title: Triclosan inhibits uropathogenic Escherichia coli-stimulated tumor necrosis factor-alpha secretion in T24 bladder cells in vitro.
abstract: OBJECTIVE
  Triclosan is an antimicrobial agent commonly used in consumer and medical products that inhibits bacterial fatty acid synthesis. In addition to its bactericidal effects, sublethal concentrations of triclosan reduce local inflammation, inhibit the growth of bacterial uropathogens, induce membrane stress, and inhibit P-fimbrial expression in uropathogenic Escherichia coli (UPEC). We tested whether sublethal concentrations of triclosan could reduce the adherence of UPEC to bladder and kidney cells and reduce the amount of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) produced by these cells during bacterial challenge in vitro.
  
  
  METHODS
  Assays of bacterial growth, adhesion, and intracellularization were performed using UPEC GR12 incubated for 4 hours on monolayers of human T24 bladder cells or A498 kidney cells with various sublethal concentrations of triclosan. The expression profile of TNF-alpha from bladder cells was evaluated using ELISA.
  
  
  RESULTS
  No significant decreases were observed in the adherence or invasion percentages of UPEC GR12 with either cell line when treated with sublethal amounts of triclosan. However, treatment with triclosan 0.5 microg/mL led to a significant decrease in the total number of UPEC GR12 recovered from T24 monolayers (P < 0.05). Importantly, a reduction in the expression of TNF-alpha by T24 cells was shown when UPEC GR12 was treated with triclosan (P < 0.05).
  
  
  CONCLUSIONS
  Sublethal concentrations of triclosan did not inhibit the adhesion or intracellularization of UPEC into kidney or bladder cell lines but did significantly reduce the amount of TNF-alpha secreted by bladder cells. Therefore, the use of triclosan on ureteral stents may prove clinically beneficial, not only by inhibiting bacterial survival and growth within the urinary tract, but by reducing local inflammation as well.
authors.affiliation: Lawson Health Research Institute, London, Ontario, Canada.
authors.forename: Chelsea N
authors.initials: CN
authors.lastname: Elwood
authors.forename: Ben H
authors.initials: BH
authors.lastname: Chew
authors.forename: Shannon
authors.initials: S
authors.lastname: Seney
authors.forename: Jana
authors.initials: J
authors.lastname: Jass
authors.forename: John D
authors.initials: JD
authors.lastname: Denstedt
authors.forename: Peter A
authors.initials: PA
authors.lastname: Cadieux
mesh_terms: D000891:Anti-Infective Agents, Local / Q000494:pharmacology*; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001422:Bacterial Adhesion / Q000187:drug effects; D002460:Cell Line; D003600:Cytosol / Q000382:microbiology; D004797:Enzyme-Linked Immunosorbent Assay; D004926:Escherichia coli / Q000187:drug effects* / Q000276:immunology*; D006801:Humans; D007668:Kidney / Q000382:microbiology; D014260:Triclosan / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*; D001743:Urinary Bladder / Q000276:immunology / Q000382:microbiology
chemical_list: D000891:Anti-Infective Agents, Local; D000893:Anti-Inflammatory Agents; D014409:Tumor Necrosis Factor-alpha; D014260:Triclosan