ABSTRACT
The bactericidal activities of macrolides (clarithromycin, roxithromycin and azithromicyn) and lansoprazole, alone and in combination, against Helicobacter pylori strains were evaluated. It was found that the association of lansoprazole and clarithromycin resulted in a marked synergism, while the combination of roxithromycin or azithromycin with lansoprazole had synergistic and additive effects.
Subject(s)
Anti-Bacterial Agents/pharmacology , Helicobacter pylori/drug effects , Omeprazole/analogs & derivatives , 2-Pyridinylmethylsulfinylbenzimidazoles , Azithromycin/pharmacology , Biopsy , Clarithromycin/pharmacology , Drug Synergism , Helicobacter pylori/isolation & purification , Humans , Kinetics , Lansoprazole , Microbial Sensitivity Tests/methods , Omeprazole/pharmacology , Roxithromycin/pharmacology , Time FactorsABSTRACT
The lethal effects occurring in neonatal (<24-h-old) BALB/c mice after challenge with 25 mg of lipopolysaccharide (LPS) per kg of body weight were significantly counteracted by pretreatment with recombinant interleukin-10 (rIL-10; 25 or 50 ng/mouse). Concordantly, blockage of endogenous IL-10 with the SXC1 monoclonal antibody increased LPS-induced mortality. Both IL-10 and SXC1 modulated the release of tumor necrosis factor alpha (TNF-alpha) so that, relative to controls, peak TNF-alpha values after LPS challenge were decreased by rIL-10 and increased by anti-IL-10.
Subject(s)
Endotoxemia/drug therapy , Interleukin-10/therapeutic use , Animals , Animals, Newborn , Antibodies, Monoclonal/pharmacology , Endotoxemia/immunology , Interleukin-10/antagonists & inhibitors , Mice , Mice, Inbred BALB C , Recombinant Proteins/therapeutic use , Tumor Necrosis Factor-alpha/metabolismABSTRACT
The aim of this study was to examine the ability of Pseudomonas aeruginosa components to induce release of cytokines from human leukocytes. Human whole-blood cultures were incubated with several concentrations of purified P. aeruginosa products, including porins, exomucopolysaccharide, lipopolysaccharide, and toxin A. Supernatants were assayed for tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) activities. All of the P. aeruginosa components except toxin A were able to stimulate the release of both cytokines. On a weight basis, porins were as effective as lipopolysaccharide and significantly more effective than exomucopolysaccharide in inducing IL-6 release (P < 0.05). Moreover, porins were more potent than either exomucopolysaccharide or lipopolysaccharide in inducing TNF-alpha release (P < 0.05). Further experiments using isolated leukocytes suggested that monocytes were the cell population predominantly responsible for the production of both cytokines. These data indicate that P. aeruginosa porins are able to induce significant cytokine production. These components may be responsible for the chronically overactive inflammatory response associated with persistent lung infection in cystic fibrosis patients.
