title: Anti-phagocytic activity of Helicobacter pylori lipopolysaccharide (LPS)--possible modulation of the innate immune response to these bacteria.
abstract: The Helicobacter pylori infections are followed by an infiltration of the gastric mucosa by neutrophils and macrophages. Accumulation of phagocytes enables them to interact with H. pylori, but a great number of infected subjects cannot eradicate these bacteria. The H. pylori inhibits its own uptake by blocking the function of phagocytes. The anti-phagocytic mechanism depends on bacterial surface structures and the presence of the cag pathogenicity island (PAI). The role of H. pylori lipopolysaccharide (LPS), during phagocytosis of these bacteria is not clear. LPS may mediate direct bacteria/phagocyte interactions and it may also regulate antibacterial activity of the phagocytes. In this study we investigated the influence of H. pylori LPS on phagocytosis of these bacteria. The H. pylori LPS inhibited an ingestion of these microbes by human peripheral blood granulocytes. This was correlated with a diminished ability of phagocytes to reduce MTT-tetrazolium salt. The anti-phagocytic effect of H. pylori LPS was reduced by recombinant lipopolysaccharide binding protein (rLBP). It is possible that in vivo H. pylori LPS may diminish elimination of these bacteria from the gastric mucosa promoting an infection persistence. However, LBP may modulate the uptake of H. pylori due to neutralization of anti-phagocytic effect of its LPS.
authors.affiliation: Department of Immunology and Infectious Biology, University of Lódź, Lódź, Poland.
authors.forename: Aneta
authors.initials: A
authors.lastname: Grebowska
authors.forename: Anthony P
authors.initials: AP
authors.lastname: Moran
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Matusiak
authors.forename: Leokadia
authors.initials: L
authors.lastname: Bak-Romaniszyn
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Czkwianianc
authors.forename: Tomasz
authors.initials: T
authors.lastname: Rechciński
authors.forename: Maria
authors.initials: M
authors.lastname: Walencka
authors.forename: Izabela
authors.initials: I
authors.lastname: Płaneta-Małecka
authors.forename: Wiesława
authors.initials: W
authors.lastname: Rudnicka
authors.forename: Magdalena
authors.initials: M
authors.lastname: Chmiela
mesh_terms: D000942:Antigens, Bacterial / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D002470:Cell Survival; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D016480:Helicobacter pylori / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000378:metabolism / Q000494:pharmacology*; D009504:Neutrophils / Q000187:drug effects*; D010587:Phagocytosis / Q000187:drug effects*
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D008070:Lipopolysaccharides; C080866:cagA protein, Helicobacter pylori; C442865:lipopolysaccharide, Helicobacter pylori