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)

We report the pathologic changes in the temporal bones of four children who died of bronchoppenumonia secondary to acute measles infection. All suffered from severe necrotizing otitis media characterized by round cell infiltration. In one case, multilobulated giant cells (Warthin-Finkelday) were found in the middle ear. These cells appear to be similar to those found elsewhere within the body during acute measles infection. Inner ear changes were seen in two cases. Severe loss of nerve fibers and ganglion cells with atrophy of the striae vascularis was present in one case. Adhesions were seen between the Reissner membrane and the tectorial membrane in one case and the Reissner membrane and the inner spiral limbus in a second case. Such findings are characteristic of those seen in the cochlear duct of persons suffering from prenatal rubella.
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PMID:Histopathologic changes in the temporal bone resulting from measles infection. 83 45

Expression of endothelial cell (EC) adhesion molecules is increased in inflammatory neurological disorders and this may regulate lymphocyte homing to the central nervous system (CNS). Viral encephalitis is characterised by lymphocytic infiltration of the CNS and one mechanism of this response may be EC adhesion molecule induction with consequent inflammatory cell/EC binding. This report characterises the effects of herpes simplex 1 (HSV1) or measles virus (MV) infection of BALB/c brain microvascular EC in vitro on adhesion of naive syngenic splenocytes and levels of ICAM-1. Adhesion was enhanced by 42% for MV-infected cells and by 73% for HSV-1-infected EC. At the multiplicities of infection employed, levels of ICAM-1 were upregulated on HSV-1-infected EC, but not on MV-infected EC. It is concluded that ICAM-1/ligand interactions do not play a role in mediation of MV enhancement of adherence, but represent one mechanism responsible for increased lymphocyte adherence to HSV-1-infected cerebral EC.
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PMID:Adhesion molecule expression and lymphocyte adhesion to cerebral endothelium: effects of measles virus and herpes simplex 1 virus. 782 75

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

Pathological changes in inflammatory bowel disease include an increase in intestinal mucosal mononuclear leukocytes and hyperplasia of the muscularis mucosae smooth muscle cells (M-SMCs). Because virus infections have correlated with disease flare, we tested the response of cultured M-SMCs to respiratory syncytial virus, measles virus, and the viral analogue, poly(I.C). Adhesion of U937 cells and peripheral blood mononuclear cells was used to measure the leukocyte-interactive potential of M-SMCs. Untreated M-SMCs, only minimally adhesive for leukocytes, bound U937 cells after treatment with respiratory syncytial virus or measles virus. Mononuclear leukocytes also bound to poly(I.C)-treated M-SMCs. Although both vascular cell adhesion molecule-1 mRNA and protein increased 3-4-fold in poly(I.C)-treated M-SMC cultures, U937 cell adhesion was not blocked by an anti-vascular cell adhesion molecule-1 monoclonal antibody. However, hyaluronidase digestion of poly(I.C)- or virus-treated M-SMCs dramatically reduced leukocyte adhesion ( approximately 75%). Fluorophore-assisted carbohydrate electrophoresis demonstrated a approximately 3-fold increase in surface-bound hyaluronan on poly(I.C)-treated M-SMCs compared with untreated controls. In addition, pretreatment of mononuclear cells with a blocking anti-CD44 antibody, greatly decreased adhesion to poly(I.C)-treated M-SMCs. Recognition of this virus-induced hyaluronan/CD44 mechanism of mesenchymal cell/leukocyte interaction introduces a new avenue in the research of gut inflammation.
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PMID:Mononuclear leukocytes preferentially bind via CD44 to hyaluronan on human intestinal mucosal smooth muscle cells after virus infection or treatment with poly(I.C). 1052 64