Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “transmigration”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed2003

Leukocyte-endothelial-cell interactions in leukocyte transmigration and the inflammatory response.

Both the innate and adaptive immune responses are dependent on the migration of leukocytes across endothelial cells. The process of diapedesis, in which the leukocyte crawls between tightly apposed endothelial cells, is a unique and complex process. Several molecules concentrated at the junctions of endothelial cells, originally described as having a role in holding the endothelial monolayer together, have also been shown to have a role in the emigration of leukocytes. Several mechanisms have been proposed for 'loosening' the junctions between endothelial cells to enable leukocyte passage. These leukocyte-endothelial-cell adhesion molecules are probably involved in regulating the signaling as well as the adhesion events of diapedesis. In addition, this Review introduces a new and unified nomenclature for the junctional adhesion molecule (JAM) family.

Animals↗
PubMed2002

Tissue-specific ICAM-1 expression and neutrophil transmigration in the copper-deficient rat.

Dietary copper deficiency promotes neutrophil accumulation in rat lungs. We have now investigated the potential mechanisms of this effect. Male weanling rats were fed a Cu-adequate (6.0 mg diet) or Cu-deficient diet (0.30 mg) for 4 wks. Endothelial intercellular adhesion molecule-1 (ICAM-1) expression was measured in vivo and in vitro using a radiolabeled monoclonal antibody to rat ICAM-1. Tissue neutrophil accumulation was measured by myeloperoxidase (MPO) content and neutrophil transendothelial migration was assessed in vitro. Dietary copper deficiency had no effects on the expression of ICAM-1 in lung, liver, heart, kidney, or cremaster. However, MPO content was significantly greater in the lungs of copper-deficient rats. Endotoxin-induced ICAM-1 expression was greater in the lungs and hearts of copper-deficient rats. Similarly, cultured rat endothelial cells that were Cu-chelated expressed more ICAM-1 after endotoxin. This correlated with the significant increase in MPO in lungs of copper-deficient rats treated with endotoxin. The results suggest a tissue-specific difference in ICAM-1 expression and neutrophil accumulation during inflammation in copper-deficient rats. The findings suggest that lung inflammatory mechanisms are particularly sensitive to copper deficiency.

Animals↗
PubMed2000

Effects of remifentanil on neutrophil adhesion, transmigration, and intercellular adhesion molecule expression.

BACKGROUND: Anaesthetic drugs are used for pain therapy and anaesthesia. Neutrophils play a significant role during the process of inflammation. The aim of the current study was to investigate the effects of remifentanil and fentanyl on neutrophil migration through endothelial cell monolayers, and on adhesion molecule expression. METHODS: After isolation of polymorphonuclear neutrophils (PMNL) we used a currently described migration assay. PMNL and/or endothelial cell monolayers (ECM) were pre-treated with remifentanil using clinically relevant, as well as higher and lower concentrations or relevant concentrations of fentanyl. RESULTS: Concentrations of remifentanil (50 ng/mL) similar to the relevant plasma concentration were able to inhibit PMNL migration through ECM significantly (migration compared to the control 82+/-7% SD; P<0.05), when both cell types were treated with the synthetic narcotic remifentanil. Fentanyl (30 ng/mL) showed a stronger inhibitory effect (migration compared to the control 67+/-9.2%; P<0.05). Endothelial cell adhesion molecule expression was reduced after either remifentanil or fentanyl. CONCLUSION: The results of the present investigation indicate that remifentanil influences interaction of ECM against human neutrophils. Compared to fentanyl, remifentanil seems to exhibit minor inhibitory effects on neutrophil migration.

Analgesics, Opioid↗
PubMed2004

Tissue eosinophilia in pemphigoid gestationis: association with eotaxin and upregulated activation markers on transmigrated eosinophils.

PROBLEM: We studied chemotactic cytokines and activation of skin-homed eosinophils in pemphigoid gestationis, a rare autoimmune bullous disease of late pregnancy. METHOD OF STUDY: Eotaxin and interleukin (IL)-5 were analysed in patients' blister fluid and serum by enzyme-linked immunosorbent assay. Lesional tissue was investigated for eotaxin deposition by immunohistochemistry. Adhesion molecules and activation markers on tissue eosinophils were analysed by immunofluorescence staining. RESULTS: Eotaxin was elevated in serum of two pemphigoid gestationis patients compared with nine healthy pregnant women. Blister fluid contained even higher amounts of eotaxin and in addition IL-5. Eotaxin was mainly expressed in subepidermal tissue in close proximity to eosinophils that expressed high levels of adhesion molecules (CD11b, CD11c, CD18 and CD49d) and the activation marker HLA-DR. CONCLUSIONS: High local levels of eotaxin and IL-5 as present in the blister fluid correspond to the high state of activation of the infiltrated eosinophils.

Antibodies↗
PubMed2002

Effects of inflammatory cytokines on the permeability of human lung microvascular endothelial cell monolayers and differential eosinophil transmigration.

BACKGROUND: Rhinovirus (RV) infections can result in asthma exacerbations in both adults and children. Respiratory epithelium, the primary site of RV replication, responds to the viral infection by generating a variety of cytokines and chemokines capable of promoting airway inflammation and hence might increase asthma severity. Some of these mediators might also affect the permeability of underlying vascular endothelium. OBJECTIVE: We hypothesized that RV infections can promote airway inflammation and thus asthma by enhancing local vascular permeability. METHODS: Confluent human lung microvascular endothelial cell (HMVEC-L) monolayers were used as an in vitro model of vascular endothelium to determine whether cytokines associated with RV-induced infections are capable of modulating endothelial cell permeability as measured by means of transendothelial electrical resistance. Recombinant cytokines and chemokines were added to confluent HMVEC-L monolayers cultured on Transwell filters, and permeability was measured as decreased electrical resistance over time. Eosinophil transendothelial migration was assessed under the same experimental conditions. RESULTS: TNF- alpha, IL-1 beta, and IFN- gamma significantly increased HMVEC-L permeability. In contrast, GM-CSF, G-CSF, IL-8, IL-6, and RANTES had no effect. Although incubation of HMVEC-L monolayers with either TNF-alpha or IL-1beta promoted eosinophil migration, IFN-gamma had no effect, indicating that enhanced permeability alone was not sufficient for eosinophil infiltration. CONCLUSION: Select cytokines, generated in response to RV infection, can increase vascular permeability and might provide a mechanism by which RV infection can lead to edema, cellular infiltration, and inflammation and thus compromised airflow.

Asthma↗
PubMed2005

Rap1 GTPase inhibits leukocyte transmigration by promoting endothelial barrier function.

The passage of leukocytes out of the blood circulation and into tissues is necessary for the normal inflammatory response, but it also occurs inappropriately in many pathological situations. This process is limited by the barrier presented by the junctions between adjacent endothelial cells that line blood vessels. Here we show that activation of the Rap1 GTPase in endothelial cells accelerated de novo assembly of endothelial cell-cell junctions and increased the barrier function of endothelial monolayers. In contrast, depressing Rap1 activity by expressing Rap1GAP led to disassembly of these junctions and increased their permeability. We also demonstrate that endogenous Rap1 was rapidly activated at early stages of junctional assembly, confirming the involvement of Rap1 during junctional assembly. Intriguingly, elevating Rap1 activity selectively within endothelial cells decreased leukocyte transendothelial migration, whereas inhibiting Rap1 activity by expression of Rap1GAP increased leukocyte transendothelial migration, providing physiological relevance to our hypothesis that Rap1 augments barrier function of inter-endothelial cell junctions. Furthermore, these results suggest that Rap1 may be a novel therapeutic target for clinical conditions in which an inappropriate inflammatory response leads to disease.

Cell Movement↗
PubMedDate not supplied

Influence of neuropeptides on neutrophil adhesion and transmigration through a lung fibroblast barrier in vitro.

The lung is richly supplied with peptidergic nerves that store and secrete substance P (SP), vasoactive intestinal peptide (VIP), and other neuropeptides known to potently modulate leukocyte function in vitro and airway inflammation in vivo. We examined the effect of SP, VIP and the novel sensory neuropeptide secretoneurin (SN), as well as of interleukin (IL)-8, IL-6, IL-1 beta, transforming growth factor (TGF)-beta, and tumor necrosis factor (TNF), all associated with acute lung injury, on human neutrophil migration across a 5-mu pore polycarbonate filter system covered by human lung fibroblast monolayers. Additionally, we tested the ability of these neuropeptides to elicit neutrophil adhesion to fibroblast monolayers. SP, but not VIP and SN, may be important in directly influencing neutrophil adhesion to and subsequent migration across a subendothelial barrier of fibroblasts and extracellular matrix towards lung inflammatory sites. The effect was mainly mediated by neurokinin (NK)-1 receptors, as evaluated by a specific NK-1 antagonist, [[(S,S)Pro-Leu(spiro-y-lactam)]9,10, Trp11]substance P (1-11), whereas a specific NK-2 receptor antagonist, [Tyr5, D-Trp6,8,9, Lys10]neurokinin A (4-10), was ineffective. The SP analog septide and the NK-1 receptor agonist ([Sar9 Met(O2)11)SP were comparably effective. Furthermore, the SP effect was concentration and time dependent. However, the other tested neuropeptides might also affect neutrophil recruitment in inflammatory lung by modulating other lung cell functions. Additionally, all tested cytokines stimulated neutrophil transfibroblast migration in vitro, except IL-6. In conclusion, SP in concert with proinflammatory cytokines may regulate neutrophil interstitial accumulation and their traffic to the alveolar space in lung inflammation.

Cell Adhesion↗
PubMed2006

Neisseria meningitidis infection of human endothelial cells interferes with leukocyte transmigration by preventing the formation of endothelial docking structures.

Neisseria meningitidis elicits the formation of membrane protrusions on vascular endothelial cells, enabling its internalization and transcytosis. We provide evidence that this process interferes with the transendothelial migration of leukocytes. Bacteria adhering to endothelial cells actively recruit ezrin, moesin, and ezrin binding adhesion molecules. These molecules no longer accumulate at sites of leukocyte-endothelial contact, preventing the formation of the endothelial docking structures required for proper leukocyte diapedesis. Overexpression of exogenous ezrin or moesin is sufficient to rescue the formation of docking structures on and leukocyte migration through infected endothelial monolayers. Inversely, expression of the dominant-negative NH(2)-terminal domain of ezrin markedly inhibits the formation of docking structures and leukocyte diapedesis through noninfected monolayers. Ezrin and moesin thus appear as pivotal endothelial proteins required for leukocyte diapedesis that are titrated away by N. meningitidis. These results highlight a novel strategy developed by a bacterial pathogen to hamper the host inflammatory response by interfering with leukocyte-endothelial cell interaction.

Cell Adhesion↗