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Extracellular proteases from Pseudomonas aeruginosa play important roles in infections in the respiratory tract. The effect of erythromycin (EM), a macrolide antibiotic, on the production of elastase by P. aeruginosa was investigated in vitro and compared with the effect of other antibiotics. Thirty-four (94.4%) of thirty-six different strains produced detectable amounts of elastase determined by the gel diffusion method. The elastase production was inhibited completely by EM in 27 (79.4%) of 34 strains at some concentrations between 0.125 and 64 micrograms/ml. At 4 micrograms/ml or less, the elastase production was inhibited completely in four (11.8%) strains and more than 50% in the other 10 (29.4%). At 8 micrograms/ml or less, the elastase production was inhibited completely in 11 (32.4%) strains and more than 50% in the other nine (26.5%). The proliferation was partially inhibited at 32 and 64 micrograms/ml. Roxithromycin inhibited the elastase production at higher concentrations than EM without inhibiting the proliferation. Midecamycin and ampicillin did not inhibit the elastase production or the proliferation. Doxycycline and ticarcillin inhibited the elastase production and/or the proliferation at concentrations greater than 16 micrograms/ml. Although ofloxacin (OFLX) inhibited both the proliferation and the elastase production in parallel at low concentrations, there were six (16.7%) strains resistant to OFLX. Among them the elastase production was inhibited in five strains by EM. These results suggest that EM acts on P. aeruginosa to inhibit extracellular production of elastase without affecting the proliferation of the bacteria.
Evidence seems to support an association between CP infection and an increased incidence of CAD. Additional and larger seroepidemiologic studies of this association need to be performed to establish a causal relationship between infection and CAD. Determination of the actual role of CP in CAD may decide the role of specific antichlamydial therapy in the management of this condition.
The effect of three macrolides (azithromycin, roxithromycin and erythromycin) on the interaction in vitro of human polymorphonuclear leukocytes (PMNs) with Staphylococcus aureus was examined. The exposure of S. aureus to 0.25 MIC of roxithromycin and erythromycin but not of azithromycin significantly increased the uptake of opsonized bacteria by human PMNs. The preincubation of PMNs with 1, 10 and 25 mg/l of the three antimicrobial agents did not affect either the uptake of S. aureus or the superoxide radical production by human PMNs. At these same concentrations the three agents showed slight but not significant intracellular activity in PMNs against S. aureus. It is concluded that treatment of S. aureus with subinhibitory concentrations of roxithromycin and erythromycin enhanced phagocytosis by PMNs, but the three macrolides tested did not directly affect the functions of human PMNs against S. aureus.
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Conformational study of methylated derivatives of macrolide antibiotics roxithromycin (6-OMe-roxithromycin and 6,11-OMe-roxithromycin) has been achieved by NMR in solution and molecular dynamics (MD) simulations and compared to 6-OMe-erythromycin (clarithromycin). A complete conformational study by NMR has been led by determination of homonuclear coupling constants and NOEs. Heteronuclear 1H-13C coupling constants were also measured to investigate the orientation of the sugar moieties with respect to the erythronolide. MD simulations were performed using the crystallographic coordinates as the starting conformation. For each compound, experimental results were compared to calculated conformations in order to identify eventual conformational equilibrium in solution. It is shown that the effect of the methylation is opposite for roxithromycin compared to erythromycin especially on motional properties as the roxithromycin derivatives gain in mobility while the erythromycin derivatives behaves as a more restrained molecule. The study of macrolide-ribosome interactions has been investigated using transferred NOESY 1H NMR experiments and the conformations weakly bound to bacterial ribosomes were determined. Biological interactions of these compounds with membranar liver protein cytochrome P450 was also discussed with regard to their structural properties.
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A 66-year-old woman with autoimmune hemolytic anemia developed hepatic veno-occlusive disease while being treated with immunosuppressive cyclophosphamide 100 mg/day in combination with roxithromycin (total dose 600 mg/day). After all drugs were stopped, the patient recovered within 2 weeks. The Naranjo probability scale indicated a probable relationship between veno-occlusive disease and treatment with cyclophosphamide in this patient.
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HPDL cells were plated at 5 x 10(5) cells/ml in 150 cm2 cell culture dishes. The confluent-stage cells were pretreated with or without 10 microg/ml of RXM or other antibiotics in 1% FBS-containing alpha-MEM for 24 hours, followed by simultaneous treatment with 10 ng/ml of TNF-alpha and 10 microg/ml of these antibiotics. After incubation for various periods, the culture supernatants and sediments were collected and analyzed by ELISA, Northern blot, and gel shift assays.
The objective of this study was to examine the effect of macrolide antibiotics, clarithromycin, erythromycin, roxithromycin, josamycin and azithromycin, on the hepatic uptake of digoxin. The uptake of [(3)H]digoxin was studied in rats in vivo, using the tissue-sampling single-injection technique, and in isolated rat hepatocytes in vitro. The uptake of [(3)H]digoxin into rat hepatocytes was concentration-dependent with a Michaelis constant (K(m)) of 445 nM. All the macrolide antibiotics inhibited the uptake of [(3)H]digoxin into rat hepatocytes in a concentration-dependent manner. However, clarithromycin did not affect the in vivo hepatic uptake of digoxin in rats. The in vivo permeability-surface area product of digoxin for hepatic uptake (PS(inf)) was estimated to be 12.5 ml/min/g liver from the present in vitro data, which is far larger than the hepatic blood flow rate (1.4 ml/min/g liver). Macrolide antibiotics at clinically relevant concentrations inhibit digoxin uptake by rat hepatocytes in vitro, but not in vivo, probably because hepatic uptake of digoxin in rats is blood flow-limited. Clinically observed digoxin-macrolide interaction in humans could be due to macrolide inhibition of hepatic digoxin uptake, if the uptake is permeation-limited.