JAC Advance Access published online on January 19, 2005
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkh525
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1 Department of Cell Biology and Histology, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
* To whom correspondence should be addressed. Background: We previously demonstrated that the quinolone moxifloxacin prevents Candida albicans pneumonitis and epithelial nuclear factor Objectives: To explore the anti-inflammatory effects of moxifloxacin directly on a lung epithelial cell line. Methods: We studied the effect of clinically relevant concentrations of moxifloxacin (2.5-10 mg/L) on cytokine-induced activation of nitric oxide (NO) secretion, inducible NO synthase (iNOS) expression and the activation of signal transduction pathways of inflammation, NF- Results: Stimulation with the cytokines interleukin-1 Conclusions: Moxifloxacin inhibits intracellular signalling, iNOS expression and NO secretion in a lung epithelial cell line. Future studies may uncover a primary site of quinolone immunomodulation, either upstream or at the cell membrane. Eventually, this quinolone might become an important therapy for inflammatory lung diseases.
Received June 9, 2004
Revised September 11, 2004
Accepted November 7, 2004
Original article
Moxifloxacin inhibits cytokine-induced MAP kinase and NF-
B activation as well as nitric oxide synthesis in a human respiratory epithelial cell line
2 Schneider Children's Medical Centre of Israel and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
3 Paediatric Department, Assaf Harofeh Medical Centre and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
Hannah Blau, E-mail: hblau{at}post.tau.ac.il
Abstract 
B (NF-B) nuclear translocation in immunosuppressed mice.B and the mitogen-activated protein kinases [extracellular signal-regulated kinases (ERK1/2) and C-Jun N-terminal kinase (JNK)], in the A549 lung epithelial cell line.
(IL-1)/interferon-
(IFN-) increased NO up to 3.3-fold and moxifloxacin inhibited this up to 68% (P < 0.05). Similarly, the increase in iNOS levels was inhibited in cells pre-treated with moxifloxacin by up to 62%. IL-1 stimulated a rapid increase in the activities of early intracellular signalling molecules, ERK1/2 and JNK. Moxifloxacin inhibited ERK1/2 by up to 100% and p-JNK activation by 100%. NF-B, as measured by electrophoretic mobility shift assay, was inhibited up to 72% by moxifloxacin. Western-blot analysis revealed that IL-1 enhanced NF-B p65 and p50 proteins by 1.7- and 3.6-fold, respectively, whereas moxifloxacin inhibited the proteins by up to 60%.
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