Disease relevance of EN 141

• We describe two mutants of Mycoplasma hominis PG-21 which show resistance to 16-membered macrolides but susceptibility to lincosamides, obtained by in vitro exposure to increasing doses of josamycin [1].
• For six clinical isolates of Chlamydia trachomatis, in vitro susceptibility to erythromycin, azithromycin, and josamycin has been determined [2].
• YM133 showed activity against erythromycin-, josamycin-, and rokitamycin-resistant (MIC greater than or equal to 100 micrograms/ml) strains of staphylococci, streptococci, Bacteroides spp., and Clostridium spp [3].
• In vitro activity of josamycin against aerobic gram-positive cocci and anaerobes [4].
• Typhus group rickettsiae were susceptible to all macrolides tested, whereas the spotted fever group rickettsiae, R. bellii, and R. canada were more resistant, with josamycin, a safe alternative for the treatment of Mediterranean spotted fever, being the most effective compound [5].

High impact information on EN 141

• Kinetics of macrolide action: the josamycin and erythromycin cases [6].
• Oral administration of clarithromycin (CAM) (5-10 mg/kg) significantly inhibited OVA- and LPS-induced mucus production and neutrophil infiltration, whereas josamycin and ampicillin showed no effect [7].
• Of the strains with the iMLS(B) phenotype, 36 exhibited a reversibly inducible MLS(B) (riMLS(B)) phenotype, i.e., blunting of the erythromycin zone of inhibition, which indicates that the 16-membered-ring macrolide josamycin is a more effective inducer than the 14-membered-ring macrolide erythromycin [8].
• We studied the effect of erythromycin, clarithromycin, josamycin, and other antibiotics on the release by eosinophils of interleukin-8 (IL-8), a potent chemokine for inflammatory cells, including eosinophils themselves [9].
• The effect of three macrolide antibiotics, midecamycin acetate, josamycin, and clarithromycin, on human T-cell function was investigated in vitro [10].

Chemical compound and disease context of EN 141

• The antimicrobial activities of josamycin, erythromycin, and spiramycin against Rickettsia conorii and R. rickettsii were evaluated in two tests: a dye-uptake assay and a plaque assay [11].
• Clindamycin, rosamicin, josamycin, and metronidazole had similar inhibitory activity against 29 clinical isolates of Bacteroides fragilis, i.e., 100% of strains were inhibited by 0.8 microng of metronidazole or josamycin/ml and 100% by 1.6 microng of clindamycin or rosamicin/ml [12].
• Streptococci isolated on media containing 64 mg/l of macrolides were mainly Streptococcus sanguis and S. mitis with one isolate of S. salivarius; the majority were resistant to 256 mg/l erythromycin, josamycin, all other macrolides tested and clindamycin [13].
• OBJECTIVES: Mycoplasma hominis is intrinsically resistant to 14- and 15-membered macrolides and to the ketolide telithromycin but is susceptible to josamycin, a 16-membered macrolide, and lincosamides [14].
• BACKGROUND: In our previous study, a triple therapy using tripotassium dicitrato bismuthate (TDB), josamycin and furazolidone achieved a suboptimal cure rate of Helicobacter pylori infection [15].

Biological context of EN 141

• The tolerance and pharmacokinetics of erythromycin stearate and josamycin base were compared in healthy dental students [16].
• Effects of josamycin on polymorphonuclear leucocyte chemotaxis [17].
• The mechanism by which josamycin exerts its activity on antibody production has been partially elucidated [18].
• Josamycin did not disturb gastrointestinal motility and no dog showed signs of discomfort [19].
• These data suggest that the bactericidal synergy between PMN and josamycin could be related, partly at least, to a direct enhancing effect of josamycin on some PMN functions such as phagocytosis, chemotaxis and FMLP-induced chemiluminescence [20].

Anatomical context of EN 141

• Midecamycin acetate and josamycin suppressed the proliferative response of peripheral blood mononuclear cells stimulated by polyclonal T-cell mitogens at concentrations between 1.6 and 8 micrograms/ml [10].
• We studied the in-vivo uptake of josamycin by alveolar macrophages recovered by broncho alveolar lavage performed in patients 3 h after ingestion of 1 g of the drug [21].
• The immunodepression depends on the stimulation of hydrogen peroxide production by monocytes and requires the actual presence of josamycin during the immune response [18].
• The effects of josamycin on the antigen-specific primary antibody responses of human peripheral blood cells have been studied by the method of haemolytic colonies in soft agar [18].
• The difference in the chemical structure of erythromycin and josamycin is the main reason for their differential effect on the gastrointestinal tract [19].

Associations of EN 141 with other chemical compounds

• OBJECTIVES: The aim of this study was to determine whether pre-incubation of peritoneal or splenic cells with different doses of the macrolides erythromycin A (14-membered ring), azithromycin (15-membered ring) and josamycin (16-membered ring) affects their phagocytic activity or cytokine production [22].
• Application of liquid chromatography-ion trap mass spectrometry to the characterization of the 16-membered ring macrolide josamycin propionate [23].
• The content of the immunoreactive protein in rat liver microsomes was increased by treatments with phenobarbital, pregnenolone 16 alpha-carbonitrile (PCN), erythromycin, erythromycin estolate, and oleandomycin but not with 3-methylcholanthrene, imidazole, ethanol, isosafrole, josamycin, midecamycin, or miocamycin [24].
• A simple and rapid method using high-performance liquid chromatography (HPLC) for the simultaneous determination of five macrolides (josamycin, kitasamycin, mirosamicin, spiramycin and tylosin) in meat has been developed [25].
• Among S. pyogenes, 30.2% were erythromycin resistant; 18.5% were also resistant to josamycin and clindamycin (MLS phenotype) [26].

Gene context of EN 141

• Addition of RXM (but not JM) at 5.0 and 7.5 microg x mL(-1) significantly suppressed the production of MMP-2 and -9 from NPF induced by TNF-alpha stimulation [27].
• Josamycin did not show definite time-dependent decreases in IC(50) for CYP 3A4, suggesting that josamycin is neither a quasi-irrversible nor an irreversible inhibitor of CYP3A4 [28].
• In addition, R compensated the negative effect of josamycin (100 micrograms/ml) on PMN adhesion and on CD18 and CD35 expression [29].
• In vitro activity of rosamicin, josamycin, erythromycin, and clindamycin against beta-lactamase-nagative and beta-lactamase-positive strains of Neisseria gonorrhoeae [30].
• Simultaneous determination of the antibiotic levels was performed on the BAL supernatant and the serum and the results compared to those obtained by incubating alveolar macrophages and blood polymorphonuclears at 2 and 8 mg/l. Josamycin concentration was measured using a high pressure liquid chromatography method [21].

Analytical, diagnostic and therapeutic context of EN 141

• Josamycin pulmonary penetration determined by broncho-alveolar lavage in man [21].
• A simple, selective and sensitive high-performance liquid chromatographic (HPLC) method has been developed for the measurement of josamycin residues in four porcine tissues (i.e., muscle, liver, kidney and fat) [31].
• The voltammetric behaviour of josamycin (a macrolide antibiotic) has been studied using direct current (DC(t)) alternating current (AC(t)) and differential pulse polarography (DPP) [32].
• In hematological examination, the platelet count was significantly (P<0.01) lower in the male groups given 0.02% or more of josamycin and in the 2.5% female group as compared with the control group values in a dose-dependent manner [33].
• Effects of troleandomycin and josamycin on thyroid hormone and steroid serum levels, liver function tests and microsomal monooxygenases in healthy volunteers: a double blind placebo-controlled study [34].

References