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At least 325 records · Page 18Linked to original sources
PubMed1988

The selective binding and transmigration of monocytes through the junctional complexes of human endothelium.

Human monocytes show a high affinity for vascular endothelium both in vitro and in vivo. To explore monocyte-endothelial interaction in greater detail, we have developed a new in vitro model for growth of human endothelial cells (EC). Human umbilical vein EC (HUVEC) cultured upon collagen gels form confluent monolayers of EC that bind silver at their intercellular border similar to cells in situ. Intercellular junctional structures, both adherens and tight junctions, were identified. In contrast, HUVEC grown on plastic surfaces did not stain with silver. The silver-staining characteristic of EC-collagen monolayers was reversible and related to their in vitro maturation and senescence. Silver staining of EC borders provided a grid by which the location of monocyte binding to the luminal surface of individual EC could be assessed. Using this technique, we found that monocytes preferentially bound to the margins of EC, in approximation to the silver-staining junctions. These results suggest that EC determinants recognized by monocytes occur in a unique topographical distribution on the apical face of EC. After binding, monocytes migrated through the EC monolayers at high basal rates. The lack of penetration of collagen gels in the absence of an EC monolayer suggested the generation of EC-specific chemotactic signal(s). Monocytes were observed to pass between EC without evidence of disruption of the monolayer. Silver stain remained present during all phases of migration, and under transmission electron microscopy, junctional complexes were found proximal to monocytes that had just completed their passage through the monolayer. After orientation to the basal surface of the EC monolayer, monocytes migrated randomly into the underlying collagen gel. Monocyte adherence, penetration, migration, and long term survival can be studied under these conditions.

Cell Adhesion↗
PubMed1976

Demonstration in vitro of postmortem bacterial transmigration.

The kinetics of the migration of intestinal bacterial flora to the peritoneal cavity upon death of the host was studied. A laboratory experiment that excluded any source of contamination was used. Samples of sterile saline solution in which a loop of the intestine was submerged were streaked onto blood agar at given intervals. Recovery of bacteria began after about 15 hours, with Staphylococcus aureus being the predominant organism. This organism showed a gradual decrease through a 36-hour period and at 48 hours was almost absent. In the same manner, other organisms such as gram-negative bacilli and spore-forming gram-positive bacilli gradually increased in numbers.

Animals↗
PubMed2000

In vitro analysis of verapamil-induced immunosuppression: potent inhibition of T cell motility and lymphocytic transmigration through allogeneic endothelial cells.

BACKGROUND: Cyclosporine A (CsA) and tacrolimus prevent proliferation but not transendothelial migration of alloreactive lymphocytes into donor organs. As a result, serious adverse effects, such as nephrotoxicity and neurotoxicity, have been observed under CsA/tacrolimus therapy. The incorporation of new drugs with infiltration blocking properties might enhance the efficacy of the current immunosuppressive protocol, allowing lower CsA/tacrolimus dosage. Because Ca2+ plays a critical role in cell-cell interaction, the Ca2+-channel blocker verapamil might be a good cany. didate for supporting CsA/tacrolimus-based therapy. METHODS: A T-cell endothelial cell coculture model or immobilized immunoglobulin G globulin chimeras were employed to investigate how S- and R- verapamil interfere with the lymphocytic infiltration process. The expression and arrangement of membranous adhesion receptors and cytoskeletal F-actin filaments were analyzed by fluorometric method in the presence of. verapamil. RESULTS: Both verapamil enantiomers strongly inhibited lymphocyte infiltration. CD4+ and CD8+ T-cells were influenced to a similar extent with regard to horizontal locomotion (CD4+=CD8+), but to a different extent with regard to adhesion and penetration (CD4+ > CD8+). Moreover, penetration was blocked to a higher extent than was adhesion. ID50-values were 31 microM (CD4+-adhesion) and 11 microM (CD4+-penetration). Verapamil reduced P-selectin expression on endothelial cells and effectively down-regulated binding of T-cells to immobilized P-selectin immunoglobulin G globulins (ID50=4.4 microM; CD4+). A verapamil-induced reduction of intracellular F-actin in T-lymphocytes was proven to be mainly responsible for diminished cell locomotion. CONCLUSIONS: The prevention of CD4+ T-cell penetration by verapamil might argue for its use as an adjunct to CsA/tacrolimus-based immunosuppressive therapy.

Cell Movement↗
PubMed1966

Transmigration of lymph nodes by tumor cells.

When either V2, Brown-Pearce, or Walker tumor cells were perfused at low pressure into the afferent lymphatic of popliteal lymph nodes or were injected into the foot pads of rabbits, they rapidly appeared in lymph draining from the node. This finding indicates that lymph nodes are not the effective barrier to dissemination of tumor cells they had previously been assumed to be.

Animals↗
PubMed2003

VCAM-1-mediated Rac signaling controls endothelial cell-cell contacts and leukocyte transmigration.

Leukocyte adhesion is mediated totally and transendothelial migration partially by heterotypic interactions between the beta1- and beta2-integrins on the leukocytes and their ligands, Ig-like cell adhesion molecules (Ig-CAM), VCAM-1, and ICAM-1, on the endothelium. Both integrins and Ig-CAMs are known to have signaling capacities. In this study we analyzed the role of VCAM-1-mediated signaling in the control of endothelial cell-cell adhesion and leukocyte transendothelial migration. Antibody-mediated cross-linking of VCAM-1 on IL-1beta-activated primary human umbilical vein endothelial cells (pHUVEC) induced actin stress fiber formation, contractility, and intercellular gaps. The effects induced by VCAM-1 cross-linking were inhibited by C3 toxin, indicating that the small GTPase p21Rho is involved. In addition, the effects of VCAM-1 were accompanied by activation of Rac, which we recently showed induce intercellular gaps in pHUVEC in a Rho-dependent fashion. With the use of a cell-permeable peptide inhibitor, it was shown that Rac signaling is required for VCAM-1-mediated loss of cell-cell adhesion. Furthermore, VCAM-1-mediated signaling toward cell-cell junctions was accompanied by, and dependent on, Rac-mediated production of reactive oxygen species and activation of p38 MAPK. In addition, it was found that inhibition of Rac-mediated signaling blocks transendothelial migration of monocytic U937 cells. Together, these data indicate that VCAM-1-induced, Rac-dependent signaling plays a key role in the modulation of vascular-endothelial cadherin-mediated endothelial cell-cell adhesion and leukocyte extravasation.

ADP Ribose Transferases↗
PubMed2006

Dissociation between alveolar transmigration of neutrophils and lung injury in hyperoxia.

The objective of this study was to quantitatively assess changes in cell adhesion molecule (CAM) expression on the pulmonary endothelial surface during hyperoxia and to assess the functional significance of those changes on cellular trafficking and development of oxygen-induced lung injury. Mice were placed in >95% O(2) for 0-72 h, and pulmonary injury and neutrophil (PMN) sequestration were assessed. Specific pulmonary CAM expression was quantified with a dual-radiolabeled MAb technique. To test the role of CAMs in PMN trafficking during hyperoxia, blocking MAbs to murine P-selectin, ICAM-1, or platelet-endothelial cell adhesion molecule-1 (PECAM-1) were injected in wild-type mice. Mice genetically deficient in these CAMs and PMN-depleted mice were also evaluated. PMN sequestration occurred within 8 h of hyperoxia, although alveolar emigration occurred later (between 48 and 72 h), coincident with rapid escalation of the lung injury. Hyperoxia significantly increased pulmonary uptake of radiolabeled antibodies to P-selectin, ICAM-1, and PECAM-1, reflecting an increase in their level on pulmonary endothelium and possibly sequestered blood cells. Although both anti-PECAM-1 and anti-ICAM-1 antibodies suppressed PMN alveolar influx in wild-type mice, only mice genetically deficient in PECAM-1 showed PMN influx suppression. Neither CAM blockade, nor genetic deficiency, nor PMN depletion attenuated lung injury. We conclude that early pulmonary PMN retention during hyperoxia is not temporally associated with an increase in endothelial CAMs; however, subsequent PMN emigration into the alveolar space may be supported by PECAM-1 and ICAM-1. Blocking PMN recruitment did not prevent lung injury, supporting dissociation between PMN infiltration and lung injury during hyperoxia in mice.

Animals↗
PubMed2006

Functional and genomic changes induced by alveolar transmigration in human neutrophils.

Although the accumulation of neutrophils in the lungs and airways is common to many inflammatory lung diseases, including acute lung injury, the alterations that neutrophils undergo as they leave the peripheral circulation and migrate into the lungs have not been well characterized. Human volunteers were exposed to endotoxin by bronchoscopic instillation. The resulting air space neutrophil accumulation and peripheral blood neutrophils were isolated 16 h later, compared with circulating neutrophils isolated before or after to the pulmonary endotoxin exposure, and compared with circulating neutrophils exposed to endotoxin in vitro. Microarray analysis was performed on air space, circulatory, and in vitro endotoxin-stimulated neutrophils. Functional analysis included the determination of neutrophil apoptosis, chemotaxis, release of cytokines and growth factors, and superoxide anion release. Dramatic gene expression differences were apparent between air space and circulating neutrophils: approximately 15% of expressed genes have altered expression levels, including broad increases in inflammatory- and chemotaxis-related genes, as well as antiapoptotic and IKK-activating pathways. Functional analysis of air space compared with circulating neutrophils showed increased superoxide release, diminished apoptosis, decreased IL-8-induced chemotaxis, and a pattern of IL-8, macrophage inflammatory protein-1beta, monocyte chemoattractant protein-1, and tumor necrosis factor-alpha release different from either unstimulated or LPS-stimulated circulating neutrophils. Many of these changes are not elicited by in vitro treatment with endotoxin. Limited differences were detected between circulating neutrophils isolated before and 16 h after pulmonary endotoxin instillation. These results suggest that neutrophils sequestered in the lung become fundamentally different from those resident in the circulation, and this difference is distinct from in vitro activation with endotoxin.

Cell Movement↗
PubMed2000

Functional properties of circulating and transmigrated neutrophils in a rat peritonitis model.

Using a rat peritonitis model, we examined the pattern of expression of adhesion molecules and H2O2 productivity of neutrophils by indirect immunofluorescence and flow cytometry. H2O2 production in blood neutrophils was significantly increased after peritonitis induction. The expression of CD11b and CD18 antigens on blood neutrophils was also significantly increased after peritonitis induction. In contrast, H2O2 production in peritoneal neutrophils was significantly lower than that in blood neutrophils. The expression of CD11b and CD45 antigens on peritoneal neutrophils was significantly higher than on blood neutrophils. Although no function has been assigned to LFA-1 on neutrophils, the expression of LFA-1 (CD11a/CD18) on peritoneal neutrophils was significantly decreased.

Animals↗
PubMed1999

Regulatory mechanisms of eosinophil adhesion to and transmigration across endothelial cells by alpha4 and beta2 integrins.

To participate in allergic airway inflammation, it is necessary for blood eosinophils (Eos) to adhere to and migrate across pulmonary vascular endothelial cells (EC). Accumulating evidence has established that Eos adhesion molecules, such as alpha4 and beta2 integrins, play central roles in these processes. We have reported that Eos spontaneously adhere to recombinant human (rh)-VCAM-1, while adhesion to rh-ICAM-1 requires a second stimulus such as GM-CSF. Furthermore, our study employing human pulmonary microvascular endothelial cells (HPMEC) revealed that although the alpha4 integrin/VCAM-1 pathway is crucial for the firm adhesion of Eos, subsequent transendothelial migration occurred dependent on the beta2 integrin/ICAM-1 pathway. We also discuss secretagogues that would affect Eos recruitment to the airways via regulation of alpha4 and beta2 integrins.

Animals↗
PubMedDate not supplied

Allergen specificity and endothelial transmigration of T cells in allergic contact dermatitis and atopic dermatitis are associated with the cutaneous lymphocyte antigen.

Recent investigations have indicated a role for antigen-specific T lymphocytes in the local skin immunity. The cutaneous lymphocyte antigen (CLA) is supposed to represent a skin-homing receptor for T cells. Inhibition experiments with specific monoclonal antibody demonstrate that CLA participates in selective transendothelial migration of memory/effector T cells in vitro by interaction with E-selectin on endothelial cell layers after activation with proinflammatory cytokines. In addition, the receptor-ligand pairs VLA-4/VCAM-1 and LFA-1/ICAM-1 are involved in this process. Moreover, only CLA+, CD45RO+ (memory/effector) T cells freshly isolated from peripheral blood of patients with allergic contact dermatitis or atopic dermatitis specifically proliferate in response to the respective allergen. CLA-, CD45RO- T cells from these patients do not respond to the allergens. In contrast, memory T cells from asthmatic individuals and patients with both asthma and atopic dermatitis express the allergen specificity in both T cell subsets. Tetanus toxoid, a systemically acting antigen, also induces a proliferative response in both CLA+ and CLA- memory/effector T cell subsets. These results strongly support the selective role of CLA in homing T cells to the cutaneous tissues and therefore playing a role in the local immunity and inflammatory reactions of the skin.

Adult↗