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)

Virus-specific T-cell responses are believed to be involved in the pathogenesis of liver cell injury secondary to hepatitis B virus infection. In this study, liver biopsy specimens from patients with chronic hepatitis B virus infection were analyzed for expression of two major pathways of adhesion used by cytotoxic T cells to interact with target cells. The lymphocyte function-associated antigen 3 was found preferentially expressed on hepatocytes of patients with active hepatitis B virus replication, whereas the expression of the intercellular adhesion molecule 1 on hepatocytes seemed more closely related with inflammatory activity. Adhesion molecules were also highly expressed on T lymphocytes found in areas of piecemeal and spotty necrosis, indicating the presence of antigen-specific "memory" T cells at the site of hepatocellular injury. This study suggests that the expression of the lymphocyte function-associated antigen 3 on hepatocytes may be important for viral elimination. The coordinate expression of the intercellular adhesion molecule 1 may regulate inflammatory response and enhance viral antigen presentation to T cells. Conversely, the absence of hepatocyte adhesion molecules might be a favorable factor for viral persistence.
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PMID:Expression of leukocyte adhesion molecules in the liver of patients with chronic hepatitis B virus infection. 170 28

Herpesviral infection of endothelial cells (ECs) induces arterial injury. We now demonstrate that such infection promoted enhanced monocyte-endothelial adhesion. Enhanced adhesion was blocked by monoclonal antibodies to the viral-encoded cell surface glycoprotein gC but not by antibodies to gD or gE. Adhesion was also blocked by treating ECs with specific thrombin inhibitors or by growing cells in prothrombin-depleted serum. We found that gC bound and promoted activation of factor X on infected ECs, thereby contributing to thrombin generation. Factor X also bound to transfected L cells that were induced to express gC. Cross-linking and immunoprecipitation studies demonstrated factor X-gC complex formation on the surface of these cells. We suggest that gC-dependent thrombin generation by herpes-infected endothelium may be an important mediator of vascular pathology during viral infection.
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PMID:Viral activation of the coagulation cascade: molecular interactions at the surface of infected endothelial cells. 216 Aug 55

The adherence of eleven strains of Haemophilus influenzae to MRC5 cells was studied and compared with adherence of the same eleven strains to MRC5 cells infected with influenza A/NWS/33 virus. Per cent Adhesion (the proportion of cells to which more than two bacteria were adhering) was estimated. Organisms grown on solid media adhered better than those grown in liquid media though the difference was not statistically significant (t test for independent means). A wide range of % Adhesion values for organisms grown on solid media to control cells was exhibited (1-88%). Ten of eleven strains grown on solid media or in broth showed increased adherence to influenza virus infected cells; this difference was significant (P less than 0.05, t test for independent means). The effect of virus infection in increasing % Adhesion was inversely proportional to the adhesiveness of the strain in question to uninfected cells. Strains that adhered most efficiently to control cells showed little increase in % Adhesion following virus infection, while strains that adhered poorly to control cells showed large increases in % Adhesion following virus infection.
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PMID:The effect of influenza virus on the adherence of Haemophilus influenzae to human cells in tissue culture. 660 64

Measles virus (MV) RNA is present in endothelial cells (Ec) in brain tissue from cases of subacute sclerosing panencephalitis (SSPE) and relatively high titres of infectious virus are produced in human cerebral Ec in vitro. Infection of Ec at the blood-brain barrier could therefore provide the opportunity for entry of virus to the CNS. Adhesion of syngeneic splenocytes to MV infected murine (Balb/c) cerebral Ec is found to be upregulated. Increased expression of endothelial adhesion molecules, following virus infection at the blood-brain-barrier, may be an important mechanism in inducing inflammatory infiltration of the CNS in SSPE.
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PMID:Measles virus infection of cerebral endothelial cells and effect on their adhesive properties. 858 7

Respiratory epithelium is both a target and an effector of airway inflammation. Adhesion molecules on epithelium play an important role in a variety of airway diseases. Respiratory syncytial virus (RSV) is the most important pathogen for airway diseases in infants. The expression of adhesion molecules on epithelium in RSV infection, however, is unclear. The expression of selected adhesion molecules and major histocompatibility complex (MHC) class I and II antigens on a human alveolar type II epithelial cell line (A549) infected with RSV was investigated by means of flow cytometry and immunocytochemistry. The results showed that intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were expressed on A549 cells at a low level. E-cadherin and MHC class I antigen were constitutively expressed on the cells. RSV infection of A549 cells significantly upregulated the expression of ICAM-1, VCAM-1 and MHC class I and II antigens on these cells. RSV infection also altered the expression of E-cadherin on A549 cells. Immunostaining showed that E-cadherin was mainly upregulated around or in RSV-induced giant cells. These data suggest that respiratory syncytial virus infection of respiratory epithelial cells enhances the expression of adhesion molecules and major histocompatibility complex antigens. These changes may play an important role in the pathophysiology of respiratory syncytial virus disease.
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PMID:Adhesion molecule expression on epithelial cells infected with respiratory syncytial virus. 1070 5

The effect of herpes virus infection on human dermal microvascular endothelial cells and herpes-virus-1-infected peripheral blood mononuclear cells on human dermal microvascular endothelial cells was studied as a model of herpes-associated erythema multiforme. After infection of human dermal microvascular endothelial cells with native herpes virus and overnight culture, 60%--90% of human dermal microvascular endothelial cells showed cytopathic effects. HLA class I molecules and CD31 (PECAM-1) surface expression in herpes-virus-infected endothelial cells were substantially downregulated, whereas CD54 (ICAM-1) remained unchanged. Cocultivation with herpes-virus-1-infected peripheral blood mononuclear cells left characteristic plaques on the human dermal microvascular endothelial cell monolayer; however, very few human dermal microvascular endothelial cells (1%--3%) were infected. Adhesion molecule expression of human dermal microvascular endothelial cells cocultivated with herpes-virus-infected peripheral blood mononuclear cells demonstrated a 5-fold increase in CD54 expression, a 2-fold increase in HLA class I expression, but no change of CD31 by fluorescence-activated cell sorter analysis. Incubation of human dermal microvascular endothelial cells with ultraviolet-C irradiated herpes-virus-infected peripheral blood mononuclear cells had no effect on morphology or adhesion molecule expression levels. Changes of adhesion molecule expression by direct infection or cocultivation with peripheral blood mononuclear cells (with native and ultraviolet-C inactivated herpes virus infection) were also documented at the mRNA level. Adhesion assays demonstrated an increased binding of herpes-virus-infected peripheral blood mononuclear cells versus noninfected peripheral blood mononuclear cells to noninfected human dermal microvascular endothelial cells. Our results suggest that incubation of herpes-virus-infected peripheral blood mononuclear cells with human dermal microvascular endothelial cells induces significant upregulation of CD54 and major histocompatibility complex class I molecules in the surrounding noninfected human dermal microvascular endothelial cells, which is associated with an increased binding of peripheral blood mononuclear cells. Our in vitro findings may serve as a model for herpes-associated erythema multiforme possibly explaining the dermal inflammatory reaction seen in that condition.
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PMID:Interaction of HSV-1 infected peripheral blood mononuclear cells with cultured dermal microvascular endothelial cells: a potential model for the pathogenesis of HSV-1 induced erythema multiforme. 1116 11

Adhesion molecules are essential for the immune response. They are involved in the regulation of cell-to-cell contact, thereby enabling leukocytes to communicate. Circulating forms of adhesion molecules are found in the serum of healthy individuals. Raised levels have been associated with disease severity in HCV and other infections and thus appear to be good markers of endothelial damage. The levels of soluble Vascular Cell Adhesion Molecule-1 (sVCAM-1) and of sP and sL-selectin in the plasma of children hospitalised for dengue in French Polynesia were monitored. Studies from the 1996/1997 dengue-2 outbreak, showed that levels of sVCAM-1 increase steadily during the febrile period, peak on day 7, and then decline relatively rapidly. Disregarding the time frame within the febrile period, sVCAM-1 levels were always higher compared to controls. There was a significant association between sVCAM-1 levels and dengue haemorrhagic fever, a severe manifestation of dengue virus infection characterised by plasma leakage. No association was apparent between sVCAM-1 levels and primary vs. secondary dengue virus infections. Levels of sP-selectin and sL-selectin were significantly higher in primary compared with secondary infection but were not different in patients presenting with plasma leakage. Lastly, sVCAM-1 levels were significantly higher in an outbreak of severe disease in 1989/1990 (dengue-3) when compared to a non-severe outbreak in 1988/1989 (dengue-1) and a mild outbreak in 1996/1997 (dengue-2). The results suggested that levels of sVCAM-1 production might prove to be a useful marker in the management of severe dengue.
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PMID:Plasma concentrations of sVCAM-1 and severity of dengue infections. 1150 50

To prepare for shortage of blood components and to avoid side effects such as blood borne infectious disease, blood substitutes such as artificial red cell (artificial oxygen carrier) and artificial platelet are being developed. As for oxygen carriers, there are several candidates such as perfluorochemicals, modified hemoglobins and liposome encapsulated hemoglobins and albuimin heme. Perfluorochemicals have limited oxygen carrying capacity and oxygen inhalation is mandatory when they are used. Modified hemoglobins such as intermolecular or intramolecular cross linked hemoglobins have side effect to cause hypertension by scavenging nitro oxide (NO) which is produced by endothelial cells, because the size of these hemoglobins are small enough to go to the adjacent place near endothelial surface. Hemoglobin vesicles (HbV) in which hemoglobins are encapsulated in liposome is most possible candidate for oxygen carrier. Usefulness and safety of the HbV is evidenced by animal shock model or exchange transfusion model and they are now being prepared for clinical trials as red blood substitutes or oxygen therapeutics. Albumin heme in which recombinant human serum albumin incorporating synthetic heme is thought an ideal resuscitation fluid as this material has colloid oncotic pressure. Short time storage and viral infection are serious concern in platelet transfusion therapy for bleeding thrombocytopenic patients. Adhesion of the platelet to the collagen surface and aggregation at the bleeding sites to plug holes in blood vessels, and to facilitate the function of the remaining platelets is a starting point in developing platelet substitutes and several platelet substitutes have been proposed on this theory.
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PMID:[Artificial blood]. 1569 96

Adhesion to epithelial surface is often the first step in bacterial and viral infection. In this process, the microbes use a variety of proteins for interaction with host carbohydrates presented as glycoconjugates on cell surfaces. Crystal structures of adhesin and lectin binding sites in complexes with oligosaccharide open the route for design and synthesis of glycomimetics, glycodendrimers, and glycopolymers that are able to block infection at an early stage.
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PMID:Glycomimetics and glycodendrimers as high affinity microbial anti-adhesins. 1861 37

Adhesion molecules are critical players in the regulation of transmigration of blood leukocytes across the blood-brain barrier in multiple sclerosis (MS). Cannabinoids (CBs) are potential therapeutic agents in the treatment of MS, but the mechanisms involved are only partially known. Using a viral model of MS we observed that the cannabinoid agonist WIN55,212-2 administered at the time of virus infection suppresses intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in brain endothelium, together with a reduction in perivascular CD4+ T lymphocytes infiltrates and microglial responses. WIN55,212-2 also interferes with later progression of the disease by reducing symptomatology and neuroinflammation. In vitro data from brain endothelial cell cultures, provide the first evidence of a role of peroxisome proliferator-activated receptors gamma (PPARgamma) in WIN55,212-2-induced downregulation of VCAM-1. This study highlights that inhibition of brain adhesion molecules by WIN55,212-2 might underline its therapeutic effects in MS models by targeting PPAR-gamma receptors.
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PMID:A cannabinoid agonist interferes with the progression of a chronic model of multiple sclerosis by downregulating adhesion molecules. 1905 82


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