Atherosclerosis is a chronic inflammatory disease characterised by the accumulation of monocytic cells and lipids within the sub-endothelial space by direct monocyte to endothelial cell contact through gap junctions (GJs). Both cell types express connexin 43 (Cx43) isoforms that permit the formation of GJs. This is enhanced by adhesion molecules in the presence of pro-inflammatory stimuli, such as tumour necrosis factor α (TNF-α). TNF-α is suggested to have a role in Cx43 expression mainly mediated through MAPK pathways over other intercellular pathways; however, to date the mechanism remains unclear. Experiments were carried out in the absence and presence of 25ng/ml TNF-α and the functional integrity of human umbilical vein endothelial cell (HUVEC) monolayers was assessed by measuring the trans-endothelial electrical resistance (TEER). The trans-endothelial migration (TEM) assay used as a model for the transmigration of monocytes to the sub-endothelial space. Monocytes were added to HUVEC ...

FUNCTION: Cell adhesion molecule that mediates homophilic cell- cell adhesion in a Ca(2+)-independent manner. Promotes neurite outgrowth in hippocampal neurons (By similarity). SUBUNIT: Can form heteromeric complexes with LRFN1, LRFN2, LRFN4 and LRFN5. Able to form homomeric complexes across cell junctions, between adjacent cells. Does not interact with DLG4 (By similarity). DOMAIN: Lacks a cytoplasmic PDZ-binding domain, which has been implicated in function of related Lrfn proteins ...

Although CD99 has been known to be critical for leukocyte transmigration for over a decade (Schenkel et al., 2002; Bixel et al., 2004, 2010; Lou et al., 2007; Dufour et al., 2008), the mechanism has remained completely unknown. Here, we report that homophilic engagement of endothelial CD99 recruits membrane from the LBRC to sites of leukocyte-endothelial contact to facilitate the passage of leukocytes through the endothelial junctions. This engagement of endothelial CD99 (Fig. 10 e, #1) signals through sAC (Fig. 10 e, #2) to activate PKA (Fig. 1 e, #3), which works through a yet-to-be-defined mechanism (Fig. 10 e, #4) to induce LBRC membrane trafficking (Fig. 10 e, #5). Furthermore, we demonstrate that CD99 and sAC are held together in a signaling complex with ezrin and PKA and that this interaction is dependent on a lysine-rich juxtamembrane region in the cytoplasmic tail of CD99. These findings represent the first description of the immediate downstream signaling mechanisms of CD99, as well as ...

Permeability oxygen through endothelial cells monolayer using time-resolved fluorescence microscopy: effect of human plasma viscosity ...

Although there is now increasing in vitro and in vivo evidence illustrating the involvement of individual endothelial cell junctional molecules in the process of leukocyte transendothelial cell migration, very few studies have addressed the potential additive/synergistic effects of multiple molecules. One such study is by Schenkel and colleagues in which an anti-PECAM-1 mAb was found to act in an additive manner with a CD99 blocker to inhibit monocyte transendothelial cell migration in vitro.31 Because in numerous inflammatory models PECAM-1 blockade/deletion results in partial suppression of leukocyte transmigration, in a final series of experiments we aimed to investigate the possibility that ICAM-2 may mediate PECAM-1-independent leukocyte transmigration. For this purpose the effect of the anti-ICAM-2 mAb, 3C4, on leukocyte transmigration in WT and PECAM-1-deficient mice was directly compared using both the cremaster muscle and peritonitis models. In line with data discussed above, ...

The recruitment of leukocytes to sites of infection and their migration through the endothelium are critical to immune responses. Transendothelial migration is essential for leukocytes to respond to foreign microorganisms, but if uncontrolled, can cause autoimmune diseases such as inflammatory bowel disease and rheumatoid arthritis. In order to evaluate the transmigration of leukocytes, we have developed a kinetic, label-free in vitro assay to automatically acquire and analyze transendothelial migration, with the added ability to monitor monolayer integrity.. Using primary T cells and Human Umbilical Vein Endothelial cells (HUVEC), we evaluated the ability of this novel assay to quantify leukocyte transmigration in the absence of cell labeling. Briefly, endothelial cells were grown to confluence on a physiological surface. Leukocytes were added to the monolayer, and the upper chamber was placed into a reservoir plate containing chemoattractant. Live cell images were captured at regular ...

Our results showed that gene expressions faithfully recapitulate immunohistochemical subtype markers, as chromogranin A in carcinoids, cytokeratin 5, p63 in SQ, and TTF1 in non-squamous types. Moreover, biological information with putative clinical relevance was revealed as potentially novel diagnostic genes for each subtype with specificity 93-100% (AUC = 0.93-1.00). Cancer subtypes were characterized by (a) differential expression of treatment target genes as TYMS, HER2, and HER3 and (b) overrepresentation of treatment-related pathways like cell cycle, DNA repair, and ERBB pathways. The vascular smooth muscle contraction, leukocyte trans-endothelial migration, and actin cytoskeleton pathways were overexpressed in normal tissue.. ...

Rabbit polyclonal antibody raised against synthetic peptide of LRFN5. A synthetic peptide corresponding to C-terminus 16 amino acids of human LRFN5. (PAB16717) - Products - Abnova

Clone 390 reacts with the cell surface protein CD31. The murine CD31 antigen is also known as PECAM-1. The encoded protein is a single-pass type I membrane protein containing six Ig-like C2-type (immunoglobulin-like) domains and functions as cell adhesion molecule. CD31 is present on mature endothelial cells as well as on most leukocyte subtypes and platelets where the expression level can vary. Besides its function in exhibiting adhesive properties, the protein is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. | Belgique

PMNL infiltrate is a common hallmark of several large bowel diseases, such as ulcerative colitis, Crohns disease, bacterial colitis, drug-induced colitis, or ischemia injury (Nash et al. 1987; Lee 1993). However, the role of PMNL-epithelial cell interaction as a proapoptotic factor in IECs was not explored. To determine whether the transmigration of PMNLs could interfere with IEC apoptosis, we used an in vitro model described by Dharmsathaphorn and Madara 1990 to study PMNL-IEC interaction. IEC apoptosis mechanisms have been assessed by both morphological and biochemical methods. Here, we provide the first evidence that neutrophil transmigration across cultured intestinal cell monolayers triggers apoptosis of epithelial cells. After PMNL transmigration for 12 h, T84 cells exhibited the morphological features of apoptotic cell death, such as brush border alteration, chromatin condensation, and cytoplasmic shrinkage. These cellular modifications have already been described in normal mice by ...

The mechanisms underlying organ vascularization are not well understood. The zebrafish intestinal vasculature forms early, is easily imaged using transgenic lines and in-situ hybridization, and develo...

We investigated the TEM of PBMC, which migrated through endothelial cell monolayers in an in-vitro model. Human umbilical vein endothelial cells (EC) were cultured to confluence on collagen gels and then incubated with human PBMC of healthy blood donors. PBMC were recollected in three groups: 1) cells that did not adhere to the endothelium, 2) cells that bound to the endothelium, 3) cells that had migrated through the endothelium, and then counted by microscope. Experiments in which PBMC as well as EC were treated with A771726 (in the absence or presence of uridine) were compared to simultaneously performed control experiments. No increased toxicity on the PBMC treated with the doses of A771726 used in our experiments, was observed. ...

The role of genetic differences among dengue virus (DENV) in causing increased microvascular permeability is less explored. In the present study, we compared two closely related DENV serotype-2 strains of Cosmopolitan genotype for their in vitro infectivity phenotype and ability to induce trans-endothelial leakage. We found that these laboratory strains differed significantly in infecting human microvascular endothelial cells (HMEC-1) and hepatocytes (Huh7), two major target cells of DENV in in vivo infections. There was a reciprocal correlation in infectivity and vascular leakage induced by these strains, with the less infective strain inducing more trans-endothelial cell leakage in HMEC-1 monolayer upon infection. The cells infected with the strain capable of inducing more permeability were found to secrete more Non-Structural protein (sNS1) into the culture supernatant. A whole genome analysis revealed 37 predicted amino acid changes and changes in the secondary structure of 3 non-translated ...

women and is the second leading cause of death from cancer. A crucial step in the progression of this disease is the transendothelial migration of tumor cells into the blood stream or lymphatic system. The factors guiding this process remain poorly understood. The development an in vitro biomimetic platform to further investigate these factors is under intensive investigation. In previous work we synthesized a tissue-engineered scaffold containing an endothelialized internal loop microchannel for microsurgical anastomosis and in vivo perfusion utilizing a sacrificial microfiber technique. Here we design a novel 3D platform to investigate tumor cell behavior in the presence of vascular cells in order to better understand the cell-cell and cell-matrix interactions that drive neoangiogenesis, invasion, metastasis and ultimately tumor progression ...

TY - GEN. T1 - TGV-based flow estimation for 4D leukocyte transmigration. AU - Frerking, L.. AU - Burger, M.. AU - Vestweber, D.. AU - Brune, Christoph. PY - 2014/8/26. Y1 - 2014/8/26. N2 - The aim of this paper is to track transmigrating leukocytes via TGV flow estimation. Recent results have shown the advantages of the nonlinear and higher order terms of TGV regularizers, especially in static models for denoising and medical reconstruction. We present TGV-based models for flow estimation with the goal to get an exact recovery of simple intracellular and extracellular flows, as well as its implication on realistic tracking situations for transmigration through barriers. To study and quantify different pathways of transmigrating leukocytes, we use large scale 4D fluorescence live microscopy data in vivo.. AB - The aim of this paper is to track transmigrating leukocytes via TGV flow estimation. Recent results have shown the advantages of the nonlinear and higher order terms of TGV regularizers, ...

According to the text: Bb is suited for extended or indefinite survival in mammalian hosts. The illness is associated with very low levels of bacteremia with primary tissue localization of the bacteria. Bb has a prediliction for certain organs/tissues. A hallmark of infection is the induction of a powerful imflamatory response despite a paucity organisms. The bacteria adhere to extraceullar matrix proteins. The bacteria has a specialized diderm membrane and a powerful flagellin which helps propel it deep into tissues, along and through endothelial cells. The bacteria can penetrate deeply into avascular cartilage and collagen. Bb can sequester in protected niches included tendonds. Bb is a sophisticated parasite, effectively co-opting host nutrtients and metabolites. Bb does not utilize oxygen or iron and metabolizes glucose via an alternative pathway. Bb is slow growing, fastidious, difficult to culture. Unique surface proteins play a role in bacterial survival. Lyme can readily change its ...

Migration of metastatic tumor cells from the bloodstream into lymph nodes is thought to be facilitated by expression of the chemokine receptors CCR7, CXCR4 and, for B cell-derived tumors, CXCR5. Expression of their respective chemokine ligands (CCL19, CCL21, CXCL12 and CXCL13) by endothelial cells inside the lymph nodes facilitates the trans-endothelial migration (TEM) of these cells through high endothelial venules into the lymph node parenchyma. It is known that CXCR7, a second CXCL12 receptor, regulates TEM of CXCR4+CXCR7+ tumor cells towards a CXCL12 source. In this study, we set out to assess the potential stimulation by CXCL12 of tumor cell TEM towards other chemokines and whether CXCR7 might be able to regulate such effects. The human Burkitts lymphoma cell line NC-37, which expresses CXCR4, CXCR5, CXCR7 and CCR7, was selected as a model system. TEM of these cells through a human HUVEC endothelial cell monolayer was used as the main model system for these studies. Regulation of their TEM

Migration of metastatic tumor cells from the bloodstream into lymph nodes is thought to be facilitated by expression of the chemokine receptors CCR7, CXCR4 and, for B cell-derived tumors, CXCR5. Expression of their respective chemokine ligands (CCL19, CCL21, CXCL12 and CXCL13) by endothelial cells inside the lymph nodes facilitates the trans-endothelial migration (TEM) of these cells through high endothelial venules into the lymph node parenchyma. It is known that CXCR7, a second CXCL12 receptor, regulates TEM of CXCR4+CXCR7+ tumor cells towards a CXCL12 source. In this study, we set out to assess the potential stimulation by CXCL12 of tumor cell TEM towards other chemokines and whether CXCR7 might be able to regulate such effects. The human Burkitts lymphoma cell line NC-37, which expresses CXCR4, CXCR5, CXCR7 and CCR7, was selected as a model system. TEM of these cells through a human HUVEC endothelial cell monolayer was used as the main model system for these studies. Regulation of their TEM

Leukocyte infiltration into the central nervous system (CNS) underlies the pathology in a wide spectrum of neuroinflammatory and neurodegenerative diseases like multiple sclerosis (MS), stroke, meningitis, and neuroAIDS. While the steps that mediate the initial adhesion of activated leukocytes to the endothelial wall has been well-characterized, not much is known about their subsequent transendothelial migration (TEM) across the blood-brain barrier (BBB), a highly restrictive paracellular barrier established by the specialized CNS endothelial cells, thus severely limiting the treatment options. In Multiple Sclerosis (MS) focal leukocyte infiltration into the CNS parenchyma early in disease is thought to be critical for the inflammatory response, and eventual neurodegeneration. Therefore, to explore the cues that regulate leukocyte TEM across the BBB in a neuroinflmmatory milieu, in this dissertation, we evaluated the role of three factors- endothelial heterogeneity, chemokine CCL2 from CNS sources,

The actin cytoskeleton is crucial for endothelial functionality. Depending on the type of vasculature, ECs contain different forms of F-actin. Under basal conditions, large arterioles of the rat mesentery are characterized by a circumferential actin rim, capillaries show diffuse actin staining, and postcapillary venules, a main site of leukocyte extravasation, display a thin peripheral actin ring with few central fibers (19). Under inflammatory conditions, the endothelial actin cytoskeleton needs to be constantly remodeled to accommodate leukocyte movement on and across the endothelium. Inflammatory mediators, such as TNF-α, induce stress fiber formation independent of the presence of leukocytes (20). In contrast, adherent leukocytes coincide with a peripheral endothelial actin ring that surrounds adherent leukocytes in vivo (21). Adhesion of lymphocytes is enabled by recruitment of ICAM-1 and VCAM-1 to tetraspanin-enriched microdomains termed endothelial adhesive platforms (22). This is ...

CD95 ligand (CD95L) is expressed by immune cells and triggers apoptotic death. Metalloprotease-cleaved CD95L (cl-CD95L) is released into the bloodstream but does not trigger apoptotic signaling. Hence, the pathophysiological role of cl-CD95L remains unclear. We observed that skin-derived endothelial cells from systemic lupus erythematosus (SLE) patients expressed CD95L, and that after cleavage, cl-CD95L promoted T helper 17 (Th17) lymphocyte transmigration across the endothelial barrier at the expense of T regulatory cells. T cell migration relied on a direct interaction between the CD95 domain called calcium-inducing domain (CID) and the Src homology 3 domain of phospholipase Cγ1. Th17 cells stimulated with cl-CD95L produced sphingosine-1-phosphate (S1P), which promoted endothelial transmigration by activating the S1P receptor 3. We generated a cell-penetrating CID peptide that prevented Th17 cell transmigration and alleviated clinical symptoms in lupus mice. Therefore, neutralizing the CD95 ...

Our results demonstrate that platelets release small molecules capable of increasing endothelial cell migration in vitro and provide evidence for the importance of dRP in mediating this response. Thus, the genetic ablation of dRP-generating TP and UP in mouse platelets or the specific inhibition of dRP-generating UP by PTAU in human platelets resulted in significantly reduced ability of protein-free supernatants to induce endothelial transmigration. Similarly, the genetic ablation of dRP-generating TP and UP in mouse platelets reduced the ability of protein-free platelet supernatants to promote endothelial monolayer repair in vitro. Both observations supported the conclusions that dRP at the concentrations released by platelets stimulates endothelial cell migration and that UP is the most important enzyme for platelet generation of this metabolite. In accordance with these conclusions, the addition of exogenous dRP to protein-free platelet supernatants reversed the inhibitory effects that ...

During the last decade, it has become increasingly clear that endothelial cells, rather than being a passive barrier, actively participate in the process of leukocyte TEM. This study focuses on a recently discovered phenomenon that occurs during TEM in which the endothelial cell extends sheets of membrane to form a cuplike structure that surrounds adherent leukocytes (Barreiro et al., 2002; Carman et al., 2003; Carman and Springer, 2004; Doulet et al., 2006). Although their precise function is unclear, evidence has been presented that these structures assist leukocytes on their way through the endothelium (Carman and Springer, 2004).. Our data reveal a new signaling pathway downstream from leukocyte adhesion that involves the small GTPase RhoG. We show here that RhoG activation is triggered through the engagement of ICAM1 and is critical for formation of the apical cups. Additionally, RhoG expression is needed for optimal leukocyte passage across the endothelium. Our data show a strong ...

TY - JOUR. T1 - Interleukin 15 induces endothelial hyaluronan expression in vitro and promotes activated T cell extravasation through a CD44-dependent pathway in vivo. AU - Estess, Pila. AU - Nandi, Animesh. AU - Mohamadzadeh, Mansour. AU - Siegelman, Mark H.. PY - 1999/7/5. Y1 - 1999/7/5. N2 - T cell recruitment to extralymphoid tissues is fundamental to the initiation and perpetuation of the inflammatory state during immune and autoimmune responses. Interleukin (IL)-15 is a proinflammatory cytokine whose described functions largely overlap with those of IL-2. The latter is attributable in large part to its binding of the heterotrimeric receptor that contains the β and γ chains of the IL-2R in combination with an unique IL- 151α chain. However, unlike IL-2, IL-15 and its receptor have a wide tissue and cell type distribution, including endothelial cells. Here, we examine the effect of IL-15 on hyaluronan expression by endothelial cells, and investigate its role in vivo in promoting the ...

Neutrophils are a key cell type of nonadaptive immune system and are the first phagocytic cell type that reaches mucosal inflammatory sites. On the last stage of their journey from the blood stream to a mucosal surface, neutrophils cross a generally sealed epithelium by migrating along the paracellu …

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PHENOTYPE: Mice homozygous for a null allele exhbit a decrease in body weight, impaired neutrophil transmigration and decreased immune and VEGF-stimulated vascular permeability. Tumor growth is inhibited due to decreased pathological angiogenesis in homozygous mutant mice. [provided by MGI curators ...

We demonstrated here in tissue culture that wild-type MV-infected human T lymphocytes are drastically impaired in their capacity to migrate through endothelial cell barriers. MV infection enhanced the adhesion of T cells to endothelial cells, and the subsequent close cell contact frequently mediated infection of the endothelial cells. The enhanced adhesion of leukocytes obviously allowed the first steps of transendothelial migration, including the formation of transmigratory cups, to take place; however, it may also be the reason why completion of the process is inhibited. Interestingly, the interaction of UV-inactivated MV with leukocytes did not inhibit transendothelial migration. This indicates that the impairment of cytoskeletal rearrangement, polarization, CD3 clustering, and cell spreading of T cells, as described earlier for a time scale of 2 h after virus-cell interaction (27), is only transient. In addition, MV infection did not strongly affect diapedesis per se. However, the capacity ...

Direct cell-to-cell contact regulates a variety of cellular functions, including cell activation and cytokine production.42 43 45 We attempted to determine whether the interaction between monocytes and endothelial cells induces MCP-1 production from these cell types, because this interaction constantly occurs in recruitment of monocytes and because production of MCP-1 would affect subsequent monocyte transendothelial migration. Our results indicate that migrated monocytes express MCP-1 protein during the process of transmigration. Cocultures of resting monocytes and unstimulated or IL-1-prestimulated endothelial cell monolayers induced an increase in the amounts of soluble MCP-1 secreted into the medium. MCP-1 secreted in supernatants exhibited chemotactic and transendothelial activities for monocytes, and its biological effect was confirmed by the disappearance of the activity in the presence of anti-MCP-1 Ab. Quantification of mRNA levels indicates that augmentation was mediated at the level ...

Transendothelial migration of myeloma cells is increased by tumor necrosis factor (TNF)-alpha via TNF receptor 2 and autocrine up-regulation of MCP-1 ...

Looking for internal transmigration? Find out information about internal transmigration. Also known as metempsychosis, transmigration is a belief in the passage of the soul into another body after death. Many religions have this belief,... Explanation of internal transmigration

The ability to seek out both junctional and non-junctional sites for barrier breach means that as endothelia increase their overall junctional strength and barrier function (i.e. with respect to fluid and solutes) the net result might be a tendency towards switching of route, rather than necessarily an abrogation of diapedesis. Importantly, in vivo, different contexts (e.g. distinct vascular beds and differing constitutive or inflammatory conditions) support broadly ranging route usage from essentially totally transcellular to almost completely paracellular diapedesis (Carman, 2009; Sage and Carman, 2009). Although lacking direct assessment of migration routes, a range of in vivo and in vitro studies support this idea. For example, engineered approaches to stabilize the VE-cadherin-actin association at adherens junctions and thereby lock closed the adherens junctions in vivo only partially reduce diapedesis in inflammatory settings, but have no effect on the extensive constitutive trafficking ...

The migration of effector or memory T cells to the graft is a critical event in the rejection of transplanted organs. The prevailing view is that the key steps involved in T cell migration - integrin-mediated firm adhesion followed by transendothelial migration - are dependent on the activation of Gαi-coupled chemokine receptors on T cells. In contrast to this view, we demonstrated in vivo that cognate antigen was necessary for the firm adhesion and transendothelial migration of CD8+ effector T cells specific to graft antigens and that both steps occurred independent of Gαi signaling. Presentation of cognate antigen by either graft endothelial cells or bone marrow-derived APCs that extend into the capillary lumen was sufficient for T cell migration. The adhesion and transmigration of antigen-nonspecific (bystander) effector T cells, on the other hand, remained dependent on Gαi, but required the presence of antigen-specific effector T cells. These findings underscore the primary role of ...

LRFN4, leucine rich repeat and fibronectin type III domain containing 4, is upregulated when monocytes differentiate into macrophages and plays a role in in monocyte/macrophage morphological changes and migration (PMID: 21704618). Overexpression of Lrfn4 has been associated with decreased survival in gastric cancer (PMID: 31089399 ...

PECAM and CD99 have been known to be critical for leukocyte extravasation in vivo for some time (reviewed in Ref. 17); however, this is a complicated, multistep process that involves transmigration across not only the endothelium, but also the basement membrane. There have been discrepancies between studies demonstrating the exact level of function of PECAM and CD99 in relation to the endothelium and basement membrane. In this report we harnessed the technology of 4D IVM to study the step in TEM at which PECAM and CD99 function in vivo in real time. We demonstrate that the role of PECAM and CD99 in leukocyte transmigration is dependent on the murine strain being studied.. The results of these studies explain the apparent inconsistencies among previous studies and largely confirm all previous conclusions. In the commonly used C57BL/6 strain, blocking PECAM or CD99 inhibits migration through the basement membrane, not the endothelium. In contrast, FVB/n mice more accurately replicate results ...

For all types of cancer, the survival rate while the tumor is still localized is significantly higher than when cancer has metastasized. Though different therapeutic methods can be applied to successfully treat primary tumors, treatment of metastasised cancer is a great challenge due to its complex and systemic nature. A deeper understanding of how cancer initiates, grows and migrates is essential for creating successful therapies. Particularly, extravasation - a process during which streaming tumor cells (TCs) adhere to the blood vessels and traverse through the vascular endothelium into the surrounding tissue - is one of the crucial steps of cancer metastasis. While cancer research has mostly focused on the initial processes of metastasis, little is known about mechanisms of transmigration of tumor cells through the vascular wall. We found that during transendothelial migration (TEM), cancers cells undergo substantial shape changes transforming from semi-spherical (with a 2D contact with the ...

Jan C.T. Eijkel is the author of this article in the Journal of Visualized Experiments: Fabrication and Validation of an Organ-on-chip System with Integrated Electrodes to Directly Quantify Transendothelial Electrical Resistance

It all happens in the local church. Just like church planting starts in the local church, so leadership development also happens in the local church. Internships exist to develop leaders for the FMCiC. To develop leaders, supervising pastors are needed who want to invest in developing leaders. Through relationship, these pastors and interns sharpen the work of ministry. We are developing leaders in the local church to pass on the DNA to fulfill the Great Commandment and the Great Commission through the vision of the FMCiC: to see healthy churches within the reach of all people in Canada and beyond.. If you are even just considering hiring a summer intern and perhaps also thinking about applying for the FMCiC internship program for this year, be sure to also apply for the Canada Summer Jobs government funding by their deadline. Please note that the government grant is based on a number of eligibility criteria and priorities, so applying for the government grant does not guarantee you will ...

Previous studies by our group and others have addressed the relationship between leukocyte infiltration into solid tumors and chemokine expression (14 , 16 , 23) . To our knowledge, this work is the first comprehensive study of CC chemokines and chemokine receptor expression in human ovarian cancer ascites.. We found that ascitic fluid is rich in CC chemokines and that the CD14-expressing cells and T cells present in ovarian cancer ascites express CC chemokine receptor mRNA and protein.. Is the extent and phenotype of the leukocyte infiltration in ovarian ascites related to chemokines and chemokine receptor expression? Gradients of chemokines usually cause tissue recruitment of leukocytes through effects on adhesion and endothelial transmigration (24) . Our data suggest that CC chemokine protein levels are significantly higher in ascitic fluid than in patient plasma samples. Therefore, chemokines present in ascites could form a gradient for leukocyte migration into the peritoneal cavity. ...

Mechanisms whereby T lymphocytes contribute to synovial inflammation in rheumatoid arthritis are poorly understood. Here we review data that indicate an important role for cell contact between synovial T cells, adjacent macrophages and fibroblast-like synoviocytes (FLS). Thus, T cells activated by cytokines, endothelial transmigration, extracellular matrix or by auto-antigens can promote cytokine, particularly TNFα, metalloproteinase production by macrophages and FLS through cell-membrane interactions, mediated at least through β-integrins and membrane cytokines. Since soluble factors thus induced may in turn contribute directly to T cell activation, positive feedback loops are likely to be created. These novel pathways represent exciting potential therapeutic targets.

POROUS MEMBRANE DEVICE THAT PROMOTES THE DIFFERENTIATION OF MONOCYTES INTO DENDRITIC CELLS - Dendritic cells (DCs) for research and clinical applications are typically derived from purified blood monocytes that are cultured in a cocktail of cytokines for a week or more. Because it has been suggested that these cytokine-derived DCs may be deficient in some important immunological functions and might not accurately represent antigen-presenting cell (APC) populations found under physiologic conditions, there is a need for methods that allow the generation of DCs in a more physiologically relevant manner. The present invention comprises a simple and reliable technique for generating large numbers of highly purified DCs, based on a single migration of blood monocytes through endothelial cells that are cultured in, for example, a Transwell® device. The resultant APCs, harvested from the lower Transwell® chamber, resemble other in vitro-generated DC populations in their expression of major ...

Lixin Liu is the author of this article in the Journal of Visualized Experiments: Tracking Neutrophil Intraluminal Crawling, Transendothelial Migration and Chemotaxis in Tissue by Intravital Video Microscopy

Inflammation is related to many diseases, such as atherosclerosis, rheumatoid arthritis and metabolic diseases. Vascular adhesion protein-1 (VAP-1) is an endothelial adhesion molecule involved in leukocyte trafficking cascades from blood circulation to the sites of inflammation. In normal condition, VAP-1 is stored in intracellular granules. During inflammation it is rapidly translocated from the intracellular storage granules to the endothelial cell surface. Siglec-9 is a leukocyte ligand of VAP-1 and Siglec-9 motif containing peptide can be used as a positron emission tomography (PET) tracer for in vivo imaging of inflammation-related diseases ...

TY - JOUR. T1 - Adherent neutrophils activate endothelial myosin light chain kinase. T2 - Role in transendothelial migration. AU - Garcia, Joe G.N.. AU - Verin, Alexander D.. AU - Herenyiova, Maria. AU - English, Denis. PY - 1998/5/1. Y1 - 1998/5/1. N2 - Increased vascular endothelial cell (EC) permeability and neutrophilic leukocyte (PMN) diapedesis through paracellular gaps are cardinal features of acute inflammation. Activation of the EC contractile apparatus is necessary and sufficient to increase vascular permeability in specific models of EC barrier dysfunction. However, it is unknown whether EC contraction with subsequent paracellular gap formation is required for PMN transendothelial migration in response to chemotactic factors. To test this possibility, we assessed migration of human PMNs across confluent bovine pulmonary arterial EC monolayers. Transendothelial PMN migration in the absence of a chemotactic gradient was minimal, whereas abluminal addition of leukotriene B4 (LTB4; 5 μM) ...

Interleukin-10 (IL-10) is a negative regulator of immune responses and was previously shown to be expressed by human nasal endothelial cells, while the adhesion molecule MECA-79 plays a role in trans-endothelial migration of immune competent cells. In this study we investigate the relationship between endothelial IL-10 and MECA-79 expression to address the question whether immune competent cells could be affected at the mucosal entry site. Nasal turbinate biopsies were taken from house dust mite allergic patients, before and after nasal allergen provocation. Subsequent slides of biopsies were stained for IL10, MECA-79, CD34, and IL10-Receptor. Capillaries, arteries/veins, and sinusoids were evaluated separately. 90% of sinusoids are IL-10 positive and all sinusoids are negative for MECA-79, while 4.8% of capillaries are positive for IL-10, and 2.2% are positive for MECA-79. Although about 47% of arteries/veins are positive for IL-10 and 57.1% are positive for MECA-79, only about 20% are positive for

In addition to decreased EGF-induced in vivo invasion of Mena11a-expressing cells, we also found that these cells express less CSF1 mRNA. Data from patients suggests that CSF1 and its receptor play crucial roles during progression of breast cancer (Kacinski et al., 1991; Scholl et al., 1994) and that CSF1 and the CSF1R are coexpressed in ,50% of breast tumors (Kacinski, 1997). Elevated circulating CSF1 was also suggested to be an indicator of early metastatic relapse in patients with breast cancer, independent of breast cancer subtype (Scholl et al., 1994; Tamimi et al., 2008; Beck et al., 2009). This suggests that lower levels of CSF1 in Mena11a-expressing cells could lead to decreased metastatic progression. The decreased invasion, intravasation and dissemination of Mena11a-expressing cells are consistent with the decrease in expression of CSF1 and the reduced sensitivity to EGF, which would make these cells less likely to participate in a paracrine signaling loop with macrophages.. A major ...

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Ueta H, Shi C, Miyanari N, Xu XD, Zhou S, Yamashita M, Ezaki T, Matsuno K. Systemic transmigration of allosensitizing donor dendritic cells to host secondary lymphoid organs after rat liver transplantation. Hepatology. 2008 Apr; 47(4):1352-62 ...

Sigma-Aldrich offers abstracts and full-text articles by [Mónica Díaz-Coránguez, José Segovia, Adolfo López-Ornelas, Henry Puerta-Guardo, Juan Ludert, Bibiana Chávez, Noemi Meraz-Cruz, Lorenza González-Mariscal].

Hi How can i find if I have BBB leakage? doctor said he cannot determine it. I was stunned. I am asking because I always feel something is happening...

Some sources say that GABA supplements dont cross the blood brain barrier (BBB), though other sources say that they do. So whos right?

- Most important Earthquake Data: Magnitude : 5.2 Local Time (conversion only below land) : 2017-12-06 10:45:56 GMT/UTC Time : 2017-12-05 23:45:56 Depth (Hypocenter) : 10 km Depth an…