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)

Cell-cell aggregation and cell-substratum adherence, two functional manifestations of granulocytes of potential clinical relevance, are widely considered to result from identical cell membrane alterations. Our study casts doubt on this assumption and defines the complement-derived adhesion-inducing (pectic)/enzyme releasing activity as an entity that is clearly separable from the chemotactic/aggregating activity (C5adesArg). Using selective activators of the alternative and the classical pathway of the complement system, unexpected dissimilarities were observed. Adhesion inducing potency that went in parallel with secondary granule content liberation, and respiratory burst activation (hexose monophosphate shunt activation), was confined to alternate pathway activators, was heat-labile (50 degrees) and could be inhibited by the protease inhibitor di-isopropylfluorophosphate. In contrast, plasma activated with aggregated gamma-globulin or cobra venom factor had no pectic/burst activating capacity but was equally potent in inducing heat- and DFP-resistant chemotactic-aggregating activity. It was further shown that, even in the presence of cytochalasin B, C5adesArg (evoked in whole plasma) does not liberate secondary granule constituents. These findings were corroborated by using highly purified C5adesArg. Our data suggest that the complement system plays a dual role in PMN accumulation at the inflammatory focus: whereas C5adesArg orientates cellular movement toward the site of bacterial invasion, the complement-dependent pexin(s) is mainly involved in confining infections localized by the adhesion-induced trapping of highly reactive cells.
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PMID:Complement-induced granulocyte adhesion and aggregation are mediated by different factors: evidence for non-equivalence of the two cell functions. 649 97

Adhesion of xerogel dressings prepared on Eudragit (E), methylcellulose (MC) and glycerol compositions, remaining within the range of 625-650 g, after addition polyvinylpyrolidone (PVP) amounts to 450-1250 g. Dissolution time from xerogel dressings without PVP additive both in water and in an artificial gastric juice amounts to 3 h. Addition of PVP results in reduction of the elution rate. In dependence upon the PVP/E/MC ratio elution time amounts to 3-3.5 h. Pharmaceutical availability of the Kunitz protease inhibitor in particular groups of then dressings depends upon concentration of hydrophilizing agent. The semi-liberation times amounts to 3.65-17.50 h.
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PMID:Studies on dressings for mucosa of the oral cavity. Part 3: Effect of preparation technology on the physical and chemical properties of stomatological xerogel dressings. 862 40

Adhesion of xerogel dressings prepared on Eudragit-E 100, methylcellulose and glycerol compositions in acetone/water mixtures, remains within the range of 317-967 g, after addition of polyvinylpyrrolidone (PVP), it increases to 633-1200 g. Dissolution time of dressings in water amounts to 6 h, in artificial gastric juice to 3 h. Addition of PVP results in decrease of the elution rate, dissolution time amounts to 2.5 h. The Kunitz protease inhibitor semi-liberation times amount to 3.3-7.6 h.
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PMID:Studies on dressings for mucosa of the oral cavity. Part 4: Influence of technology used in the preparation of dental xerogel dressings in the presence of acetone on their properties. 967 69

Polymorphonuclear leukocytes (PMNs) and endothelial cells interact at sites of vascular injury during inflammatory response and during the development of atherosclerotic lesions. Such close proximity leads to the modulation of several of the biological functions of the 2 cell types. Because we have shown previously that PMNs enhance release of growth factors from resting endothelial cells, we decided to evaluate whether coincubation of PMNs with interleukin-1beta (IL-1beta)-stimulated human umbilical vein endothelial cells (HUVEC) could further modulate mitogen release from HUVEC. We found that PMN-HUVEC coincubation resulted in a 10-fold increase in mitogen release, compared with HUVEC alone (14+/-6 versus 1.3+/-0.1). When PMNs were incubated with IL-1beta-treated HUVEC, a further increase in mitogen release (up to 35-fold) was observed. The mitogenic activity was immunologically related to platelet-derived growth factor (PDGF) because the activity was abolished by an anti-PDGF antibody. PDGF-AB antigen, detected in low concentrations in conditioned medium from HUVEC alone, was increased 4-fold when IL-1beta or PMNs were incubated with HUVEC and dramatically upregulated (up to 40-fold) when PMNs were cocultured with IL-1beta-treated HUVEC. The presence of the protease inhibitor eglin C abolished mitogenic activity generation, suggesting a role for PMN-derived elastase and cathepsin G. Indeed, purified elastase and cathepsin G mimicked PMN-induced mitogen release from HUVEC. Because PMNs firmly adhered to IL-1beta-treated HUVEC, we investigated the role of cell-cell adhesion in mitogen release. Adhesion and PDGF release were inhibited by approximately 60% in the presence of anti-CD11a/CD18 and anti-intercellular adhesion molecule-1 monoclonal antibodies. This study suggests a new role for PMNs and their interaction with endothelium in pathological conditions in which intimal hyperplasia is a common feature.
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PMID:Polymorphonuclear leukocytes induce PDGF release from IL-1beta-treated endothelial cells: role of adhesion molecules and serine proteases. 976 23