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 × 103 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.

Keywords:
Chlamydia pneumoniae, Interleukin 6, Levofloxacin, HEp-2 cells
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© 2003 S. Karger AG, Basel
2003
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