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)

Adhesion molecules are responsible for PMN-endothelial cell interactions involved in both PMN-mediated endothelial injury (e.g., after ischemia-reperfusion injury) and PMN-mediated host defense against bacterial infection. Inhibition of PMN-endothelial adherence with CD18 and P-selectin mAb has been shown to ameliorate the tissue injury resulting from ischemia and reperfusion under a variety of experimental conditions. However, interference with PMN function may result in an increased risk of bacterial infection. Previous investigations suggest that CD18 blockade can lead to increased infectious risk. Little is known of the infectious risks associated with selectin blockade. We report the effects of P-selectin blockade (using mAb PB1.3) on bacteria-induced PMN emigration into the peritoneum and subcutaneous (s.c.) tissue in rabbits. Leukocyte and PMN emigration into the peritoneum 4 h after inoculation with 10 ml of 10(9) CFU/ml Escherichia coli was significant in saline-treated animals, and not different in animals pretreated with mAb PB1.3. Similarly, the incidence and severity of abscess formation 7 days after s.c. inoculation with Staphylococcus aureus (10(7), 10(8), or 10(9) CFU) was not increased in rabbits pretreated with mAb PB1.3 compared to saline. PMN emigration to the s.c. S. aureus was also similar in both saline and mAb PB1.3-treated animals, as determined by light microscopy. We conclude that P-selectin blockade with mAb PB1.3: 1) does not interfere with acute, E. coli-induced PMN emigration into the peritoneum, 2) does not increase the incidence or severity of S. aureus abscess formation in s.c. tissue, and 3) interferes less with PMN antibacterial host defense mechanisms than inhibition of CD18-mediated PMN adherence.
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PMID:P-selectin blockade does not impair leukocyte host defense against bacterial peritonitis and soft tissue infection in rabbits. 769 61

Oxidants generated by endothelial xanthine oxidase (XO) can help trigger free radical-mediated tissue injury. An important event in oxidant-mediated tissue injury is neutrophil-endothelial adhesion. Although activation of endothelial XO increases adhesion, little is known about xanthine in the adhesive effect of XO. This study examined administered xanthine on the adhesion of neutrophils. Endothelial [human umbilical vein endothelial cells (HUVEC)] monolayers were exposed to xanthine (15 min), and neutrophils were allowed to adhere to HUVEC in an adhesion assay. Adhesion was dose dependently increased by xanthine (3-100 microM). Either catalase (1,000 U/ml), oxypurinol (XO inhibitor; 100 microM), or platelet-activating factor (PAF) receptor antagonist (WEB 2086; 10 microM) reduced neutrophil adhesion. Superoxide dismutase (1,000 U/ml) had no effect. Pretreatment of HUVEC with 50 microM tungsten also blocked xanthine-induced adherence. Adhesion was also inhibited by preincubation with 100 U/ml heparin. Finally, anti-P-selectin antibody (PB1.3; 20 micrograms/ml) attenuated adhesion. Our results indicate that xanthine may promote neutrophil-endothelial adhesion via a hydrogen peroxide- and PAF-mediated P-selectin expression.
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PMID:Exogenous xanthine promotes neutrophil adherence to cultured endothelial cells. 927 12

Adhesion molecules are key molecules for inflammatory cardiovascular diseases and are known to be up-regulated by inflammatory cytokines. However, the role of adhesion molecules in the cytokine-induced myocardial dysfunction in vivo remains unclear. This role was examined in our novel canine model, in which chronic treatment of the heart with IL-1 beta-bound microspheres (MS), but not control MS, causes sustained myocardial dysfunction in vivo. The expression of P-selectin (mRNA and immunoreactivity) was more prominent in the IL-1 beta group than in the control group (treated with control MS alone) after MS injection. The extent of neutrophil infiltration and myocardial myeloperoxidase (MPO) activity were significantly increased in the IL-1 beta group (P < 0.01). Pre-treatment with SLeX-OS (a novel oligosaccharide analog of sialyl LewisX) or PB1.3 (a monoclonal antibody to P-selectin) prevented the myocardial dysfunction and significantly suppressed the neutrophil infiltration and the increase in myocardial MPO activity induced by IL-1 beta (P < 0.01 each). These results indicate that adhesion molecules play an important role in the pathogenesis of the cytokine-induced sustained myocardial dysfunction in dogs in vivo.
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PMID:Inhibition of adhesion molecules markedly ameliorates cytokine-induced sustained myocardial dysfunction in dogs in vivo. 999 May 35