title: 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 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.
authors.affiliation: Stratton Veterans Affairs Medical Center and Albany Medical College, Albany, NY 12208, USA. Aldona.Baltch@med.va.gov
authors.forename: Aldona L
authors.initials: AL
authors.lastname: Baltch
authors.forename: Raymond P
authors.initials: RP
authors.lastname: Smith
authors.forename: William J
authors.initials: WJ
authors.lastname: Ritz
authors.forename: Andrea
authors.initials: A
authors.lastname: Carpenter-Knaggs
authors.forename: Phyllis B
authors.initials: PB
authors.lastname: Michelsen
authors.forename: Cynthia J
authors.initials: CJ
authors.lastname: Carlyn
authors.forename: Lawrence H
authors.initials: LH
authors.lastname: Bopp
authors.forename: Jonathan R
authors.initials: JR
authors.lastname: Hibbs
mesh_terms: D000890:Anti-Infective Agents / Q000494:pharmacology*; D002277:Carcinoma; D002690:Chlamydia Infections / Q000188:drug therapy; D016993:Chlamydophila pneumoniae / Q000187:drug effects*; D022781:Hepatocytes / Q000378:metabolism*; D006801:Humans; D015850:Interleukin-6 / Q000096:biosynthesis*; D064704:Levofloxacin; D008113:Liver Neoplasms; D015242:Ofloxacin / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
chemical_list: D000890:Anti-Infective Agents; D015850:Interleukin-6; D064704:Levofloxacin; D015242:Ofloxacin