Levofloxacin kills Chlamydia pneumoniae and modulates interleukin 6 production by HEp-2 cells
Abstract
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 x 10(3) inclusion-forming units (IFU)/ml] by centrifugation for 30 min and incubation at 37 degrees C for 1 h. Infected monolayers were treated with levofloxacin (3 or 8 microg/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 >or=98% of C. pneumoniae…
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