PubMed · 8743259
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P Nickel, H Näher. 1996. Nongonococcal urethritis.. https://pubmed.ncbi.nlm.nih.gov/8743259/
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Lung transplantation is hampered by bronchiolitis obliterans syndrome (BOS), although recently azithromycin treatment has a published response rate of about 42% in patients with established BOS. We linked this improvement to a reduction in airway neutrophilia and IL8. In the present study, we further investigated the intracellular mechanisms of azithromycin, looking at the possible involvement of mitogen-activated-protein kinases (MAPK) and oxidative stress. Simultaneously, currently used immunosuppressive agents were investigated. Human primary airway smooth muscle cells were stimulated with IL17 and incubated with increasing concentrations of steroids, immunosuppressive agents (tacrolimus, cyclosporine and rapamycin) or macrolides (erythromycin and azithromycin). We measured supernatant IL8 protein, 8-isoprostane and cell lysate MAPK. IL17-induced IL8 production was decreased by both erythromycin and azithromycin. In nonstimulated condition, IL8 production only increased at the highest dose of azithromycin. Dexamethasone failed to attenuate IL8 production, whereas immunosuppressive agents significantly increased IL8 production in both IL17-stimulated and nonstimulated conditions. 8-isoprostane production and MAPK activation proved to be decreased by the macrolides. We conclude that macrolides (but not steroids/immunosuppressive agents) inhibit IL17-induced IL8 production in human primary airway smooth muscle cells via a reduction in MAPK activation and 8-isoprostane production. In BOS patients, these phenomena may explain the anti-inflammatory effects of azithromycin.
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From 2002 to 2003, a total of 381 consecutive S. pyogenes isolates were obtained from throat swabs (n = 337) and samples of pus (n = 31), sputum (n=10) and blood (n = 3) at Hacettepe University Hospital. The susceptibility of the isolates to erythromycin was tested by the agar dilution method. Erythromycin resistant strains were then tested for their MICs to azithromycin, clindamycin, and penicillin, their phenotype of resistance to macrolides-lincosamides-streptogramin B (MLSB) and for the presence of macrolide resistance genes. The rate of resistance to erythromycin was 6.8%. Constitutive (cMLSB), inducible (iMLSB), and M phenotypes of resistance were detected in 7.7, 30.8, and 57.7% of resistant strains, respectively. One strain had both cMLSB and iMLSB phenotypes. All M phenotypes carried the mefA gene, all iMLSB phenotype carried the ermTR gene, 1 isolate with cMLSB phenotype harboured the ermB gene, and 1 isolate with cMLSB phenotype carried both the ermB and mefA genes. One strain which showed cMLSB and iMLSB phenotypes harboured the ermB gene.