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)

Tissue factor pathway inhibitor(TFPI) is the major inhibitor of the extrinsic pathway of the blood coagulation cascade. Our previous study showed that TFPI could obviously prolong the blood coagulation time on the surface of polyethelene(PE) and polyvinylchloride(PVC) membranes in vitro and decrease the generation of thrombus on Dacron membrane in vivo. In the present study, the effect of TFPI on the adhesion of platelet onto PE and PVC membranes was investigated. PE or PVC membrane was cut into small pieces and incubated in 96-well culture plate with GST or GST-TFPI fusion protein at 4 degrees C over night. Freshly collected rabbit blood was mixed with 3.8% sodium citrate. Platelet-rich plasma was separated by centrifugation and then incubated with the treated membranes at 37 degrees C for 30 minutes. The membranes were then washed, fixed, and freeze-dehydrated Adhesion of platelet was observed through scanning electronic microscope. The result showed that GST-TFPI treatment significantly decreased the number of platelet adhered on the membrane when compared with the GST and control group, and it suggested that TFPI might have a great potential to be used as an anticoagulant for improving the hemocompatibility of biomaterials.
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PMID:[Effect of tissue factor pathway inhibitor on the adhesion of platelet onto polyethylene and polyvinylchloride membranes]. 1133 28

1. The nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), inhibits both rat and human eosinophil chemotaxis in vitro. Here, the role of nitric oxide (NO) in human eosinophil cell surface integrin expression and function was investigated. 2. Human peripheral blood eosinophils were treated with L-NAME (0.01 - 1.0 mM) and their adhesion to human fibronectin and serum observed. Adhesion of cells to fibronectin and serum increased by 24.0+/-4.6 and 43.8+/-4.7%, respectively, when eosinophils were treated with 1.0 mM L-NAME. Increased adhesion by L-NAME could be abolished when cells were co-incubated with VLA-4- and Mac-1-specific monoclonal antibodies (mAbs). 3. The NO donor, sodium nitroprusside (2.5 mM), significantly inhibited eosinophil adhesion to fibronectin and serum by 34.3+/-4.5 and 45.2+/-5.6%, respectively. This inhibition was accompanied by a 4 fold increase in the levels of intracellular cyclic GMP. 4. Flow cytometrical analysis demonstrated that L-NAME induced an increased expression of CD11b (Mac-1) on the eosinophil cell surface of 36.3+/-7.4%. L-NAME had no effect upon CD49d (VLA-4) expression. 5. Treatment of human eosinophils, in vitro, with H-[1,2,4] oxadiazolo quinoxalin-1-one (ODQ) (0.1 mM), an inhibitor of soluble guanylate cyclase, also significantly increased eosinophil adhesion to fibronectin and serum by 73.5+/-17.9 and 91.7+/-12.9%, respectively. This increase in adhesion could also be inhibited by co-incubation with the Mac-1 and VLA-4-specific mAbs. 6. In conclusion, results indicate that NO, via a cyclic GMP-dependent mechanism, inhibits the adhesion of human eosinophils to the extracellular matrix (ECM). This inhibition is accompanied by a decrease in the expression and function of the eosinophil's adhesion molecules, in particular, the expression of the Mac-1 integrin and the function of the VLA-4 integrin.
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PMID:Nitric oxide regulates human eosinophil adhesion mechanisms in vitro by changing integrin expression and activity on the eosinophil cell surface. 1158 18

The aim of this paper was to determine the adhesion of two physico-chemically characterized bacterial strains to a surface hydrophilic (CL A, water contact angle 57 degrees) and hydrophobic (CL B, water contact angle 106 degrees) hydrogel contact lens (CL) with and without an adsorbed tear film in a parallel plate flow chamber. Hydrophobicity (by water contact angles), charge (by particulate microelectrophoresis) and elemental composition (by XPS) of the surfaces of seven bacterial strains were characterized, after which two strains were selected for further studies. On CL surfaces, hydrophobicity, elemental composition, and mean surface roughness (by AFM) were determined, as well as the protein composition of tear films adsorbed on these lenses (by sodium dodecylsulphate-polyacrylamide gel electrophoresis (SDS-PAGE)). Bacterial cell surfaces were relatively uncharged and water contact angles on lawns of different strains ranged from hydrophobic to hydrophilic. After adsorption of tear film components, N/C elemental surface concentrations increased on CL A and CL B and differences in water contact angles between both lenses reduced to range from 57 degrees (CL A) to 69 degrees (CL B). However, different protein compositions were inferred. The surface roughness of CL A increased from 4 to 13 nm. while it remained 16 nm for CL B. Adhesion of hydrophobic Pseudomonas aeruginosa #3 was more extensive than of hydrophilic Staphylococcus aureus 799, with no differences between both lenses. The hydrophobicity of P. aeruginosa #3 after cell surface damage decreased and its adhesion was reduced on CL A and strongly on CL B. In addition, passage of an air-liquid interface yielded more detachment of S. aureus 799 than of P. aeruginosa #3 from the CL surfaces. In conclusion, the hydrophobicity of CL surfaces dictates the composition of the adsorbed tear film and therewith plays an important role in bacterial adhesion to lenses. Adhesion of hydrophobic P. aeruginosa #3 was more tenacious than of hydrophilic S. aureus 799.
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PMID:Bacterial adhesion to surface hydrophilic and hydrophobic contact lenses. 1170 Jul 93

Mast cells have been implicated in the ethiopathology of post-operative peritoneal adhesions. However an evaluation of their role in this condition is missing. Adhesions were induced in rats using small intestinal scraping. These rats or rats injected ip with either Stem Cell Factor (SCF) or nedocromil sodium or compound 48/80 (day 0-20) were sacrificed for grading of peritoneal adhesions, for evaluating mast cells and inflammatory cells in adhesions and peritoneal lavage (histochemical staining) and for histamine content (peritoneal lavage, radioenzymatic assay) on days 1-21. Mast cell sonicate was added to intestinal fibroblast and their proliferation was assessed (cell counting). All the rats developed adhesions (day 1) and after 3 days the adhesion score remained constant. Early adhesions were avascular and made of fibrinous exudate containing many mast cells. Thereafter adhesions became denser, and the number of stainable mast cells decreased and then stabilized. On the first few days, inflammatory cells in the peritoneal lavage increased while mast cells and histamine content were significantly reduced indicating their activation. Injection of SCF for 1 week slightly increased peritoneal adhesion formation while nedocromil sodium reduced their development. Compound 48/80 had no significant influence. Addition of mast cell sonicate to normal intestine or to peritoneal adhesion fibroblasts resulted in a significant increase of fibroblast proliferation. In conclusion, mast cell presence correlated with the establishment of peritoneal adhesions, and their pharmacological modulation influenced adhesion formation. In vitro mast cell induced fibroplasia. Therefore, mast cells have a profibrogenic role in this model of peritoneal adhesions.
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PMID:Mast cell dynamics and involvement in the development of peritoneal adhesions in the rat. 1185 32

Adhesion to the intestinal mucosa is generally considered an important property of probiotic microorganisms and has been related to many of their health benefits. This study investigated some factors that could affect or be involved in the adherence of Propionibacterium acidipropionici CRL 1198, a dairy strain with suggested probiotic effects and high adherence in vitro and in vivo to intestinal epithelial cells. In vitro adhesion of propionibacteria was decreased by gastric digestion but not affected by bile and pancreatic enzymes. Adherence was also decreased by pretreatment of bacterial cells with protease, sodium metaperiodate, and trichloroacetic acid, revealing that different features of the cell surface, like protein factors, carbohydrates, and teichoic acids, are involved in the process. Adherence to intestinal epithelial cells was enhanced by calcium and was dependent on other divalent cations. Adhesion to intestinal mucus was also demonstrated. The results should explain the metabolic effects in the host previously obtained with this strain and support the potential of Propionibacterium for development of new probiotics.
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PMID:Some factors affecting the adherence of probiotic Propionibacterium acidipropionici CRL 1198 to intestinal epithelial cells. 1210 85

This study examines effects of alpha(2)-macroglobulin (alpha(2)M) on adhesion of fibroblasts. Native alpha(2)M and transformed form of alpha(2)M, alpha(2)M-plasmin, were bound to plastic. Adhesion of mouse L929 and human embryo M-19 fibroblasts to immobilized alpha(2)M was estimated under various conditions by counting adherent cells using videomicroscopy and computer-assisted image analysis. alpha(2)M-plasmin, bound to plastic, induced adhesion and spreading of mouse L929 and human M-19 fibroblasts. Neither native alpha(2)M nor plasmin alone did not induce fibroblast adhesion. The adhesion to alpha(2)M-plasmin was undetectable at 4 degrees C, as well as when sodium azide was added or divalent ions were removed. These findings provide novel information on alpha(2)M functions. On the basis of these observations we hypothesized that alpha(2)M, immobilized in the extracellular matrix, can participate in the regulation of microenvironment effects on the cells, and, in particular, influence on fibroblast adhesion.
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PMID:Adhesion of Fibroblasts to Immobilized alpha(2)-Macroglobulin. 1268 59

Adhesions between viscera and mesh may result in intestinal obstruction and fistulae formation. Fewer adhesions with sodium carboxymethylcellulose (SCMC)-coated polypropylene mesh (PM) has been reported, but impaired wound healing was the major concern. We investigated the adhesion-prevention effect of SCMC in different concentrations, as coating only on visceral face of PM and its effects on wound healing. A full-thickness abdominal wall defect was created in 28 rats, which were then divided into three groups. In Group I (control), the defect was repaired with PM only; in Group II and Group III, the defects were repaired with 1% and 1.6% SCMC-coated-PM, respectively. All animals were sacrificed at day 30, and histological evaluation and adhesion scoring were done. Animals in the group in which 1.6% SCMC-coated PM was used developed significantly fewer adhesions compared with other animals (P=0.04). Histological evaluation using a semiquantitative scoring system showed no difference between the groups in fibrosis and inflammation scores (P=0.9 and P=0.3, respectively), and thickness of fibrosis on mesh was also similar (P=0.5). SCMC in 1.6% concentration as coating only on the visceral face of PM reduced the incidence and severity of adhesions without impairing wound healing.
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PMID:Carboxymethylcellulose coated on visceral face of polypropylene mesh prevents adhesion without impairing wound healing in incisional hernia model in rats. 1268 27

PURPOSE: Lanreotide, a long-acting somatostatin analogue, inhibits intestinal, bile and pancreatic secretions and decreases intestinal motility. The purpose of this experimental study was to evaluate the effects of lanreotide on the healing of intestinal anastomoses following small bowel obstruction. METHODS: Two groups of 16 Wistar rats (average weight 310 g) were used. Basal diameters of ileus were measured prior to the ligation of the bowel, 15 cm from the ileocecal valve. Luminal fluid was also withdrawn proximal to the obstructed bowel for sodium and potassium analysis. Lanreotide was administered intramuscularly in a single dose (5.4 mg/kg) in the first group, while the same volume of saline was used in the control group. 48 h later rats were re-operated upon. Diameters of the obstructed segments were measured, and luminal fluid of the obstructed bowel was withdrawn and sodium and potassium levels were measured. A segment of 1 cm of the obstructed bowel was resected and end-to-end intestinal anastomosis was performed. Rats were sacrificed on day 7 following the second operation. Anastomoses were examined macroscopically and resected including a 2.5 cm of small bowel on either side. Bursting pressures were measured and the specimens were send for histological examination. RESULTS: The diameter of obstructed bowel increased significantly in both groups. The increase was more prominent in the control group (P < 0.001). Total luminal electrolyte contents for sodium and potassium were stastistically higher in the control group compared to the lanreotide group (P < 0.001). Adhesion formation was more extensive in the control group. Bursting pressures were significantly higher in the lanreotide group compared to the control group (P=0.003). Histological examination of anastomoses showed a more profound inflammatory reaction in the control group compared to the lanreotide group while microscopical healing of the anastomoses was almost the same in both groups. CONCLUSIONS: Lanreotide administration in rats with small bowel obstruction decreases significantly distension and electrolyte losses and seems to improve strength of small bowel anastomoses.
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PMID:Effects of lanreotide on the healing of small bowel anastomoses following obstructive ileus in rats. 1278 Jun 50

The fungal pathogen Cryptococcus neoformans has a predilection for the central nervous system (CNS), resulting in devastating meningoencephalitis. At present, it is unclear how C. neoformans traverses the blood-brain barrier (BBB) and causes CNS infection. The present study has examined and characterized the interaction of C. neoformans with human brain microvascular endothelial cells (HBMEC), which constitute the BBB. Adhesion of and transcytosis of HBMEC by C. neoformans was inoculum- and time-dependent and occurred with both encapsulated and acapsulated strains. C. neoformans induced marked morphological changes in HBMEC, for example membrane ruffling, irregular nuclear morphology and swelling of the mitochondria and the ER. These findings suggest that C. neoformans induced actin cytoskeletal reorganization of the host cells. In addition, it was observed that the dephosphorylated form of cofilin was increased during cryptococcal adherence to HBMEC, concomitant with the actin rearrangement. Cryptococcal binding to HBMEC was increased in the presence of Y27632, a Rho kinase (ROCK)-specific inhibitor. Since ROCK activates LIM kinase (LIMK), which phosphorylates cofilin (inactive form), this suggests the involvement of the ROCK-->LIMK-->cofilin pathway. In contrast, the phosphatase inhibitor sodium orthovanadate decreased adherence of Cryptococcus to HBMEC, concomitant with the increase of phosphorylation of cofilin. Furthermore, the tight junction marker protein occludin became Triton-extractable, indicating alteration of tight junctions in brain endothelial cells. This is the first demonstration that C. neoformans is able to adhere to and transcytose across the HBMEC monolayer and alter the cytoskeleton morphology in HBMEC. Further characterization of the interactions between C. neoformans and HBMEC should help the development of novel strategies to prevent cryptococcal meningitis and its associated morbidity.
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PMID:Cryptococcus neoformans induces alterations in the cytoskeleton of human brain microvascular endothelial cells. 1453 40

We report on an optimized method for the in vitro culture of tissue cyst-forming Neospora caninum bradyzoites in Vero cells and the separation of viable parasites from host cells. Treatment of tachyzoite-infected Vero cell cultures with 17 microM sodium nitroprusside for 8 days severely scaled down parasite proliferation, led to reduced expression of tachyzoite surface antigens, and induced the expression of the bradyzoite marker NcBAG1 and the cyst wall antigen recognized by the monoclonal antibody MAbCC2. Transmission electron microscopy demonstrated that intracellular parasites were located within parasitophorous vacuoles that were surrounded by a cyst wall-like structure, and the dense granule antigens NcGRA1, NcGRA2, and NcGRA7 were incorporated into the cyst wall. Adhesion-invasion assays employing purified tachyzoites and bradyzoites showed that tachyzoites adhered to, and invaded, Vero cells with higher efficiency than bradyzoites. However, removal of terminal sialic acid residues from either the host cell or the parasite surface increased the invasion of Vero cells by bradyzoites, but not tachyzoites.
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PMID:In vitro induction of Neospora caninum bradyzoites in vero cells reveals differential antigen expression, localization, and host-cell recognition of tachyzoites and bradyzoites. 1468 39


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