Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of demethylbellidifolin (DMB), a major compound of Swertia davidi Franch, on the adhesion of monocytes to endothelial cells induced by oxidized low-density lipoprotein (ox-LDL) was studied. Adhesion of monocytes to endothelial cells was induced by treatment with ox-LDL (100 microg/mL) for 48 h. Levels of tumor necrosis factor-alpha (TNF-alpha) and asymmetric dimethylarginine (ADMA, an endogenous inhibitor of NOS) in conditioned medium and the activity of dimethylarginine dimethylaminohydrolase (DDAH) in endothelial cells were measured. DMB (3 or 10 micromol/L) significantly inhibited the adhesion of monocytes to endothelial cells, attenuated an increase in levels of TNF-alpha and ADMA, and a decrease in the activity of DDAH by ox-LDL. The present results suggest that DMB inhibits the increased adhesion of monocytes to endothelial cells induced by ox-LDL, and that the effect of DMB is related to reduction of the ADMA concentration via reduction of TNF-alpha production in cultured endothelial cells treated with ox-LDL.
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PMID:Demethylbellidifolin inhibits adhesion of monocytes to endothelial cells via reduction of tumor necrosis factor alpha and endogenous nitric oxide synthase inhibitor level. 1475 34

Adhesion and migration of leukocytes into the surrounding tissues is a crucial step in inflammation, immunity, and atherogenesis. Expression of cell adhesion molecules by endothelial cells plays a leading role in this process. Butyrate, a natural short-chain fatty acid produced by bacterial fermentation of dietary fiber, has been attributed with anti-inflammatory activity in inflammatory bowel disease. Butyrate in vitro is active in colonocytes and several other cell types. We have studied the effect of butyrate on expression of endothelial leukocyte adhesion molecules by cytokine-stimulated human umbilical vein endothelial cells (HUVEC). Pretreatment of HUVEC with butyrate-inhibited tumor necrosis factor-alpha (TNFalpha)-induced expression of vascular cell adhesion molecule-1 (VCAM-1) and intracellular cell adhesion molecule-1 (ICAM-1) in a time and concentration-dependent manner. Butyrate at 10 mM/L inhibited interleukin-1 (IL-1)-stimulated VCAM-1 and ICAM-1 expression. The effect of butyrate on cytokine-stimulated VCAM-1 expression was more pronounced than in the case of ICAM-1. Butyrate decreased TNFalpha-induced expression of mRNA for VCAM-1 and ICAM-1. Suppressed expression of VCAM-1 and ICAM-1 was associated with reduced adherence of monocytes and lymphocytes to cytokine-stimulated HUVEC. Butyrate inhibited TNFalpha-induced activation of nuclear factor-kappaB (NF-kappaB) in HUVEC. Finally, butyrate enhanced peroxisome proliferator-activated receptor-alpha (PPARalpha) expression in HUVEC. These results demonstrate that butyrate may have anti-inflammatory properties not only in colonocytes but also in endothelial cells. The anti-inflammatory and (perhaps) antiatherogenic properties of butyrate may partly be attributed to an effect on activation of NF-kappaB and PPARalpha and to the associated expression of VCAM-1 and ICAM-1. The present findings support further investigations on the therapeutic benefits of butyrate in several pathological events involving leukocyte recruitment.
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PMID:Butyrate inhibits cytokine-induced VCAM-1 and ICAM-1 expression in cultured endothelial cells: the role of NF-kappaB and PPARalpha. 1506 15

Mild hypothermia impairs resistance to infection and, reportedly, impairs phagocytosis and oxidative killing of unopsonized bacteria. We evaluated various functions at 33 degrees-41 degrees C in neutrophils taken from volunteers. Adhesion on endothelial cells was determined using light microscopy. Adhesion molecule expression and receptors, phagocytosis, and release of reactive oxidants were assessed using flow cytometric assays. Adhesion protein CD11b expression on resting neutrophils was temperature-independent. However, up-regulation of CD11b with tumor necrosis factor (TNF)-alpha was increased by hypothermia and decreased with hyperthermia. Neutrophil adhesion to either resting or activated endothelial cells was not temperature-dependent. Bacterial uptake was inversely related to temperature, more so with Escherichia coli than Staphylococcus aureus. Temperature dependence of phagocytosis occurred only wi thopsonized bacteria. Hypothermia slightly increased N-formyl-L-methionyl-L-leucyl-phenylalanine receptors on neutrophils: hyperthermia decreased expression, especially with TNF-alpha. N-formyl-L-methionyl-L-leucyl-phenylalanine-induced H2O2 production was inversely related to temperature, especially in the presence of TNF-alpha. Conversely, phorbol-13-myristate-12-acetate, an activator of protein kinase C, induced an extreme and homogenous release of reactive oxidants that increased with temperature. In contrast to nonreceptor-dependent phagocytosis and oxidative killing, several crucial receptor-dependent neutrophil activities show temperature-dependent regulation, with hypothermia increasing function. The temperature dependence of neutrophil function is thus more complicated than previously appreciated.
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PMID:Mild hyperthermia down-regulates receptor-dependent neutrophil function. 1528 45

Polysaccharides isolated from fungi, Phellinus spp. is well-known material with anti-tumor and anti-inflammatory properties. We have assessed the adhesion- and abscess-reducing capacity of carboxymethylcellulose (CMC) and polysaccharides from Phellinus spp. combination in a rat peritonitis model. In 72 Sprague-Dawley rats, experimental peritonitis was induced by means of the cecal ligation and puncture model (CLP). After 24 hr, the abdomen was reopened and the ligated cecum was resected. Peritoneal fluid samples were taken for microbiological examination. Rats were randomly assigned to 6 groups: ringer lactate solution (RL group), polysaccharides from Phellinus gilvus (PG group) and Phellinus linteus (PL group), carboxymethylcellulose (CMC group), and their combinations (PG+CMC and PL+CMC groups). Adhesions and abscesses were noted at day 7 after CLP. RT-PCR assay for urokinase-type plasminogen activator (uPA), its cellular receptor (uPAR), and tumor necrosis factor (TNF)-alpha was performed to assess the cecal tissue. Microbiological examination showed polymicrobial bacterial peritonitis. Adhesion formation was significantly reduced in PG+CMC and PL+CMC groups (P<0.05). The incidence of abscesses was reduced in all treated groups except the RL group (P<0.05). uPA, uPAR, and TNF-alpha mRNA were highly expressed in the PG+CMC and PL+CMC groups, as compared to the RL group. We concluded that the combination of polysaccharides and CMC had significant adhesion- and abscess-reducing effects compared with their single treatment and the effects may act by modifying the fibrinolytic capacity of uPA, uPAR and TNF-alpha produced from activated macrophages in a rat peritonitis model.
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PMID:The effect of polysaccharides and carboxymethylcellulose combination to prevent intraperitoneal adhesion and abscess formation in a rat peritonitis model. 1552 50

Adhesion molecules, which play a crucial role in the development of atherogenesis, are produced by endothelial cells following stimulation with various inflammatory cytokines. The current studies examined the effect of a potent water-soluble antioxidant, protocatechuic aldehyde (derived from the Chinese herb, Salvia miltiorrhiza), on the expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis factor-alpha (TNF-alpha). Protocatechuic aldehyde appeared to specifically downregulate the TNF-alpha-induced cell surface expression of vascular adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) on HUVECs as well as the release of soluble VCAM-1and ICAM-1 from HUVECs in a dose-response manner at pharmacologically relevant concentrations (0.15-1.35 mM). We also observed a dose-dependent lowering of mRNA expression of VCAM-1 and ICAM-1 in the presence of protocatechuic aldehyde. Furthermore, protocatechuic aldehyde (0.15, 0.45, and 1.35 mM) notably inhibited TNF-alpha-induced upregulation of U937 cell adhesion to HUVECs to 83.7%, 60.9%, and 40.8%, respectively. A gel shift assay further showed that protocatechuic aldehyde inhibited the TNF-alpha-activated NF-kappaB and AP-1 DNA binding activities in a dose-dependent manner. Collectively, these results indicate that protocatechuic aldehyde inhibits TNF-alpha-stimulated VCAM-1 and ICAM-1expression in HUVECs through a mechanism that involves NF-kappaB and AP-1.
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PMID:Protocatechuic aldehyde suppresses TNF-alpha-induced ICAM-1 and VCAM-1 expression in human umbilical vein endothelial cells. 1587 4

The influence of different surface modifications with poly(ethyleneglycol) (PEG) layers on the adsorption of fibrinogen and the adhesion and activation of macrophage-like human leukocytes was investigated. Poly(ethylene terephthalate) (PET) was modified using pulsed AC plasma polymerization with two types of starting monomers to generate: 1) a reactive acid surface using maleic anhydride (MAH) as monomer, and 2) a PEG-like surface using diethyleneglycol methyl vinyl ether (DEGVE) as monomer. The MAH surface was used as a reactive platform to graft linear chains of non-fouling mPEG via an intermediate layer of poly(ethyleneimine) (PEI) under lower critical solution temperature (LCST) conditions of the mPEG. The DEGVE monomer is used to create PEG-like layers by use of low power plasma conditions. The ability of the surfaces to resist protein adsorption was investigated quantitatively using (125)I-radiolabeled human fibrinogen, and the conformation of the adsorbed protein was tested using an anti-fibrinogen monoclonal antibody in an enzyme-linked immunosorbent assay. The results showed that PEGylated surfaces adsorbed significantly less (up to 90% less) fibrinogen, and that unfolding of adsorbed fibrinogen was more pronounced on the linear mPEG layers than on the PEG-like plasma polymer surfaces. Adhesion of in-vitro differentiated macrophage-like U937 cells was reduced on both the PEG-like plasma polymer surfaces and the linear mPEG layers compared to the unmodified PET surface, but cells adhering to the PEG-like plasma polymer surfaces secreted less tumor necrosis factor-alpha (TNF-alpha) than cells adhering to the linear mPEG layers. In conclusion, the method for preparing non-fouling surfaces for long-term implanted devices influence surface-induced cellular responses of the host.
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PMID:The method of surface PEGylation influences leukocyte adhesion and activation. 1655 12

Recent studies have underscored the role of B-cell-activating factor (BAFF), a member of the tumor necrosis factor superfamily, in promoting the survival of malignant B cells, including human multiple myeloma. We here characterized the functional significance of BAFF in the interaction between multiple myeloma and bone marrow stromal cells (BMSC) and further defined the molecular mechanisms regulating these processes. BAFF is detected on BMSCs derived from multiple myeloma patients as evidenced by flow cytometry. BAFF secretion is 3- to 10-fold higher in BMSCs than in multiple myeloma cells, and tumor cell adhesion to BMSCs augments BAFF secretion by 2- to 5-fold, confirmed by both ELISA and immunoblotting. Adhesion of MM1S and MCCAR multiple myeloma cell lines to KM104 BMSC line transfected with a luciferase reporter vector carrying the BAFF gene promoter (BAFF-LUC) significantly enhanced luciferase activity, suggesting that nuclear factor-kappaB (NF-kappaB) activation induced by multiple myeloma adhesion to BMSCs mediates BAFF up-regulation. Moreover, BAFF (0-100 ng/mL) increases adhesion of multiple myeloma lines to BMSCs in a dose-dependent manner; conversely, transmembrane activator and calcium modulator and cyclophylin ligand interactor-Ig or B-cell maturation antigen/Fc blocked BAFF stimulation. Using adenoviruses expressing dominant-negative and constitutively expressed AKT as well as NF-kappaB inhibitors, we further showed that BAFF-induced multiple myeloma cell adhesion is primarily mediated via activation of AKT and NF-kappaB signaling. Importantly, BAFF similarly increased adhesion of CD138-expressing patient multiple myeloma cells to BMSCs. These studies establish a role for BAFF in localization and survival of multiple myeloma cells in the bone marrow microenvironment and strongly support novel therapeutics, targeting the interaction between BAFF and its receptors in human multiple myeloma.
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PMID:Role of B-cell-activating factor in adhesion and growth of human multiple myeloma cells in the bone marrow microenvironment. 1681 41

Intestinal adhesions are bands of fibrous tissue that connect the loops of the intestine to each other, to other abdominal organs or to the abdominal wall. Fibrous tissue formation is regulated by the balance between plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (tPA), which reciprocally regulate fibrin deposition. Several components of the inflammatory system, including cytokines, chemokines, cell adhesion molecules and neuropeptide substance P, have been reported to participate in adhesion formation. We have used cecal cauterization to develop a unique experimental mouse model of intestinal adhesion. Mice developed severe intestinal adhesion after this treatment. Adhesion development depended upon the interferon-gamma (IFN-gamma) and signal transducer and activator of transcription-1 (STAT1) system. Natural killer T (NKT) cell-deficient mice developed adhesion poorly, whereas they developed severe adhesion after reconstitution with NKT cells from wild-type mice, suggesting that NKT cell IFN-gamma production is indispensable for adhesion formation. This response does not depend on STAT4, STAT6, interleukin-12 (IL-12), IL-18, tumor necrosis factor-alpha, Toll-like receptor 4 or myeloid differentiation factor-88-mediated signals. Wild-type mice increased the ratio of PAI-1 to tPA after cecal cauterization, whereas Ifng(-/-) or Stat1(-/-) mice did not, suggesting that IFN-gamma has a crucial role in the differential regulation of PAI-1 and tPA. Additionally, hepatocyte growth factor, a potent mitogenic factor for hepatocytes, strongly inhibited intestinal adhesion by diminishing IFN-gamma production, providing a potential new way to prevent postoperative adhesions.
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PMID:Interferon-gamma is a therapeutic target molecule for prevention of postoperative adhesion formation. 1834 12

Cartilage engineering is the object of intense research as a result of major medical needs and therapeutic prospects. Porcine xenogeneic cells/tissues may help in the development of clinical applications such as articular cartilage repair. However, unmodified porcine cartilage is rejected in primates by humoral and cellular mechanisms. We previously showed that porcine articular chondrocytes (PAC) isolated from H-transferase (HT) transgenic pigs show markedly reduced expression of the Galalpha1,3Gal antigen (alphaGal) and prolonged survival when transplanted into alpha1,3galactosyltransferase-deficient mice. In this work, we further studied the protective mechanisms of HT transgenic expression in cartilage, particularly its effects on monocyte adhesion. To this end, PAC isolated from control and HT transgenic pigs were assayed for human complement deposition and adhesion to the human monoblastic cell line U937. Consistent with a reduction in complement activation by the classical pathway, the HT transgenic PAC showed a 2-fold reduction in the deposition of complement components C4 and C3 relative to controls. Adhesion of U937 cells to HT PAC was also diminished under various conditions. This reduction was more dramatic at high effector:target ratios and especially observed when combined with anti-alphaGal antibodies (5-fold difference). Nevertheless, this effect was also observed in the absence of anti-alphaGal. antibodies and after tumor necrosis factor treatment. These results suggest that HT expression on porcine chondrocytes protects them from both humoral and cellular rejection.
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PMID:Characterization of cartilage from H-transferase transgenic pigs. 1837 27

Dendritic cells (DCs) have been increasingly implicated in the pathogenesis of neuroinflammation, and there is evidence that they are recruited to the brain across the blood-brain barrier. The molecular mechanisms mediating DC trafficking to the central nervous system are poorly understood. This study used an in vitro model of the human blood-brain barrier and monocyte-derived DCs to investigate the role of endothelial cell (EC) adhesion molecules and their ligands in the adhesion of immature and mature DCs to cerebral microvascular ECs. Adhesion of DCs to resting brain ECs was minimal, but activation of ECs with tumor necrosis factor significantly upregulated adhesion. Immature DCs adhered to activated ECs more avidly than mature DCs; this correlated with differences in the expression of adhesion molecule ligands between the mature and immature DCs. Blocking studies indicated that adhesion to cytokine-activated blood-brain barrier endothelium is mediated by intercellular adhesion molecule (ICAM)-1, ICAM-2, platelet-EC adhesion molecule (PECAM)-1, vascular cell adhesion molecule 1, CD18, and DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN) for immature DCs and ICAM-1, CD18, DC-SIGN, and PECAM-1 for mature DCs. These results suggest that DC adhesion to cerebral ECs depends on the maturation state of DCs and the activation state of the endothelium, and that it is regulated by specific receptor-ligand interactions. This study thus further highlights the active role of human brain microvascular ECs in neuroinflammation.
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PMID:Dendritic cell adhesion to cerebral endothelium: role of endothelial cell adhesion molecules and their ligands. 1922 7


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