title: Potential role of LPS in the outcome of Helicobacter pylori related diseases.
abstract: In this study we asked a question whether H. pylori LPS with or without LewisXY (Le) determinants as well as LBP (lipopolysaccharide binding protein) and sCD 14 molecules recognizing bacterial LPS may be involved in atherogenesis. Sera from 57 patients with coronary heart disease (CHD), 27 H. pylori infected dyspeptic patients-H.p.(+) and 49 healthy controls (HC) were tested for IgM and IgG to H. pylori LPS expressing LeX (LPS LeX) or LeXY (LPS LeXY) determinants and to a glycine acid extract (GE). Immune complexes (ICs) of Lewis antigens and specific IgM or IgG were also determined. The prevalence of anti-GE IgG and IgA was significantly higher in CHD as compared to HC and the same as in the H.p.(+) group. The highest levels of anti-GE IgG were detected only for CHD group. CHD patients showed upregulation of IgG to LPS LeX and LeXY. In contrast, an upregulation of IgM to such LPSs was found for healthy subjects. The levels ofLeY-anti-LeY IgG ICs were higher in CHD patients than in healthy controls similarly to the levels of LBP. There was no difference in sCD14 concentration between CHD and HC groups. The results obtained in this study indicate that H. pylori infections may be the risk factors of atherosclerosis due to: 1) an enhanced humoral response to H. pylori surface antigens, 2) a host predisposition to respond to Lewis determinants present in H. pylori LPS by IgG, 3) increased levels of serum LBP.
authors.affiliation: Department of Immunology and Infectious Biology, University of Lódź, 90-237 Lódź, Banacha 12/16, Poland.
authors.forename: Aneta
authors.initials: A
authors.lastname: Grebowska
authors.forename: Tomasz
authors.initials: T
authors.lastname: Rechciński
authors.forename: Leokadia
authors.initials: L
authors.lastname: Bak-Romaniszyn
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Czkwianianc
authors.forename: Anthony
authors.initials: A
authors.lastname: Moran
authors.forename: Magdalena
authors.initials: M
authors.lastname: Druszczyńska
authors.forename: Magdalena
authors.initials: M
authors.lastname: Kowalewicz-Kulbat
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Owczarek
authors.forename: Michał
authors.initials: M
authors.lastname: Dziuba
authors.forename: Maria
authors.initials: M
authors.lastname: Krzemińska-Pakuła
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: D000209:Acute-Phase Proteins / Q000276:immunology*; D000328:Adult; D000368:Aged; D000936:Antigen-Antibody Complex / Q000097:blood / Q000276:immunology; D002352:Carrier Proteins / Q000097:blood / Q000276:immunology*; D003324:Coronary Artery Disease / Q000276:immunology / Q000382:microbiology*; D004415:Dyspepsia / Q000382:microbiology; D016481:Helicobacter Infections / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology*; D008562:Membrane Glycoproteins / Q000097:blood / Q000276:immunology*; D008875:Middle Aged; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D000936:Antigen-Antibody Complex; D002352:Carrier Proteins; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D000099231:Lipopolysaccharide-Binding Protein; C442865:lipopolysaccharide, Helicobacter pylori