title: Helicobacter pylori susceptible/resistant to antibiotic eradication therapy differ in the maturation and activation of dendritic cells.
abstract: BACKGROUND
  The natural course of Helicobacter pylori infection, as well as the success of antibiotic eradication is determined by the immune response to bacteria. The aim of the study is to investigate how different Helicobacter pylori isolates influence the dendritic cells maturation and antigen-presenting function in order to elucidate the differences between Helicobacter pylori strains, isolated from the patients with successful antibiotic eradication therapy or repeated eradication failure.
  
  
  METHODS
  Dendritic cells maturation and antigen presentation were monitored by flow cytometry analysis of the major histocompatibility complex class II (MHC-II), Toll-like receptor (TLR) and costimulatory molecules expression, and by determining cytokine secretion.
  
  
  RESULTS
  Dendritic cells stimulated with Helicobacter pylori isolated from patients with repeated antibiotic eradication failure expressed less human leukocyte antigen (HLA-DR), CD86, TLR-2, and interleukin-8 (IL-8) compared to Helicobacter pylori strains susceptible to antibiotic therapy; the latter expressed lower production of IL-10. Polymyxin B inhibition of lipopolysaccharide reduces IL-8 secretion in the group of Helicobacter pylori strains susceptible to antibiotic therapy. The differences in IL-8 secretion between both groups are lipopolysaccharide dependent, while the differences in secretion of IL-10 remain unchanged after lipopolysaccharide inhibition. Inhibitor of cathepsin X Mab 2F12 reduced the secretion of IL-6, and the secretion was significantly lower in the group of Helicobacter pylori strains isolated from patients with repeated antibiotic eradication failure.
  
  
  CONCLUSIONS
  Helicobacter pylori strains, susceptible/resistant to antibiotic eradication therapy, differ in their capability to induce DCs maturation and antigen-presenting function.
authors.affiliation: Medical Faculty Ljubljana, Institute of Microbiology and Immunology, University of Ljubljana, Ljubljana, Slovenia.
authors.forename: Andreja N
authors.initials: AN
authors.lastname: Kopitar
authors.forename: Miha
authors.initials: M
authors.lastname: Skvarc
authors.forename: Bojan
authors.initials: B
authors.lastname: Tepes
authors.forename: Janko
authors.initials: J
authors.lastname: Kos
authors.forename: Alojz
authors.initials: A
authors.lastname: Ihan
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology*; D024881:Drug Resistance, Bacterial; D005260:Female; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000276:immunology* / Q000382:microbiology; D016480:Helicobacter pylori / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology; D016753:Interleukin-10 / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D016209:Interleukin-8 / Q000276:immunology; D008297:Male; D051193:Toll-Like Receptors / Q000276:immunology
chemical_list: D000900:Anti-Bacterial Agents; D015850:Interleukin-6; D016209:Interleukin-8; D051193:Toll-Like Receptors; D016753:Interleukin-10; D007371:Interferon-gamma
keywords: Helicobacter pylori; Innate immune response; antimicrobial response; cathepsin X; cytokines; polymyxin B