Levofloxacin Kills Chlamydia pneumoniae and Modulates Interleukin 6 Production by HEp-2 Cells

• Published in: Chemotherapy (Basel) Vol. 49; no. 1-2; pp. 27 - 32
• Main Authors: Baltch, Aldona L., Smith, Raymond P., Ritz, William J., Carpenter-Knaggs, Andrea, Michelsen, Phyllis B., Carlyn, Cynthia J., Bopp, Lawrence H., Hibbs, Jonathan R.
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Karger 01.05.2003; S. Karger AG
• Subjects: Anti-Infective Agents - pharmacology; Antibacterial agents; Antibiotics. Antiinfectious agents. Antiparasitic agents; Biological and medical sciences; Carcinoma; Chlamydia Infections - drug therapy; Chlamydophila pneumoniae; Chlamydophila pneumoniae - drug effects; Hepatocytes - metabolism; Humans; Interleukin-6 - biosynthesis; Levofloxacin; Liver Neoplasms; Medical sciences; Microbiology; Ofloxacin - pharmacology; Pharmacology. Drug treatments; Tumor Cells, Cultured; Interleukin 6; Levofloxacin; HEp-2 cells; Chlamydia pneumoniae; Cell culture; Chlamydiaceae; Cytokine; Inflammation; In vitro; Biological activity; Bactericidal effect; Antibiotic; Fluoroquinolone derivatives; Modulation; Production; Chlamydiales; Bacteria; Antibacterial agent; Quinolone derivatives
• ISSN: 0009-3157; 1421-9794
• DOI: 10.1159/000069775

Background:Chlamydia pneumoniae is known to cause acute respiratory infection and more recently it has been studied as a pathogen causing inflammatory changes in chronic diseases such as atherosclerosis. This study addresses the antichlamydial effect of levofloxacin and its role in modulation of a proinflammatory cytokine IL-6 production by uninfected and infected HEp-2 cells. Methods: HEp-2 cell monolayers were infected with previously prepared and frozen aliquots of C. pneumoniae [1 × 10 3 inclusion-forming units (IFU)/ml] by centrifugation for 30 min and incubation at 37°C for 1 h. Infected monolayers were treated with levofloxacin (3 or 8 µg/ml) immediately after infection (0 h) or 24 h after infection. Monolayers were examined daily for 96 h after infection by counting inclusions with fluorescently labeled antichlamydial monoclonal antibody. Aliquots of disrupted monolayers were titrated to determine the numbers of viable C. pneumoniae IFU/ml. IL-6 concentrations in cell supernatants were determined by ELISA assays. Results: Infected HEp-2 cells produced IL–6. Noninfected HEp-2 cells demonstrated modulation of IL-6 production by levofloxacin. No viable C. pneumoniae were detected in infected HEp-2 cells when the monolayer was treated with levofloxacin immediately after infection (0 h). In contrast, when cells were treated 24 h after infection, a gradual decline in the number of viable C. pneumoniae occurred; by 96 h into the assay ≧98% of C. pneumoniae were killed. IL-6 concentrations were similar in the supernatants of levofloxacin-treated and nontreated HEp-2 cells. Conclusions: (1) Levofloxacin is effective in eliminating C. pneumoniae from infected HEp-2 cells; (2) although levofloxacin modulates the production of IL-6 in untreated HEp-2 cells, no evidence for such modulation was observed in HEp-2 cells infected with C. pneumoniae. (3) Presence of viable C. pneumoniae may not be necessary for IL-6 production by infected and treated HEp-2 cells.