Effect of levofloxacin on the viability of intracellular Chlamydia pneumoniae and modulation of proinflammatory cytokine production by human monocytes.

Although antibiotics are known to affect the intracellular growth of Chlamydia pneumoniae in acute infections, their efficacy in therapy for chronic infections, including atherosclerosis, remains debatable. Human monocyte-derived macrophages (MDM) obtained from monocytes of healthy donors were infected with C. pneumoniae AR-39 and treated with levofloxacin (8 microg/mL) immediately after infection (0 hours) or 24 hours after infection. Levofloxacin treatment at 24 hours, but not at 0 hours, resulted in a significant decrease in the number of C. pneumoniae inclusions within the MDM (p < 0.05). Also decreased were concentrations of proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, and IL-8 in the extracellular medium (p < 0.01). Viable counts in titrations remained similar to those in untreated controls. In summary, levofloxacin administered to MDM at serum-attainable levels 24 hours after C. pneumoniae infection significantly decreased inclusion counts and proinflammatory cytokine production, but did not eliminate the C. pneumoniae infection.

Molecular subtyping to detect human listeriosis clusters.

We analyzed the diversity (Simpson's Index, D) and distribution of Listeria monocytogenes in human listeriosis cases in New York State (excluding New York City) from November 1996 to June 2000 by using automated ribotyping and pulsed-field gel electrophoresis (PFGE). We applied a scan statistic (p

Levofloxacin kills Chlamydia pneumoniae and modulates interleukin 6 production by HEp-2 cells.

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.