resulted in a 7.2-fold induction of mRNA for monocyte chemotactic protein 1 (MCP-1), a 2.5-fold increase in the levels of MCP-1 protein in the coculture supernatants, and a 7.1-fold increase in the transmigration of monocytes into the subendothelial space of the cocultures. Monocyte migration was inhibited by 91% by antibody to MCP-1. Media collected from the cocultures that had been incubated with LDL induced target endothelial cells (EC) to bind monocyte but not neutrophil-like cells. Media collected from cocultures that had been incubated with LDL-induced monocyte migration into the subendothelial space of other cocultures that had not been exposed to LDL. In contrast, media from separate cultures of EC or smooth muscle cells (SMC) containing equal number of EC or SMC compared to coculture and incubated with the same LDL did not induce monocyte migration when incubated with the target cocultures. High density lipoprotein HDL, when presented to cocultures together with LDL, reduced the increased monocyte transmigration by 91%. Virtually all of the HDL-mediated inhibition was accounted for by the HDL2 subfraction. HDL3 was essentially without effect. Apolipoprotein AI was also ineffective in preventing monocyte transmigration while phosphatidylcholine liposomes were as effective as HDL2 suggesting that lipid components of HDL2 may have been responsible for its action. Preincubating LDL with beta-carotene or with alpha-tocopherol did not reduce monocyte migration. However, pretreatment of LDL with probucol or pretreatment of the cocultures with probucol, beta-carotene, or alpha-tocopherol before the addition of LDL prevented the LDL-induced monocyte transmigration. Addition of HDL or probucol to LDL after the exposure to cocultures did not prevent the modified LDL from inducing monocyte transmigration in fresh cocultures. We conclude that cocultures of human aortic cells can modify LDL even in the presence of serum, resulting in the induction of MCP-1, and that HDL and antioxidants prevent the LDL induced monocyte transmigration.

Antioxidants↗
PubMed1987

Effects of polymorphonuclear leukocyte transmigration on the barrier function of cultured intestinal epithelial monolayers.

We describe a model to study the effects of polymorphonuclear leukocyte (PMN) transmigration on the intestinal epithelial barrier. Human PMN were induced to transmigrate across high resistance monolayers of a cultured human intestinal epithelial cell line (T84 cells) by chemotactic gradients produced by formyl methionyl leucyl phenylalanine (FMLP). With maximal transmigration monolayer resistance decreased by 48 +/- 12.6% in 15 min and by 83 +/- 1.6% in 60 min. This response was dependent on the size of the FMLP gradient and the density of PMN transmigration. The decrease in resistance correlated with number of PMN migrating across monolayers, and was accompanied by increases in flux of paracellular tracers. Macromolecular tracer studies localized the leak sites to foci at which PMN impaled the epithelium. Removal of the chemotactic gradient led to restoration of baseline resistance within 18 h. PMN transmigration across intestinal epithelial monolayers occurs via intercellular occluding junctions and may be associated with a reversible increase in epithelial permeability.

Cell Line↗
PubMed1992

ICAM-1-independent lymphocyte transmigration across high endothelium: differential up-regulation by interferon gamma, tumor necrosis factor-alpha and interleukin 1 beta.

The adhesion of lymphocytes to cytokine-treated high endothelium was studied using cultured high endothelial cells (HEC). Pretreatment of the HEC layer with a variety of cytokines caused up-regulation of lymphocyte adhesion with the effects ordered interferon gamma (IFN-gamma) greater than tumor necrosis factor-alpha (TNF-alpha) greater than or equal to interleukin 1 beta (IL 1 beta). Increased lymphocyte adhesion was found to be independent of ICAM-1 as expression by HEC was not increased by cytokines and antibodies against ICAM-1 did not block adhesion. The peptide CS1 and anti-beta 1 integrin subunit antibodies, however, caused partial inhibition of lymphocyte adhesion thus indicating a role for fibronectin on HEC and alpha 4 beta 1 on lymphocytes. Study of the kinetics of lymphocyte adhesion showed that the effects of IFN-gamma and TNF-alpha were persistent and remained detectable 2.5 h after removal of the cytokines whereas the effects of IL 1 beta were transient and were not sustained beyond 1 h. All of the cytokines used caused transient increases in the number of surface-bound lymphocytes with IFN-gamma greater than TNF-alpha greater than or equal to IL 1 beta, however, the most dramatic effect was on the transmigration of lymphocytes across the HEC. Both IFN-gamma and TNF-alpha caused sustained increased transmigration with IFN-gamma having the greater effect. IL 1 beta had little effect on transmigration. This model demonstrates that the binding and transmigration of lymphocytes across HEC can be differentially regulated by the actions of individual cytokines. These results support the concept that locally produced cytokines regulate HEC function within the lymph node.

Animals↗
PubMed1992

Association of murine CD31 with transmigrating lymphocytes following antigenic stimulation.

Human CD31 is a recently characterized molecule present on leukocytes, platelets, and endothelium. Its function is not known. Because it is a member of the immunoglobulin superfamily and structurally homologous to carcinoembryonic antigen, a putative intercellular adhesion molecule, it is believed that CD31 may function also as an adhesion molecule. In this report, we characterize the cellular reactivity of a monoclonal antibody to a murine protein that is homologous to CD31. To delineate the cellular reactivity of the murine CD31 homologue recognized by our monoclonal antibody, we used immunoperoxidase and immunoelectron microscopic techniques. The most striking finding was that the putative murine homolog of CD31 is expressed in particularly high amounts on endothelium-adherent lymphocytes transmigrating across sinusoidal or venular vascular boundaries. Such a distribution was apparent in draining murine lymph nodes during the peak of an immune response after immunization with a protein antigen in adjuvant, a situation in which there are many transmigrating lymphocytes. Immunoelectron microscopic analysis also shows that CD31 is predominantly distributed on portions of transmigrating lymphocytes that are in contact with or adjacent to areas of contact with endothelial cells. These findings suggest a previously undescribed role for CD31 in lymphocyte recruitment and transmigration.

Amino Acid Sequence↗
PubMed1985

Transmigration of impacted mandibular cuspids.

Transmigration of impacted mandibular cuspid is a rare finding. A cuspid is classified as "transmigrated" when more than half of its length has passed the mid-line. 13 cases of transmigration of impacted mandibular cuspids are presented, 3 of which occurred in pairs, raising the total number of teeth to 16. Radiographs showed positions ranging from a vertical impaction, to a cuspid having crossed the mid-line completely, reaching the first molar area of the opposite side.

Adolescent↗
PubMed1992

Monocyte-selective transendothelial migration: dissection of the binding and transmigration phases by an in vitro assay.

We describe a quantitative assay of transendothelial migration (TEM) that allows us to selectively study the interaction of monocytes with confluent human endothelial cell (HEC) monolayers. The HEC are grown on hydrated collagen gels; the monocytes need not be purified. 100% of monocytes transmigrated the monolayer within 1 h at 37 degrees C and accumulated in the subendothelial collagen; TEM of lymphocytes was not detected within this time. Migration of neutrophils from the same donor was much slower and incomplete, with only 14% of PMN transmigrating in 2 h. This rapid TEM occurs in the absence of exogenous chemoattractants, and HEC in this system do not express cytokine-inducible leukocyte adhesion molecules. A slight modification of the TEM assay allowed us to separate binding to the apical HEC surface from TEM. We found that tight apical surface binding was the rate-limiting step for TEM. Two-thirds of this binding and TEM could be blocked by a monoclonal antibody against the leukocyte beta 2 integrin chain CD18. This assay will allow us to dissect the mechanisms of both the binding and transmigration stages of diapedesis.

Cell Cycle↗
PubMed1992

IL-4 controls the selective endothelium-driven transmigration of eosinophils from allergic individuals.

The mechanism leading to selective accumulation of eosinophils in allergic inflamed tissue is still unknown. In this article, transendothelial migration of circulating eosinophils from normal and allergic individuals is characterized by means of human umbilical vein endothelial cells cultivated on extracellular matrix from human fibroblasts. IL-4 pretreatment of these vascular constructs induced adherence and impressive layer penetration of eosinophils but not of neutrophils. For layer penetration, blood eosinophils from nonallergic donors needed in vitro priming by granulocyte/macrophage-CSF, IL-3, or IL-5. In contrast, freshly isolated blood eosinophils from a group of patients with atopic dermatitis spontaneously penetrated IL-4-activated vascular constructs. The here described selective pathway of eosinophil transmigration was 1) specifically induced by IL-4; 2) inhibited by the IL-4 specific, neutralizing mAb 8F12; and 3) dependent upon endothelial mRNA synthesis. Both eosinophil adherence and transmigration were present at an IL-4 concentration of 1 U/ml. The effect of endothelial preincubation with IL-4 culminated at 16 h and persisted up to 48 h. A linear increase of subendothelial accumulating eosinophils was observed within 2 h, reaching almost 100% after 4 h of coincubation. From inhibition experiments using different mAb, we conclude that the integrins CD11a/CD18, CD11b/CD18, and very late Ag-4 (CDw49d/CD29) are involved in this selective pathway of eosinophil transmigration. Taken together, this study demonstrates a novel mechanism which allows in vitro or in vivo primed eosinophils to leave the vascular compartment without influencing emigration of neutrophils.

Adult↗
PubMed1991

[The transmigration of the permanent lower canine].

A rare dental anomaly--the transmigration--is analysed. This condition, which is sparsely recorded in the literature, typically affects the mandibular canine. Twelve cases in which an unerupted mandibular canine has crossed the midline, are described and discussed. Reference is made to considerations put forward in the past by other Authors on this subject, after which personal conclusions are drawn on the diagnosis, etiology and therapy of this rare but serious behaviour of the mandibular canine. The anomaly can be properly diagnosed only by an attentive radiographic evaluation which is primarily based on the orthopantomogram. A series of successive panoramic radiographs taken over years documents the progressive ectopic movement of an unerupted mandibular canine from its developmental site, through the symphysis of the mandible. Lateral, postero-anterior cephalometric films and periapical radiographs, provide additional important information. After having analysed the most frequent etiological factors of mandibular canine impaction, the authors present their considerations concerning the probable pathogenetic mechanism of transmigration. In addition to the proinclination of the lower incisors and the increasing axial inclination of the unerupted canine, already pointed out by other authors, an enlargement of the symphyseal cross-sectional area has been observed and documented. In conclusion it is important, also from a therapeutical point of view, to keep under control, by periodical panoramic radiographs, all those clinical situations considered at risk due to their possible evolution in transmigration and which are characterized by: 1) an unerupted canine which can be palpated in a mesial position in the labial sulcus; 2) an enlarged symphyseal cross-sectional area; 3) an obstacle to normal eruption (cysts, odontomas, ecc.); 4) a proinclination of the lower incisors. A progressive worsening of the position of the unerupted canine should induce to consider the possibility of an early interception of this anomalous condition, which, once established, results in the definitive impaction of the tooth.

Adolescent↗
PubMed1987

[Studies on the metabolic fate of 14C-rokitamycin. III. Transmigration to fetus or milk].

Transmigration of 14C-radioactivity to fetus or milk were studied in 17-18 day-pregnant rats and mother rats on the 14th day after parturition after a single oral administration of 14C-rokitamycin (TMS-19-Q) at a dose of 200 mg/kg. The blood concentration of the drug in the mother reached a maximum level of 22.8 micrograms/ml at 2 hours after administration. Maximum concentrations of TMS-19-Q in placenta, ovary and uterus were attained in 2 hours, and were 28.9, 26.0 and 26.2 micrograms/g, respectively. The distribution to these tissues were considered good. The maximum concentration of TMS-19-Q in the amniotic fluid was attained in 2 hours, at a level of 5.4 micrograms/ml. The transmigration to the amniotic fluid was considered poor. The maximum concentration of the drug in the fetus was achieved in 2 hours at a level of 13.7 micrograms/g. Maximum concentrations of the drug in fetal liver and brain were attained in 4 hours, and were 32.8 and 11.4 micrograms/g, respectively. Whole body autoradiography was done when the radioactivity in maternal blood reached peak concentration. It was found that radioactivities in placenta and fetal membrane were similar to the radioactivity in maternal blood, while the radioactivity in fetal brain was considerably lower than that in maternal blood. Maximum concentrations were found at 1 hour in the blood and at 4 hours in the milk, and were 14.8 and 21.5 micrograms/ml, respectively. Transmigration to the milk was good.

Amniotic Fluid↗
PubMed1985

Transmigration of titanium dioxide (TiO2) particles in rats after inhalation exposure.

Titanium dioxide (TiO2) has been used extensively in the manufacturing of white pigment and has generally been regarded as a nuisance dust in animals and man. After inhalation exposure, little is known about transmigration routes and potential toxic effects of translocated particles in other organs. In order to answer these questions, rats were exposed to TiO2 by inhalation exposure at concentrations of 0, 10, 50, and 250 mg/m3 for 2 years. A few free particles were retained in the nasal and tracheobronchial epithelium without any cellular damage, but aggregates of dust-laden macrophages (dust cells) were found in the lymphoid tissue of the submucosa. Inhaled particles were mostly engulfed by alveolar macrophages and confined sharply to the alveolar duct region at 10 and 50 mg/m3, while dust cells were scattered throughout alveoli at 250 mg/m3. A fraction of the inhaled particles was retained in the membranous pneumocytes and interstitial macrophages. A dense accumulation of dust cells was found in the perivascular and peribronchial lymphoid tissue. Some dust cells entered peribronchial lymphatics or pulmonary blood vessels and the general circulation. Dust cells in the hyperplastic peribronchial lymphoid tissue were exposed directly in the luminal surface of the airways and were subsequently eliminated via airways. Massive dust deposition was observed in the tracheobronchial lymph nodes. Dust transmigration was markedly reduced in the cervical lymph nodes, and only a trace amount of dust particles was found in the mesenteric lymph nodes. Some dust cells entered either blood or lymphatic vessels in the lymph nodes and then migrated into the general circulation. The incidence of extrapulmonary dust deposition in the liver or spleen was increased in a dose-related fashion similar to the lung dust burden. Since there was no tissue response to translocated particles in the lymph nodes, spleen, or liver, potential adverse health effects appear to be negligible.

Administration, Intranasal↗
PubMed1987

Role of transmigration and abnormal embryogenesis in ectopic pregnancy.

Transmigration of ovum and/or sperm may occur, as deduced by the presence of EP in the fallopian tube contralateral to the corpus luteum. The frequency of occurrence of transmigration is relatively low, and, in many cases, other routes of ovum and sperm transport (i.e., intrauterine migration, tubal recanalization, fistula formation) may lead to the ectopic implantation site. In our view, the percentage of abnormal embryos associated with EP is no different from those associated with spontaneous abortions of intrauterine origin. Embryos from spontaneous abortions-of either intrauterine or extrauterine origin-seem to have more abnormalities than embryos from induced abortions. Other etiologic factors such as tubal disease, strictures of the fallopian tube, or endocrinopathies seem to contribute more significantly to the incidence of EP than does abnormal embryogenesis.

Abdomen↗
PubMed1991

Transmigration of permanent mandibular canines. Case report.

Transmigration is the migration of a tooth across the midline of the jaw. This phenomenon is found only in relation to the permanent mandibular canines. Two cases are reported. In both, the cause of this deviation was an odontome found in the site normally occupied by the mandibular canine. The literature on transmigration is reviewed.

Adult↗
PubMed1985

SEM observations on the cellular transmigration through the wall of blood vessels in cancer of the human larynx.

Human larynges, removed surgically for advanced planoepithelial carcinoma were used for study. After employing appropriate preparation procedure the obtained material was examined in scanning electron microscope (SEM). The predominant findings were: the human cancer cells transmigrate through the venule lining at/or near the sites of the endothelial intercellular junction, capillaries and postcapillary venules constitute a territory within the transmigration of lymphocytes, piercing the body of the endothelial cell, occur in both directions, the cellular elements of the immune system are relatively more numerous gathered in the peripheral areas of the primary tumor, the obtained results are consistent with in vivo and in vitro experimental data.

Carcinoma↗
PubMed1991

Gastrostomy tube transmigration: a rare cause of small bowel obstruction.

A 77-year-old woman with an indwelling gastrostomy tube presented with a clinical picture of pneumonia and small bowel obstruction. During gastrostomy closure and performance of a feeding jejunostomy, inadvertent transmigration of the gastrostomy tube was found to be the etiology of the small intestinal obstruction. This case illustrates a rare complication of enteric feeding tubes.

Aged↗
PubMed1992

The belief in the transmigration of souls: psychotherapy of a Druze patient with severe anxiety reaction.

In this paper the culture-sensitive psychotherapy of a 19-year-old Druze patient with severe anxiety reaction is described. The patient explained his anxiety and his symptoms as stemming from violent death in his former life and subsequent transmigration. The therapists joined the patient's explanatory model and previous traditional healing, adding hypnotic suggestion which relieved the symptoms. The relationship of patient symptomatology to cultural background, multiple personality disorder, possession and dissociation is discussed. The strategic combination of culture-specific and modern psychiatric approaches is advocated in similar cases.

Adult↗
PubMed1986

Transmigration of mitochondrial GOT in cholestatic liver injury.

Cholestatic liver injury was experimentally induced in rats by administration of alpha-naphthylisothiocyanate (ANIT) and the peak activity of mitochondrial L-aspartate: 2-oxoglutarate aminotransferase (m-GOT) released in the serum was found to precede the peak of total GOT activity. To investigate the permeability of the mitochondrial inner membrane to m-GOT, liver mitochondria obtained from rats given ANIT were fractionated into two subfractions: one containing the matrix and the inner and outer membranes, and the other containing the intermembrane space, and the m-GOT in these fractions was determined. As a result, 12 hours after ANIT administration, the relative activity of GOT in the subfraction containing the matrix and the membranes was significantly lower than the control value. In the same period, the ratio of GOT activity to the activity of glutamate dehydrogenase, which is a marker enzyme for the matrix, and the ratio of GOT activity to the activity of cytochrome c oxidase, which is a marker enzyme for the inner membrane, were both decreased by half. In contrast, the relative GOT activity for the subfraction containing the intermembrane space was significantly increased 12 hours after administration. Also, the ratio of GOT activity to the activity of adenylate kinase, a marker enzyme for the intermembrane space, was doubled. These results suggest that m-GOT, which is originally located in the mitochondrial matrix, transmigrated to the intermembrane space via the inner membrane under the effect of ANIT administration.

1-Naphthylisothiocyanate↗