“…Buccal mucosal cells were collected by scraping the mucosa with a blunt spatula. The scrapings were minced by passage through a 50-mesh grid, and the epithelial cells were dispersed by homogenization and settled by centdfugation (12,13).…”
Section: Methodsmentioning
confidence: 99%
“…The microtiter wells were precoated with monoclonal anti-TNF-c~ to capture TNF-c~ from the homogenates of buccal mucosa derived from the animals on the ethanol or control diets, and after washing away the excess of reagent the wells were probed with horseradish peroxidase-conjugated polyclonal anti-TNF-~. The complex was then incubated with TMB substrate solution and TNF-c~ quantified spectrophotometrically (12).…”
SUMMARYIn this study we investigated buccal mucosal cells' apoptosis and the expression of regulatory cytokJnes, tumor necrosis factor-~ (TNF-~) and inetrleukin-4(IL-4) with chronic ethanol ingestion. The buccal mucosa of rats maintained for 23 days on alcohol-containing and control liquid diet was assessed for IL-4 and TNF-c~ content, and the extent of epithelial cells apoptosis. While the expression of TNF-c~ in alcohol diet group showed a significant increase (1.9-fold) over that of the controls, less apparent differences between the two groups were observed in the content of IL-4 (141.8 ___28.2 vs. 119.8 _+7.3 pg/mg protein). The DNA fragmentation assays revealed that alcohol diet group also exhibited a 3.5-fold enhancement in buccal mucosal cells apoptosis. Moreover, the apoptotic index showed positive correlation (r = 0.53) with the extent of induced changes in TNF-~. These results demonstrate that ethanol-induced buccal mucosal cells apoptosis is triggered by the enhancement in TNF-~ expression.
“…Buccal mucosal cells were collected by scraping the mucosa with a blunt spatula. The scrapings were minced by passage through a 50-mesh grid, and the epithelial cells were dispersed by homogenization and settled by centdfugation (12,13).…”
Section: Methodsmentioning
confidence: 99%
“…The microtiter wells were precoated with monoclonal anti-TNF-c~ to capture TNF-c~ from the homogenates of buccal mucosa derived from the animals on the ethanol or control diets, and after washing away the excess of reagent the wells were probed with horseradish peroxidase-conjugated polyclonal anti-TNF-~. The complex was then incubated with TMB substrate solution and TNF-c~ quantified spectrophotometrically (12).…”
SUMMARYIn this study we investigated buccal mucosal cells' apoptosis and the expression of regulatory cytokJnes, tumor necrosis factor-~ (TNF-~) and inetrleukin-4(IL-4) with chronic ethanol ingestion. The buccal mucosa of rats maintained for 23 days on alcohol-containing and control liquid diet was assessed for IL-4 and TNF-c~ content, and the extent of epithelial cells apoptosis. While the expression of TNF-c~ in alcohol diet group showed a significant increase (1.9-fold) over that of the controls, less apparent differences between the two groups were observed in the content of IL-4 (141.8 ___28.2 vs. 119.8 _+7.3 pg/mg protein). The DNA fragmentation assays revealed that alcohol diet group also exhibited a 3.5-fold enhancement in buccal mucosal cells apoptosis. Moreover, the apoptotic index showed positive correlation (r = 0.53) with the extent of induced changes in TNF-~. These results demonstrate that ethanol-induced buccal mucosal cells apoptosis is triggered by the enhancement in TNF-~ expression.
“…[210] Des Weiteren wurden in Magenbiopsien von mit H. pylori infizierten Patienten niedrigere Sulfomucinspiegel festgestellt. [212] Man geht davon aus, dass der erhöhte Mucinabbau durch Mucin-Sulfatasen die Schwere eines Krankheitsbildes entscheidend beeinflusst. [201] Weiterhin spielen Mucin-Sulfatasen vermutlich eine Rolle bei der Invasion der opportunistischen Pathogene P. aeroginosa und Burkholderia cepacia in Lungengewebe, besonders bei Patienten mit beeinträchtigter Mucin-Clearance, wie sie bei einer zystischen Fibrose (CF) typisch ist.…”
Section: Bakterielle Sulfatasen Und Pathogenitätunclassified
“…[216] Diese Annahme wird durch den Befund gestützt, dass zwei gebräuchliche antiulcerative Wirkstoffe gegen Infektion mit H. pylori, Nitecapon und Sulcrasulfat, die Desulfonierungsaktivität von Mucin-Sulfatasen signifikant herabsetzen. [205,212] Eine Umlagerung der Sulfatstruktur wurde auch als Ursache für die Pathogenität bestimmter Stämme von Mycobacterium vorgeschlagen. In bioinformatischen Studien wurde gefunden, dass die in diesen Organismen ubiquitären Sulfatasesequenzen für Enzyme codieren könnten, die Glycosaminoglycane so modifizieren, dass die für eine Infektion essenziellen Bindungsstellen entstehen.…”
Section: Bakterielle Sulfatasen Und Pathogenitätunclassified
Sulfatasen – d. h. Sulfatester spaltende Enzyme – spielen eine entscheidende Rolle bei der Regulierung von Sulfatierungszuständen, die über die Funktion vieler physiologischer Moleküle entscheiden. Die Substrate der Sulfatasen reichen von kleinen cytosolischen Steroiden wie dem Östrogensulfat bis hin zu komplexen Kohlenhydraten auf Zelloberflächen, etwa den Glycosaminoglycanen. Die Umwandlung dieser Moleküle wurde mit wichtigen zellulären Funktionen in Verbindung gebracht, z. B. mit der Hormonregulation, dem zellulären Abbau und der Modulation von Signalisierungsprozessen. Sulfatasen hängen mit dem Ausbruch etlicher pathophysiologischer Erscheinungen zusammen, etwa mit hormonabhängigen Krebsformen. Bis heute sind zwar zahlreiche Sulfatasen identifiziert worden, die Aufklärung des weitreichenden Spektrums ihrer biologischen Aktivitäten befindet sich aber erst am Anfang. Dieser Aufsatz gibt einen Überblick über den derzeitigen Wissensstand zu den Strukturen, Mechanismen und der Inhibition von Sulfatasen.
“…Sofalcone has antibacterial activity that induces morphological changes of H. pylori, inhibits adhesion of H. pylori to gastric mucin, and inhibits the lipolytic activity of H. pylori [19][20][21]. Sucralfate contains aluminum and reduces H. pylori enzyme activities and inhibits H. pylori attachment to gastric surface epithelium [22,23]. Also sucralfate enhanced the susceptibility of H. pylori to antibiotics [24].…”
Triple therapy with a proton pump inhibitor plus two antibiotics is recently standard regimen for treatment of H. pylori infection. However, the agents that are used for H. pylori eradication are not always limited to drugs whose primary use is as an antimicrobial agent. Anti-H. pylori activity has been reported for nontraditional antimicrobials such as proton pump inhibitors, bismuth compounds, mucosal defensive agents, and some other agents. Proton pump inhibitors and their acid-activated derivatives have significant activities against H. pylori, potent inhibitors of urease, proton motive force, and ATPase of H. pylori. Some bismuth compounds and compound of a mixture of ranitidine hydrochloride and bismuth citrate were shown to inhibit the growth of H. pylori in vitro, to eradicate H. pylori in vivo, and to decrease the development of H. pylori secondary resistance to antibiotics. The mechanism of bactericidal action of bismuth compounds has not been clear. Mucosal defensive agents that enhance defense factors of gastro-duodenal mucosa are locally acting anti-ulcer drugs. Each mucosal defensive agent was found to have direct or indirect different activities against H. pylori in vitro. Though studies attempting to improve the eradication rate by the addition of mucosal defensive agents to conventional therapy have been tried, additive effects of these agents were equivocal. Therapeutic approaches with other agents such as Lactobacillus, lactoferrin, and dietary constituents to cure H. pylori infection are under investigation.Non-traditional antimicrobials by them selves are unable to cure H. pylori infection in spite of anti-H. pylori activities. Studies are needed to establish the clinical utility of non-traditional antimicrobial agents in prevention and eradication of H. pylori infection since eradication of antibiotic resistance H. pylori would become a difficult problem.
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