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

Fronto-ethmoidal mucocoeles have the capacity to destroy bone. Sinus lining tissue has been obtained at surgery from patients with mucocoeles, from those with chronic sinusitis undergoing endoscopic sinus surgery and from patients undergoing craniofacial resection. Tissues have been frozen, sectioned, and subjected to immunohistochemical examination with monospecific antibodies for the presence of the potent osteolytic cytokines interleukins-1 and -6 and tumour necrosis factor alpha. In addition, the chemotactic intercrine--interleukin-8 was investigated. The presence of the cytokine-inducible vascular endothelial adhesion receptors--Inter-Cellular Adhesion Molecule (ICAM)-1 and E-Selectin (also known as Endothelial Leukocyte Adhesion Molecule--ELAM) was also determined. Normal sinus tissue showed no immunoreactivity with the antibodies to these various moieties. Surprisingly, only a small proportion of tissues from patients with chronic sinusitis showed the presence of cytokines or vascular adhesion receptors. In contrast, all specimens of fronto-ethmoidal mucocoeles showed positive staining for IL-1 alpha and beta and for ICAM-1 and E-selectin. IL-1 immunostaining was restricted to the epithelial cell population not being found in infiltrating leukocytes. In 40% of mucocoeles infiltrating macrophage-like cells showed the presence of tumour necrosis factor alpha. The presence of the potent osteolytic cytokine--IL-1 in all specimens of fronto-ethmoidal mucocoeles coupled to the finding of the IL-1-inducible adhesion molecules ICAM-1 and E-Selectin argues strongly that IL-1 is released from the epithelial cells and that this cytokine may be the factor causing the erosion of bone overlying the expanding mucocoele. The nature of the signals inducing cytokine synthesis remain, however, unidentified.
 ...
PMID:Involvement of cytokines and vascular adhesion receptors in the pathology of fronto-ethmoidal mucocoeles. 769 Oct 23

Venous and arterial large vessel endothelial cells (EC) were compared for their constitutive and TNF-alpha-induced expression of the cell-surface adhesion molecules ICAM-1 and -2, VCAM-1 and ELAM-1 by FACS analysis. Human iliac venous and arterial EC (HIVEC and HIAEC) constitutively express ICAM-1 and ICAM-2. TNF-alpha increases the expression of ICAM-1, but not ICAM-2, and induces the expression of ELAM-1 on both EC types. However, TNF-alpha induces VCAM-1 cell-surface expression and mRNA only in venous, but not in arterial EC. We next investigated the function of these adhesion molecules and their ligands, LFA-1, very late activation Ag (WLA-L) and sialylated Lewis x glycoprotein (sLe(x)), in adhesion assays with the monocyte-like cell line U937. Untreated U937 cells do not adhere to untreated HIVEC or HIAEC and adhesion is much lower to TNF-alpha-treated arterial than to TNF-alpha-treated venous EC. In adhesion-inhibition assays we demonstrate that U937 cell adhesion to TNF-alpha-treated HIVEC is mediated by VCAM-1/VLA-4 and ELAM-1/sLe(x) interaction, whereas the lower adhesion to TNF-alpha-treated HIAEC is only mediated by ELAM-1/sLe(x) interaction. U937 cells treated with the phorbol ester PMA for 3 days adhere to both HIVEC and HIAEC; this adhesion is mediated by LFA-1 interaction with ICAM-1 and/or -2. Adhesion of PMA-treated U937 cells is increased by TNF-alpha treatment of EC. This increased adhesion is mediated in part by the TNF-alpha-induced VCAM-1 expression on venous EC. Therefore, the cell-surface adhesion molecule VCAM-1 is differentially induced on these two EC types and the differential expression is functionally important in U937 cell adhesion.
 ...
PMID:Differential induction of VCAM-1 on human iliac venous and arterial endothelial cells and its role in adhesion. 769 6

Monocytes but not unstimulated lymphocytes adhered to human neurons and astrocytes in primary culture, as demonstrated by double labeling. The expression of VCAM-1 was higher on neurons than on astrocytes, whereas that of beta 1, alpha 1, alpha 2, alpha 4 and alpha 5 chains from the integrins and of ICAM-1 was identical on both types of cells. The expression on neurons of ICAM-1, but not of integrins, was up-regulated by exogenous tumor necrosis factor (TNF) alpha, interleukin (IL)-1 alpha and interferon (IFN)-gamma. The same was observed on astrocytes associated with a sharp increase in the expression of VCAM-1. Adhesion between monocytes and neurons or astrocytes was 80% inhibited by mAbs directed against the CR3 determinant on monocytes or against ICAM-1 on neural cells but not by any of the other mAbs against adhesion proteins that were tested. Finally, the level of endogenous production of IL-1 alpha and TNF alpha was greatly increased after the adhesion of monocytes to CNS cells.
 ...
PMID:Adhesion to human neurons and astrocytes of monocytes: the role of interaction of CR3 and ICAM-1 and modulation by cytokines. 770 27

Three families of cell-surface proteins are largely responsible for the adherence of leukocytes to cells and matrices: integrins, immunoglobulin (Ig)-related molecules and selectins. Blood monocytes express beta 1 integrins VLA-4, -5 and -6 and beta 2 integrins CD11a/CD18, CD11b/CD18 and CD11c/CD18. These cells also express the Ig-related molecules ICAM-1, -2 and -3, ligands for the beta 2 integrins. In addition, monocytes express L-selectin and the oligosaccharides Lex and sialyl Lex, ligands for the endothelial selectins E- and P-. In vitro studies with blocking antibodies have identified adhesion molecules participating in the adherence of monocytes to one another, to T lymphocytes and to vascular endothelial cells. These antibodies also block adhesion-dependent monocyte activities, such as cytotoxicity of tumor cells, antigen presentation, phagocytosis of large particles, induction of cytokine secretion, formation of multinucleated giant cells and HIV-induced syncytium formation. In vivo studies in animals have demonstrated participation of L-selectin and CD11b/CD18 in monocyte accumulation in inflamed peritoneum. Moreover, treatment with anti-CD11b antibodies potentiates primary listeriosis and inhibits the macrophage recruitment and granuloma formation, and anti-CD18 antibodies block ear swelling in Mycobacterium tuberculosis-immunized animals following challenge with PPD. Adhesion molecules may also play key roles in the pathogenesis of tuberculosis and AIDS.
 ...
PMID:Adhesion molecules mediating recruitment of monocytes to inflamed tissue. 771 61

We have previously shown that lymphocytic cells bind to cultured syncytiotrophoblast and that this may be important in the lymphocyte-mediated infection of trophoblast with the human immunodeficiency virus (HIV). Leukocyte-trophoblast adhesion may also have implications for normal trophoblast function. The following experiments were designed to characterize the adhesion systems that mediate the attachment of lymphocytic cells to trophoblast. Adhesion was assayed by labelling lymphocytic MOLT-4, clone 8 cells with the fluorescent marker, calcein-AM, and then incubating them with primary cultures of human syncytiotrophoblast. Adhesion was stimulated by pretreatment of the trophoblast cultures with several cytokines either alone or together. These included tumor necrosis factor-alpha (TNF-alpha), granulocyte/macrophage-colony stimulating factor (GM-CSF), interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma). Stimulation was time- and dose-dependent. In contrast, preincubation of trophoblast cultures with anti-TNF-alpha antibodies for 2 days reduced MOLT adhesion by almost 50%. Preincubation with other anti-cytokine antibodies had no significant effect on adhesion. In other experiments, adhesion was measured in the presence of antibodies to known adhesion molecules. Adhesion was reduced by 50% in the presence of antibodies to alpha 4 integrin or beta 1 integrin. When present together, these antibodies reduced adhesion by almost 85%. Incubation in the presence of antibodies to the very late activation antigen-4 (VLA-4; alpha 4 beta 1 integrin) counter-receptors, VCAM-1 and CS-1, was without effect. Adhesion was also unaffected by antibodies to LFA-1, ICAM-1, ICAM-2, LFA-2, or LFA-3. These results suggest that adhesion is mediated by an adhesion system consisting of lymphocyte VLA-4 (alpha 4 beta 1) and an as yet unidentified counter receptor on trophoblast.
 ...
PMID:Effect of cytokines and anti-adhesion molecule antibodies on the adhesion of lymphocytic cells to human syncytiotrophoblast. 780 71

Endothelial damage, synovial oedema, fibrin deposition, polymorphonuclear cell (PMN) invasion, and mild lining cell hyperplasia characterize acute inflammatory arthritis. Later on, perivascular tissue is infiltrated by mononuclear cells. The early events are mediated by interactions between PMNs and endothelial cells. Both parts in the adhesion event are activated with multiple stimuli resulting in complex interactions of varying intensity and duration. Adhesion molecules present on the surface of PMNs (L-selectin) or induced by inflammatory stimuli (beta 2-integrins) mediate PMN adhesion to activated endothelium, which has counter receptors (E-selectin for L-selectin and ICAM-1 and ICAM-2 for beta 2-integrins). At the initial phase L-selectin initiates the rolling of PMNs on endothelial cells. Further stimuli result in a more prolonged adhesion between PMNs and endothelium. At the side of endothelium, induction of P-selectin and PAF by histamine, thrombin and LTC4 contribute to the acute rolling of PMNs on endothelial surface. Tumor necrosis factor (TNF), interleukin-1 (IL-1) and lipopolysaccharide activate endothelial cells to synthesize interleukin-8 (IL-8), a potent chemotactic and proadhesive mediator for PMNs, and further adhesion molecule (E-selectin), a mediator of long-term adhesion between PMN and endothelium. After adhesion and migration to the focus of inflammation, PMNs induce inflammation by aggregating, releasing hydrolyzing enzymes, generating lipid peroxidation products such as prostaglandins and LTB4, and oxygen derived free radicals. In studies on the pathogenesis of seronegative spondyloarthropathies, we have shown persistently aberrant PMN function evidenced by enhanced chemotaxis and high production of toxic oxygen derived free radicals by PMN.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The present knowledge of the inflammatory process and the inflammatory mediators. 781 74

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.
 ...
PMID:Adhesion molecule expression and lymphocyte adhesion to cerebral endothelium: effects of measles virus and herpes simplex 1 virus. 782 75

Adhesion molecules play a major role in the recruitment of neutrophils to the site of inflammation. Currently, two congenital hereditary Leukocyte Adhesion Deficiency (LAD) syndromes are recognized. LAD I is due to the absence of the beta subunit of the integrin molecule, while LAD II is caused by a deficiency of Sialy1 Lewis X, the neutrophil ligand for selectins. Clinically, both syndromes are characterized by recurrent bacterial infections, more severe in LAD I. Developmental abnormalities (growth and mental retardation) constitute a prominent feature of LAD II and may be attributed to a general defect found in fucose metabolism in LAD II. Neutrophil motility was found to be defective in both syndromes. Using activated umbilical endothelial cells, we showed that LAD I neutrophil do not bind to cells expressing ICAM-1, while LAD II cells do not bind to endothelial cells expressing E- or P-selectin. Skin window technique showed a marked decrease in margination in both syndromes. Using intravital microscopy we were able to show that the basic defect in LAD II is in the "rolling" phase, while in LAD I, firm adhesion and transmigration are defective. Studies of these two rare conditions emphasized the important in vivo roles of adhesion molecules in host defense mechanism.
 ...
PMID:Adhesion molecule deficiencies and their clinical significance. 782 63

Adhesion molecules play a critical role in leukocyte emigration to a site of inflammation. In order to assess the potential therapeutic benefit of blocking adhesion molecule function in anterior uveitis, the efficacy of antibodies to specific adhesion molecules was tested in 3 separate rabbit models of anterior uveitis. Antibodies to two different leukocyte molecules, CD11a and CD18, and antibodies to the endothelial ligand for CD11a/CD18, ICAM-1 (intercellular adhesion molecule-1, CD54), were studied in inflammation after intravitreally injected interleukin-1, intravitreally injected endotoxin, or an ocular reversed passive Arthus reaction. The CD18 antibody (2 mg/kg intravenously) reduced the cellular infiltrate with each of these 3 models. The antibody to CD11a was equally effective but was tested only in the IL-1-induced model. The antibody to ICAM-1 reduced the cellular infiltrate associated with this model, but the results did not reach statistical significance. None of the antibodies was able to reduce the associated increase in vascular permeability as measured by protein in the aqueous humor. The antibody to CD18 failed to reduce the inflammation if it was administered 24 hours after the intravitreally injected endotoxin. These observations demonstrate that leukocyte migration into the anterior segment of the eye is dependent on the CD11a/CD18 complex.
 ...
PMID:Efficacy of antibodies to adhesion molecules, CD11a or CD18, in rabbit models of uveitis. 790 35

In the airways inflammation observed in asthma, activated macrophages are present in increased numbers. Adhesion molecules are required for the cell:cell contacts between leukocytes and endothelial cells or other leukocytes, and they are induced by inflammatory stimuli. We studied the expression of two adhesion molecules (ICAM-1 and LFA-1) on alveolar macrophages recovered by bronchoalveolar lavage from 11 normal subjects and 13 asthmatic patients by using immunocytochemistry. Two specific monoclonal antibodies were used, and the reaction was revealed by the alkaline phosphatase-antialkaline phosphatase (APAAP) method. The percentage of cells expressing ICAM-1 or LFA-1 was significantly increased in asthmatic patients, as compared with normal subjects (P < 0.001 and P < 0.002, respectively; Mann-Whitney U test), and there was a significant correlation with the percentage of cells expressing both markers in asthma (P < 0.03, Spearman rank test). This study highlights the importance of macrophages in the inflammation of asthma and suggests that macrophage interactions with other cells play a role in this inflammation.
 ...
PMID:Increased expression of adhesion molecules (ICAM-1 and LFA-1) on alveolar macrophages from asthmatic patients. 790 25


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>