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PubMed2006

Effects of saliva contamination on dentin bond strength using all-in-one adhesives.

PURPOSE: To evaluate the effects of saliva contamination on microtensile bond strengths of all-in-one adhesives to dentin. MATERIALS AND METHODS: Flat superficial occlusal dentin surfaces of extracted human molars were used and randomly divided into 2 groups depending on two all-in-one adhesives: One-Up Bond F Plus (Tokuyama Dental) and Adper Prompt L-Pop (3M ESPE). For each adhesive, the teeth were allocated to 7 subgroups in which one group was bonded without contamination with saliva, serving as a control. The other groups, either before or after the polymerization of adhesives, were contaminated with saliva and dried; contaminated, dried, and adhesives re-applied; contaminated, rinsed, and the adhesives re-applied. Resin composite was then placed on the treated dentin surfaces. After 24 h storage in distilled water at 37 degrees C, the teeth were sectioned perpendicular to the adhesive interface in x and y directions, obtaining multiple beam-shaped specimens with a cross-sectional area of approximately 1.0 mm2. Specimens were stressed in tension at 1 mm/min until rupture of the bond. Data were analyzed using one-way ANOVA and the Games-Howell test. RESULTS: For both all-in-one adhesives, saliva-contaminated groups showed lower bond strengths than the controls. Re-application of the adhesives after drying or rinsing the saliva off restored the dentin bond strengths to the control levels. CONCLUSION: Saliva contamination reduced the dentin bond strengths of all-in-one adhesives. Supplementary application of the adhesive after cleaning the saliva from the dentin surface is an empirical recommendation for restoring bond strength.

Adhesives↗
PubMed1992

Platelet adhesion to laminin: role of Ca2+ and Mg2+ ions, shear rate, and platelet membrane glycoproteins.

The adhesion of platelets to purified laminin under flow conditions was investigated. Adhesion to laminin was strongly dependent on the presence of divalent cations. In the absence of cations platelet adhesion (8% coverage in 5 minutes) was maximal at a shear rate of 100/s and no adhesion could be detected at shear rates above 800/s. In the presence of 0.8 mmol/L Mg2+ and 2 mmol/L Ca2+ platelet adhesion reached its maximum (30% coverage) around 800/s. At 1,800/s platelets still adhered to purified laminin (coverage of 6%). Antibodies against the E8 domain of laminin and antibodies against the alpha 6 and beta 1 chains of platelet membrane glycoprotein very late activation antigen-6 (VLA-6), completely inhibited adhesion. No inhibition was found with antibodies against glycoprotein IIb:IIIa, against the alpha 2 chain of VLA-2, and against the alpha 5 chain of VLA-5. Fibronectin and von Willebrand factor were not involved in laminin-dependent adhesion. Anti-VLA-6 partly inhibited platelet adhesion to the extracellular matrix of endothelial cells at shear rates below 800/s. Preincubation of the matrices with antilaminin E8 antibodies did not influence the adhesion. These results show that purified laminin supports platelet adhesion and that the presence of VLA-6 is important for platelet adhesion under flow conditions. The protein in the matrix with which VLA-6 interacts is currently unknown.

Adsorption↗
PubMed1991

Modulation of antigen presentation and peptide-MHC-specific, LFA-1-dependent T cell-macrophage adhesion.

Incubation of peritoneal macrophages in vitro before fixation increased their ability to present exogenous peptides to 3A9 T hybridoma cells. The enhanced level of presentation correlated with a greatly increased, peptide-specific adhesion of 3A9 cells to the macrophages, whereas peptide-independent adhesion was minimal and essentially unaltered. 3A9 cells exhibited rapid peptide-specific adhesion (plateau by 5 to 10 min) and deadhesion (complete reversal by 5 min). Peptide-specific adhesion was blocked by anti-I-Ak and anti-LFA-1. Interaction of T cell receptors and CD-4 with peptide-I-Ak complexes appeared to provide little direct contribution to the avidity of T cell-macrophage adhesion, but activated a LFA-1-mediated adhesion mechanism. In addition, anti-T cell receptor, anti-CD3, and anti-CD4 antibodies themselves activated LFA-1-dependent adhesion in the absence of peptide. Unlike the peptide-induced adhesion, this adhesion was similar for macrophages whether or not they were incubated in vitro before fixation. We conclude that the different macrophage populations supported LFA-1-mediated adhesion equally. Therefore, the enhancement of T cell stimulation observed after in vitro incubation of macrophages was due to increased peptide presentation and consequently increased triggering of LFA-1-mediated adhesion. Mechanisms may exist to regulate the effectiveness with which peptide-class II MHC complexes are displayed for T cell recognition.

Animals↗
PubMed1986

Interferon-gamma induction of LFA-1-mediated homotypic adhesion of human monocytes.

Cell-cell adhesion plays an important role in monocyte function. To investigate the molecular basis for monocyte adhesion, we used recombinant interferon-gamma to induce the formation of homotypic monocyte adhesions. The induction of homotypic adhesions correlated with the increased expression of the LFA-1 membrane molecule. LFA-1 surface expression was increased twofold, whereas expression levels of other monocyte surface molecules including CR3 and p150,95 were unchanged. The direct involvement of LFA-1 in monocyte adhesion was addressed by anti-LFA-1 monoclonal antibody inhibition of homotypic adhesions. Two monoclonal antibodies to distinct epitopes on the LFA-1 alpha-chain completely inhibited homotypic adhesions. Antibodies to a variety of other monocyte surface molecules, often present at higher cell surface density than LFA-1, did not inhibit homotypic adhesion. A panel of monoclonal antibodies that recognized different functional epitopes on the LFA-1 alpha-chain inhibited homotypic monocyte in a hierarchy identical to that observed in previous studies of cell-mediated cytotoxicity. These findings suggest that LFA-1 serves an adhesive function for human mononuclear phagocytes. In addition to providing a molecular basis for homotypic monocyte adhesions, the results suggest a more general role for LFA-1 in monocyte adhesion reactions.

Animals↗
PubMedDate not supplied

Adhesion re-formation in the rabbit uterine horn model: I. Reduction with carboxymethylcellulose.

Adhesion re-formation frequently complicates the performance of adhesiolysis in reproductive pelvic surgery. To assess the ability of carboxymethylcellulose (CMC) to reduce adhesion re-formation, a rabbit uterine horn model was employed. Adhesions were created at laparotomy by scraping a 5-cm segment of each uterine horn. This injury reproducibly creates adhesions. Two weeks later, repeat laparotomy was performed, at which time all adhesions were lysed by sharp dissection. Animals were then randomly assigned to the control or CMC (20 mL of 2% solution) group. Necropsy was performed 2 weeks later. At both the second operative procedure and the time of necropsy, adhesions were graded in a blind fashion for severity and tenacity. There was no difference in adhesion score in the control and CMC-treated rabbits at the time of adhesiolysis. Subsequently, at the time of necropsy, the mean adhesion reformation score in the control group was 3.96 (median = 4.0). In contrast, adhesion re-formation in the CMC-treated group was significantly less (mean score = 2.15; median = 2.0; sign test, P less than .01). In summary, CMC significantly reduced adhesion re-formation in the rabbit uterine horn model. The mechanism by which CMC was able to reduce adhesion reformation is uncertain, but may be related to "hydroflotation" or "siliconizing" effects.

Animals↗
PubMed1978

Effect of shear rate on platelet interaction with subendothelium in citrated and native blood. I. Shear rate--dependent decrease of adhesion in von Willebrand's disease and the Bernard-Soulier syndrome.

Previous studies have demonstrated impaired adhesion of platelets to the subendothelium in von Willebrand's disease. These studies were performed by circulating (in a closed system) citrated whole blood through a chamber containing everted segments of rabbit aorta from which the endothelium had been removed by balloon catheter. The average wall shear rate was 800 sec-1, and the perfusion time was 10 min. In the present study we measured the interaction of platelets with subendothelium in native (nonanticoagulated) blood, using a recently described technique in which the vessel segments are perfused with directly sampled venous blood. The system was open; that is, the blood was not recirculated. We used blood flow rates of 20, 40, and 50 ml/min, which correspond to calculated shear rates of 1300, 2600, and 3300 sec-1 and perfusion times of 3, 2, and 2 min, respectively. For comparison, parallel studies at 1300 sec-1 were also obtained with citrated blood. In normal subjects, at a shear rate of 1300 sec-1, platelet adhesion was less in native blood than in citrated blood, but thrombus formation was greater. Platelet adhesion in five patients with von Willebrand's disease was decreased in both citrated and native blood. The magnitude of the adhesion defect was strongly dependent on the shear rate. Thus, in citrated blood studied at a shear rate of 1300 sec-1, adhesion was 75% less than in normal subjects, whereas in previous studies at 800 sec-1 the reduction in adhesion was 29%. In native blood, adhesion in von Willebrand's disease was normal at a shear rate of 1300 sec-1, whereas 53% and 77% reductions in adhesion were obtained at shear rates of 2600 and 3300 sec-1, respectively. The latter shear rates studied, adhesion of platelets in native blood was also decreased in the Bernard-Soulier syndrome but was normal in hemophilia and afibrinogenemia. Our findings with native blood provide further evidence that impaired adhesion of platelets to the vessel wall accounts for the hemostatic defect in von Willebrand's disease. In addition, this adhesion defect is shear rate-dependent.

Adolescent↗
PubMed1988

Molecules mediating adhesion of T and B cells, monocytes and granulocytes to vascular endothelial cells.

Leucocytes interact with vascular endothelial cells (EC), and adhesion between these two cell types in vitro is modulated by phorbol ester. Monocytes were found to display the highest basal adhesion to EC, followed by Epstein-Barr virus-immortalized normal B cells (EBV-B), T cells and granulocytes. Phorbol ester treatment increased the adhesion of all types of leucocytes, except monocytes. In the presence of this compound, monoclonal antibody 60.3 to GP90 (CD18, a leucocyte-adhesion protein which is non-covalently associated to either GP160, GP155, or GP130) was found to inhibit the adhesion of the four types of leucocytes to a considerable extent, while anti-lymphocyte function-associated antigen-1 (LFA-1) antibody to GP160 (CD11a) inhibited the adhesion of T and B cells only. Antibody 60.1 to GP155 (CD11b) had a major inhibitory activity exclusively on granulocytes, while antibody LB-2, which recognizes a distinct adhesion molecule (GP84) and, in contrast to the previous antibodies, reacts with EC, mainly inhibited adhesion of EBV-B and did not increase the inhibition obtained with antibody 60.3 alone. Fab fragments of antibody 60.3 inhibited leucocyte adhesion more efficiently, in either the absence or presence of phorbol ester, than the intact antibody molecule. It is concluded the GP90, either alone or associated to the larger glycoproteins, mediates the adhesion in all types of leucocytes, while GP84 mediates the adhesion of the activated B cells.

Antibodies, Monoclonal↗
PubMed1988

Increased expression of adhesive proteins on leukocytes by TNF alpha.

To further elucidate the role of tumor necrosis factor alpha (TNF alpha) in cell adhesion, we investigated the effect of TNF alpha on the expression of surface adhesive protein. After treatment with TNF alpha for 1 h, the increased expression of surface adhesive proteins (beta subunit) was observed on granulocytes but not on monocytes or lymphocytes. The expression of Mac-1 (3,4-fold increase) was consistently enhanced more than p 150,95 (1.4-fold increase) and LFA-1 expression was unchanged. Dose-response and time course studies indicated a parallel relationship between TNF alpha-increased expression of surface adhesive proteins and TNF alpha-induced granulocyte adhesion. The anti-inflammatory drug Dexamethasone suppressed both TNF alpha-induced granulocyte adhesion and TNF alpha-induced expression of surface adhesive proteins. The inhibition of granulocyte adhesion correlated with the reduction of surface adhesive protein expression. The data suggest that one contributing factor in the mechanism by which Dexamethasone inhibited TNF alpha-induced granulocyte adhesion may be diminished expression of surface adhesive proteins.

Antigens, Surface↗
PubMed1987

CTL adhesion and antigen recognition are discrete steps in the human CTL-target cell interaction.

Th initial step in cytolytic T lymphocyte (CTL)-mediated cytolysis involves target cell adhesion and antigen recognition. To investigate these initial events in the CTL-target interaction, we used HLA-A2- and HLA-B7-specific human CTL clones and HLA-typed B lymphoblastoid target cells. By using two different adhesion assays, we demonstrated antigen nonspecific CTL-target cell adhesion. To more precisely define the contribution of the antigen-specific receptor to CTL-target cell adhesion, we used the HLA-A2, HLA-B7, and mock transfected RD target cells. Consistent with the results when using B lymphoblastoid target cells, the CTL clones demonstrated equivalent adhesions to the RD target cells whether or not they expressed HLA-A2 or HLA-B7. These results suggested that CTL-target cell adhesion occurred independent of the T cell receptor. By using the calcium-sensitive dye Indo-1 and flow cytometry, we assessed CTL-target cell adhesion and CTL activation. Simultaneous measurement of adhesion and intracellular free calcium demonstrated that CTL-target cell adhesion alone did not activate CTL clones. Both CTL-target cell adhesion and the presence of the appropriate HLA target molecule were necessary for the efficient activation of human CTL. MAb inhibition studies indicated that antigen nonspecific adhesion is largely regulated by the LFA-1, CD2 (LFA-2/T11), and LFA-3 cell surface molecules. These antigen nonspecific cell-cell interaction molecules appear to play an important role in facilitating antigen recognition and subsequent target cell lysis.

Antibodies, Monoclonal↗
PubMed1994

Ligation of MHC class I and class II molecules can lead to heterologous desensitization of signal transduction pathways that regulate homotypic adhesion in human lymphocytes.

Engagement of lymphocyte MHC class I and class II Ags activates an array of intracellular signal transduction pathways that up-regulates the activity of cell-surface adhesion receptors, resulting in homotypic cell-cell aggregation. In this study, engagement of MHC class I and class II molecules with specific mAbs was shown to also inhibit lymphocyte homotypic adhesion. Two mAbs reactive with class II Ag, homotypic adhesion blocking mAb (HAB)-2, and HAB-3, and one mAb reactive with class I Ag, HAB-4, were generated that inhibited homotypic adhesion of activated lymphocytes and B and T cell lines at concentrations as low as 0.1 microgram/ml. Binding of these mAbs resulted in heterologous desensitization of other surface signal transduction molecules as homotypic adhesion induced through class I, class II, CD19, CD20, CD39, CD40, Leu-13, and PMA was also inhibited. The spontaneous adhesion exhibited by some cell lines was also abrogated by binding of these mAbs. Abs that either induced, blocked, or had no effect on adhesion bound to distinct epitopes on class I, whereas the anti-class II mAbs recognized either distinct or overlapping epitopes. Thus, engagement of distinct epitopes on MHC molecules can result in homologous or heterologous desensitization of cell-surface signaling molecules. The induction or inhibition of homotypic adhesion through class I molecules did not require the presence of the cytoplasmic domain, as deletion of this portion of the class I molecule had no effect. In contrast, the transmembrane region was essential for signal transduction as the mAbs binding to a chimeric molecule in which the transmembrane and cytoplasmic domains of class I were exchanged with those of the HB15 molecule did not induce or inhibit homotypic adhesion. Although this report is the first demonstration that homotypic adhesion can be influenced in a negative manner through MHC molecules, these findings demonstrate a considerable level of cross-talk between MHC molecules and other cell-surface receptor systems and their signal transduction pathways, and suggests that MHC class I and class II molecules may serve important roles in the regulation of adhesive events during lymphocyte activation.

Animals↗
PubMed1994

The putative RGD-dependent cell adhesion activity of matrix Gla protein is due to higher molecular weight contaminants.

This study was carried out to further characterize the RGD-dependent cell adhesion activity which was previously observed in the vitamin K-dependent matrix Gla protein (MGP) (Loeser, R. F., and Wallin, R. (1992) J. Biol. Chem. 267, 9459-9462). We have found that this cell adhesion activity can be completely removed from the 10-kDa MGP by gel filtration over Sephacryl S-200-HR. The higher molecular weight contaminants removed by the gel filtration step display potent cell adhesion activity. The additional evidence previously adduced in support of the putative cell adhesion activity of MGP is that heat decarboxylation of the vitamin K-dependent gamma-carboxyglutamate residues in MGP abolished the adhesion activity. The heat decarboxylation conditions used, however, appear to cause other chemical changes in proteins in addition to decarboxylation, as evidenced by the fact that the cell adhesion activity of fibronectin, which is not a vitamin K-dependent protein, is also destroyed by this procedure. The present evidence that the putative cell adhesion activity of MGP is caused by contaminating higher molecular weight cell adhesion proteins accounts for two apparent anomalies in the previously reported cell adhesion activity of MGP, the failure of antibodies raised against a synthetic peptide corresponding to the C-terminal 19 residues of bovine MGP to inhibit the cell adhesion activity of the intact, 79-residue bovine protein, and the potent inhibition of the cell adhesion activity of MGP by a synthetic peptide containing an RGD sequence, even though MGP does not contain this sequence.

Animals↗
PubMed1994

Prevention of postoperative pericardial adhesions with a hyaluronic acid coating solution. Experimental safety and efficacy studies.

Postoperative pericardial adhesions complicate reoperative cardiac procedures. Topical application of solutions containing hyaluronic acid have been shown to reduce adhesions after abdominal and orthopedic surgery. The mechanism by which hyaluronic acid solutions prevent adhesion formation is unknown but may be due to a cytoprotective effect on mesothelial surfaces, which would limit intraoperative injury. In this study, we tested the efficacy and safety of hyaluronic acid coating solutions for the prevention of postoperative intrapericardial adhesion formation. Eighteen mongrel dogs underwent median sternotomy and pericardiotomy followed by a standardized 2-hour protocol of forced warm air desiccation and abrasion of the pericardial and epicardial surfaces. Group 1 (n = 6) served as untreated control animals. Group 2 (n = 6) received topical administration of 0.4% hyaluronic acid in phosphate-buffered saline solution at the time of pericardiotomy, at 20-minute intervals during the desiccation/abrasion protocol, and at pericardial closure. The total test dose was less than 1% of the circulating blood volume. Group 3 (n = 6) served as a vehicle control, receiving phosphate-buffered saline solution as a topical agent in a fashion identical to that used in group 2. At resternotomy 8 weeks after the initial operation, the intrapericardial adhesions were graded on a 0 to 4 severity scale at seven different areas covering the ventricular, atrial, and great vessel surfaces. In both the untreated control (group 1, mean score 3.2 +/- 0.4) and vehicle control (group 3, mean score 3.3 +/- 0.2) animals, dense adhesions were encountered. In contrast, animals treated with the hyaluronic acid solution (group 2, mean score 0.8 +/- 0.3) characteristically had no adhesions or filmy, transparent adhesions graded significantly less severe than either the untreated control (group 2 versus group 1, p < 0.001) or vehicle control (group 2 versus group 3, p < 0.001) animals. In separate experiments, six baboons were infused with 0.4% hyaluronic acid in phosphate-buffered saline solution in volumes equivalent to 2.5%, 5%, and 10% of the measured circulating blood volume. The 2.5% and 5% infusions had no effect on the parameters measured; infusion of the 10% volume produced transient hemodynamic, coagulation, and gas exchange abnormalities. Hyaluronic acid solutions are efficacious in the prevention of pericardial adhesions in this model, and they appear safe in doses five times the amount needed to prevent adhesions. Further studies investigating the mechanism by which these solutions prevent adhesions, their optimal dose and method of application, and documentation of their safe use in humans are warranted.

Animals↗
PubMed1994

Prevention of postoperative adhesions in the rat by in situ photopolymerization of bioresorbable hydrogel barriers.

OBJECTIVE: To assess the efficacy of a novel resorbable hydrogel barrier for preventing postoperative adhesions in animals. METHODS: A hydrogel barrier was formed in situ by photopolymerizing a solution of a macromolecular prepolymer in buffered saline using long-wavelength ultraviolet light. Two models in the rat were evaluated. In a primary adhesion model, devascularization and serosal injury were performed on the uterine horns using bipolar electrocautery. The prepolymer solution was applied to the horns and illuminated to form the barrier. On the seventh postoperative day, the fraction of the length of the horns involved in adhesions was scored, as was the quality of the adhesions. In a readhesion model, adhesions were formed as described and were surgically lysed on the seventh day, then were treated subsequently with the barrier and scored after 7 additional days. Each group in both models consisted of seven animals per treatment condition. Four prepolymer concentrations were examined in the primary adhesion model, and the optimal one was examined in the readhesion model. RESULTS: A conformal hydrogel barrier coating was formed upon in situ photopolymerization and adhered to the treated tissues. No residual hydrogel barrier was observed 7 days after application of the optimal gel concentrations. In the primary adhesion model, the mean fraction of the horns involved in adhesions was reduced significantly, from 76% in controls to 10% (P < .0001), and treatment with a 10% solution of prepolymer was determined to be optimal (P = .025). In the readhesion model, surgical lysis of adhesions alone did not reduce adhesions significantly (from 86% to 79%; P = .3), whereas lysis with barrier treatment did (79% to 28%; P = .002). CONCLUSIONS: In situ photopolymerization allowed the formation of adherent, conformal barriers, which demonstrated high efficacy in the prevention of adhesion formation and reformation in animals. This efficacy and ease of use warrant clinical evaluation.

Animals↗
PubMed1993

Characterization of FN-C/H-V, a novel synthetic peptide from fibronectin that promotes rabbit corneal epithelial cell adhesion, spreading, and motility.

PURPOSE: Fibronectin promotes corneal epithelial cell adhesion and motility in vitro and plays an important role in corneal re-epithelialization during corneal wound healing. Multiple domains contribute to the adhesion- and motility-promoting activity of fibronectin. The aim of this study was to identify amino acid sequences that contribute to the rabbit corneal epithelial (RCE) cell adhesion- and motility-promoting activity of the 33 and 66 kD carboxy-terminal heparin-binding fragments of fibronectin. METHODS: Synthetic peptides derived from the 33/66 kD fragments of fibronectin were tested for their ability to directly promote RCE cell adhesion, spreading, and motility. To assess the contribution of these peptides to the activity of fibronectin and the 33/66 kD fragments of fibronectin, synthetic peptides, and antibodies against these peptides were tested for their ability to block RCE cell adhesion, spreading, and motility. RESULTS: In this study, we identified a novel peptide sequence derived from the 33/66 kD fragments of fibronectin, FN-C/H-V (WQPPRARI), that directly promotes the adhesion, spreading, and migration of RCE cells in a concentration-dependent manner. A second peptide from the 33/66 kD fragments of fibronectin, FN-C/H-IV (SPPRRARVT), promoted RCE cell adhesion and spreading, but did not promote RCE cell migration. In contrast, two synthetic peptides from the 33/66 kD fragments of fibronectin that were previously shown to promote RCE cell adhesion (FN-C/H-I and FN-C/H-III) did not promote RCE cell spreading or migration. Soluble FN-C/H-V inhibited RCE cell adhesion to surfaces coated with FN-C/H-V, the 33/66 kD fragments of fibronectin, and to fibronectin. In addition, polyclonal anti-FN-C/H-V IgG inhibited RCE cell adhesion to FN-C/H-V, the 33/66 kD fragments of fibronectin, and to fibronectin. Finally, polyclonal anti-FN-C/H-V IgG also inhibited RCE cell haptotactic migration on the 33/66 kD fragments. CONCLUSIONS: These data suggest that the amino acid sequence defined by peptide FN-C/H-V contributes to the adhesion-, spreading-, and motility-promoting activity of the 33/66 kD carboxy-terminal heparin-binding fragments of fibronectin. Given the important role of fibronectin in corneal wound healing, these findings provide additional insight into the complex molecular basis of corneal epithelial cell interactions with fibronectin and may be important in the context of corneal wound healing.

Amino Acid Sequence↗
PubMed1996

Glycoprotein IV-independent adhesion of sickle red blood cells to immobilized thrombospondin under flow conditions.

The abnormal adherence of red blood cells (RBC to the blood vessel wall is believed to contribute to the vascular occlusion observed in patients with sickle call anemia. The cell adhesion receptors GPIV (CD36) and integrin alpha 4 beta 1 (CD49d/CD29) were previously identified on circulating sickle reticulocytes, and shown to mediate sickle RBC adhesion to the endothelium. The presence of damaged endothelium in these patients suggests that exposed extracellular matrix proteins could provide a potential substrate for sickle RBC adhesion. To determine whether RBC adhesion receptors could mediate adhesion to extracellular matrix proteins, we tested their ability to adhere to a variety of immobilized, purified proteins under flow conditions. Neither sickle nor normal RBC adhered to fibronectin, vitronectin, fibrinogen, or collagen. In contrast, we observed substantial adhesion of sickle but not normal RBC to thrombospondin (TSP). The adhesion was not inhibited with known antagonists of the GPIV-TSP interaction, nor by inhibitors of several other known binding domains in TSP. Moreover, the adhesion was resistant to inhibition by soluble TSP, suggesting that immobilization of TSP exposes an adhesive site that is cryptic on TSP in solution. However, the glycosaminoglycans, chondroitin sulfate A, and dextran sulfate were potent inhibitors of this adhesion. These results suggest that a mechanism distinct from GPIV is responsible for sickle RBC adhesion to immobilized TSP under flow conditions.

Aggrecans↗
PubMed1996

Effect of interleukin-5 exposure during in vitro eosinophilopiesis on MAC-1 adhesion molecule expression and function on cultured human eosinophils.

We examined the selective effects of interleukin (IL-5) in regulating the maturational expression of surface adhesion molecules on human eosinophils and adhesion to endothelial cells during eosinophiiopolesis in vitro. Expression of the beta 2 integrins (CD11/CD18) and the beta 1 integrin, VLA-4 (CD49d/ CD29), was assessed during development in culture with IL-3, IL-5, and granulocyte-macrophage colony stimulating factor in cultures of human umbilical cord blood-derived eosinophil (CDE) precursor cells. Expression of both CD11b and CD18 subunits of Mac-1 was lower on CDE which were continuously (= chronically) exposed to IL-5 than on CDE which were cultured without IL-5 for the final week of culture. CD11b expression on cells grown without IL-5 was 71.3 +/- 5.92 (mean specific fluorescence value [MSF] as measured by flow cytometry) versus 52.5 +/- 4.48 MSF for Mac-1 alpha (CD11b) on CDE grown in the continued presence of 2 x 10 - 11 mol/L IL-5 (P < .01). Although expression of VLA-4 decreased as CDE matured, expression of CD29 and CD49d were similar regardless of cytokine exposure for the final week of culture. For eosinophils cultured without IL-5, acute stimulation with 10 - 8 mol/L IL-5 increased CD11b surface expression and increased the number of cells adhering to unstimulated human umbilical vein endothelial cells (HUVEC) from 4,570 +/- 780 cells (9.14 +/- 1.56% adhesion) to 8,385 +/- 515 cells (16.8 +/- 1.03% adhesion) (P < .01). Basal adhesion to unstimulated HUVEC of CDE cultured continuously with IL-5 was comparable (8.62 +/- 1.12% adhesion; P = NS), but neither CD11b expression (50.3 +/- 11.8 MSF; P = NS v control) nor adhesion to HUVEC (6.77 +/- 1.35%; P = NS) was enhanced in these eosinophils after acute stimulation with IL-5. Blockade of adhesion to IL-1-stimulated HUVEC caused by the anti-CD49d monoclonal antibody (MoAb), HP2/1, was comparable for cells cultured with IL-5 and without IL-5. However, the anti-CD18 MoAb, R15.7, caused 47.6 +/- 5.08% inhibition of adhesion of eosinophils cultured without IL-5 and only 25.8 +/- 5.20% for cells cultured continuously with IL-5 (P < .01), and failed to block significantly the adhesion of only the latter cells to IL-4-stimulated HUVEC. Our data show that continuous, chronic exposure to low concentrations of IL-5 causes decreased expression of Mac-1 and refractoriness to acute stimulation with IL-5 of adhesion to HUVEC. These data further demonstrate that CDE maturing in the continued presence of IL-5 adhere to HUVEC predominantly through VLA-4 ligation.

Cell Adhesion↗
PubMed1996

Platelet/polymorphonuclear leukocyte interaction in dynamic conditions: evidence of adhesion cascade and cross talk between P-selectin and the beta 2 integrin CD11b/CD18.

Adhesion between platelets and polymorphonuclear leukocytes (PMN) is a key event in thrombosis and inflammation. Double color fluorescence-activated cell sorter (FACS) analysis was used to determine the extent and kinetics of adhesion of thrombin-activated platelets to resting or activated PMN when mixed cell populations were incubated in dynamic conditions. Activated platelets bound very rapidly to PMN. Mixed cell conjugates reached a maximum at 1 minute and were reversible within 10 minutes. Platelet/PMN adhesion required both Ca2+ and Mg2+ and was markedly increased by the presence of Mn2+. The latter made mixed cell conjugates stable up to 10 minutes. Adhesion of platelets required metabolic activity of PMN and was abolished by tyrosine kinase inhibitors. Furthermore, adhesion of platelets to PMN resulted in binding of a monoclonal antibody (MoAb 24) known as beta 2 integrins "activation reporter." When PMN were activated by exogenous stimuli, the adhesion of platelets was markedly increased: fMLP induced a rapid and transient effect, while PMA resulted in a slower, but stable, increase in mixed conjugates formation. The hypothesis that activated PMN beta 2 integrins are able to bind a counter-receptor on platelets was directly demonstrated by the increase of mixed cell conjugates following PMN treatment with KIM127 and KIM185, two anti-CD18 antibodies able to induce the active conformation of beta 2 integrins. Consistently, two other anti-CD18, as well as an anti-CD11b inhibitory antibody abolished platelet/PMN adhesion. PMN beta 2 integrin activation was not the only mechanism for activated platelet/PMN adhesion to occur: indeed, this phenomenon could also be inhibited by two anti-P-selectin antibodies. Resting platelets did not adhere to resting PMN, but markedly adhered to fMLP- or PMA-activated PMN. Resting platelet/fMLP-activated PMN adhesion was abolished by anti-CD18 antibodies, but not by anti-P-selectin antibodies. In conclusion, activated platelet/PMN interaction can be modeled as an adhesion cascade involving a P-selectin-dependent recognition step and a functional signal. The latter proceeds through tyrosine kinase activation and enables a beta 2 integrin-dependent adhesion to a not yet identified counter-receptor constitutively expressed on platelet surface.

Antibodies, Monoclonal↗
PubMed1997

Adhesions: preventive strategies.

Adhesions, which occur after 67% to 93% of abdominal operations, represent a major clinical problem, resulting in intestinal obstruction, infertility, and pain and incurring considerable economic costs. The magnitude and seriousness of the problem of adhesions have been underappreciated. Moreover, efforts to prevent or reduce adhesions largely have been unsuccessful, hindered by their empirical basis, the lack of good predictive animal models, and the biochemical complexities of adhesiogenesis. The two major strategies for adhesion prevention or reduction are adjusting surgical technique and applying adjuvants. Modifications in technique that all surgeons should implement include minimizing the invasiveness of surgery, minimizing surgical trauma, such as ischemia from peritoneal suturing, and avoiding the introduction of foreign material, e.g., starch glove powder, into the body. Given the adhesiogenic nature of peritoneal repair, however, improvements in surgical technique alone will help decrease but not prevent adhesion formation. Adjuvant therapy is necessary. Adjuvants fall into two main categories, drugs and barriers. Nonsteroidal anti-inflammatory drugs have shown questionable clinical efficacy, possibly because of difficulties in drug delivery. Corticosteroids, alone or with antihistamines, also have had equivocal clinical results and may be immunosuppressive and delay wound healing. Experimentally, fibrinolytics such as tissue plasminogen activator (tPA), administered systemically or intraperitoneally (i.p.), have demonstrated conflicting results and hemorrhagic complications. However, recently, tPA, administered topically in a carboxymethylcellulose (CMC) gel, has been effective in reducing and preventing adhesions in rabbits. Phosphatidylcholine, given i.p. or orally, also has shown promise in animal studies. Barriers, by separating traumatized surfaces for the critical first five to seven days of peritoneal re-epithelialization, are useful adjuvants, and include macromolecular solutions and mechanical devices. Dextran, a macromolecular solution, has been studied widely, but has not demonstrated consistent clinical efficacy and has been largely abandoned as an anti-adhesion barrier. A newly developed hyaluronic acid-phosphate-buffered saline solution applied intraoperatively to protect peritoneal surfaces from indirect surgical trauma effectively and safely reduced adhesions in a large multicenter study of women undergoing gynecological laparotomy. Three recently developed mechanical barriers also have demonstrated clinical progress in adhesion prevention. A bioresorbable membrane consisting of hyaluronic acid and CMC has gained regulatory approval for clinical use in both general and gynecological surgery following demonstration of efficacy and safety in reducing adhesions. A barrier made of expanded polytetrafluoroethylene and another developed from oxidized regenerated cellulose are currently available for gynecological surgery. With continued research, new and improved approaches hopefully will become available to prevent adhesion formation.

Adrenal Cortex Hormones↗

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