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1
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0025823864
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Essential role of urease in pathogenesis of gastritis induced by Helicobacter pylori in gnotobiotic piglets
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Eaton KA, Brooks CL, Morgan DR, Krakowka S: Essential role of urease in pathogenesis of gastritis induced by Helicobacter pylori in gnotobiotic piglets. Infect Immun 1991, 59:2470-2475.
-
(1991)
Infect Immun
, vol.59
, pp. 2470-2475
-
-
Eaton, K.A.1
Brooks, C.L.2
Morgan, D.R.3
Krakowka, S.4
-
2
-
-
0029620934
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Essential role of urease in vitro and in vivo Helicobacter pylori colonization study using a wild-type and isogenic urease mutant strain
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Karita M, Tsuda M, Nakazawa T: Essential role of urease in vitro and in vivo Helicobacter pylori colonization study using a wild-type and isogenic urease mutant strain. J Clin Gastroenterol 1995, 21 (Suppl 1):S160-S163.
-
(1995)
J Clin Gastroenterol
, vol.21
, Issue.1 SUPPL.
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-
Karita, M.1
Tsuda, M.2
Nakazawa, T.3
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3
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0031003615
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Localization of Helicobacter pylori urease and heat shock protein in human gastric biopsies
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Dunn BE, Vakil NB, Schneider BG, Miller MM, Zitzer JB, Peutz T, Phadnis SH: Localization of Helicobacter pylori urease and heat shock protein in human gastric biopsies. Infect Immun 1997, 65:1181-1188.
-
(1997)
Infect Immun
, vol.65
, pp. 1181-1188
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Dunn, B.E.1
Vakil, N.B.2
Schneider, B.G.3
Miller, M.M.4
Zitzer, J.B.5
Peutz, T.6
Phadnis, S.H.7
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4
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0030021824
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Surface localization of Helicobacter pylori urease and a heat shock protein homolog requires bacterial autolysis
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Phadnis SH, Parlow MH, Levy M, Ilver D, Caulkins CM, Connors JB, Dunn BE: Surface localization of Helicobacter pylori urease and a heat shock protein homolog requires bacterial autolysis. Infect Immun 1996, 64:905-912. This morphologic study, as well as Dunn et al.'s (Infect Immun 1997, 65:1181-1188), indicates that urease and HspB are cytoplasmic proteins of H. pylori. It is proposed that the presence of these proteins at the bacterial surface in late cultures and in vivo is secondary to bacterial autolysis and passive adsorption by surviving bacteria. The observation that urease and HspB are present at the cell surface in vivo, and are thus accessible to the host immune response, is consistent with the efficacy of mucosal immunization with urease and HspB.
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(1996)
Infect Immun
, vol.64
, pp. 905-912
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Phadnis, S.H.1
Parlow, M.H.2
Levy, M.3
Ilver, D.4
Caulkins, C.M.5
Connors, J.B.6
Dunn, B.E.7
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5
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0029815909
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The effect of environmental pH on the proton motive force of Helicobacter pylori
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Meyer-Rosberg K, Scott DR, Rex D, Melchers K, Sachs G: The effect of environmental pH on the proton motive force of Helicobacter pylori. Gastroenterology 1996, 111:886-900. Using a pH-sensitive dye technique, this study shows that urease activity at the bacterial surface expands the acidic pH range over which H. pylori can maintain an active proton motive force, thereby enhancing its survival in acidic media. In contrast, urease activity may limit H. pylori survival in nonacidic conditions.
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(1996)
Gastroenterology
, vol.111
, pp. 886-900
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Meyer-Rosberg, K.1
Scott, D.R.2
Rex, D.3
Melchers, K.4
Sachs, G.5
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6
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0029916337
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Capacity of Helicobacter pylori to generate ionic gradients at low pH
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Matin A, Zychlinsky E, Keyhan M, Sachs G: Capacity of Helicobacter pylori to generate ionic gradients at low pH. Infect Immun 1996, 64:1434-1436.
-
(1996)
Infect Immun
, vol.64
, pp. 1434-1436
-
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Matin, A.1
Zychlinsky, E.2
Keyhan, M.3
Sachs, G.4
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7
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0030835739
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The complete genome sequence of the gastric pathogen Helicobacter
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Tomb JF, White O, Kerlavage AR, Clayton RA, Sutton GG, Fleischmann RD, Ketchum KA, Klenk HP, Gill S, Dougherty BA, Nelson K, Quackenbush J, Zhou L, Kirkness EF, Peterson S, Loftus B, Richardson D, Dodson R, Khalak HG, Glodek A, McKenney K, Fitzegerald LM, Lee N, Adams MD, Venter JC: The complete genome sequence of the gastric pathogen Helicobacter. Nature 1997, 388:539-547. The entire genome of H. pylori has been sequenced and 1590 open-reading frames identified. Sequence analysis and homology searches lead to the identification of many proteins potentially expressed at the bacterial surface, including adhesins, lipoproteins, and other outer membrane proteins, which may have a role in host-pathogen interactions. The complexity of these interactions may be further increased by antigenic variation. Several mechanisms of antigen variation exist in the genome of H. pylori: sequence-related membrane proteins, homopolymeric repeats, and dinucleotide repeats. These mechanisms, already described in other mucosal pathogens, may explain host adaptation, variation in disease outcome, and escape from the immune response.
-
(1997)
Nature
, vol.388
, pp. 539-547
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Tomb, J.F.1
White, O.2
Kerlavage, A.R.3
Clayton, R.A.4
Sutton, G.G.5
Fleischmann, R.D.6
Ketchum, K.A.7
Klenk, H.P.8
Gill, S.9
Dougherty, B.A.10
Nelson, K.11
Quackenbush, J.12
Zhou, L.13
Kirkness, E.F.14
Peterson, S.15
Loftus, B.16
Richardson, D.17
Dodson, R.18
Khalak, H.G.19
Glodek, A.20
McKenney, K.21
Fitzegerald, L.M.22
Lee, N.23
Adams, M.D.24
Venter, J.C.25
more..
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8
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0031042034
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Synthesis and activity of Helicobacter pylori urease and catalase at low pH
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Bauerfeind P, Garner R, Dunn BE, Mobley HL: Synthesis and activity of Helicobacter pylori urease and catalase at low pH. Gut 1997, 40:25-30. This study shows that urease synthesis is not induced by exposure of H. pylori to low pH. In fact, intracelluar urease activity is reduced. This may result from the observed global reduction in protein synthesis at low pH. Alternatively, urease may be exported to the cell surface upon exposure to low pH.
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(1997)
Gut
, vol.40
, pp. 25-30
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Bauerfeind, P.1
Garner, R.2
Dunn, B.E.3
Mobley, H.L.4
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9
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0029781599
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Adhesion of Helicobacter pylori to polarized T84 human intestinal cell monolayers in pH dependent
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Corthésy-Theulaz I, Porta N, Pnngault E, Racine L, Bogdanova A, Kraehenbuhl JP, Blum AL, Michetti P: Adhesion of Helicobacter pylori to polarized T84 human intestinal cell monolayers in pH dependent. Infect Immun 1996, 64:3827-3832. Polarized epithelial cell monolayers grown on filters establish separate apical and basolateral compartments. This study shows that adhesion of H. pylori to the apical surface of these cells is enhanced at low pH. Upon adhesion, actin condensation and brush border effacement occur, resulting in an intimate association.
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(1996)
Infect Immun
, vol.64
, pp. 3827-3832
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Corthésy-Theulaz, I.1
Porta, N.2
Pnngault, E.3
Racine, L.4
Bogdanova, A.5
Kraehenbuhl, J.P.6
Blum, A.L.7
Michetti, P.8
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10
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0029929131
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Acidic pH changes receptor binding specificity of Helicobacter pylori: A binary adhesion model in which surface heat shock (stress) proteins mediate sulfatide recognition of host cell proteins
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Huesca M, Borgia S, Hoffman P, Lingwood CA: Acidic pH changes receptor binding specificity of Helicobacter pylori: a binary adhesion model in which surface heat shock (stress) proteins mediate sulfatide recognition of host cell proteins. Infect Immun 1996, 64:2643-2648.
-
(1996)
Infect Immun
, vol.64
, pp. 2643-2648
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Huesca, M.1
Borgia, S.2
Hoffman, P.3
Lingwood, C.A.4
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11
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0031036214
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Identification of the N-acetylneuraminyllactose-specific laminin-binding protein of Helicobacter pylori
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Valkonen KH, Wadstrom T, Moran AP: Identification of the N-acetylneuraminyllactose-specific laminin-binding protein of Helicobacter pylori. Infect Immun 1997, 65:916-923. This article describes the identification of a 25 kD laminin binding protein of H. pylori. By analogy with laminin-binding proteins of other pathogenic bacteria, this receptor may have an important role in promoting and/or maintaining mucosal tissue damage by allowing H. pylori to compete with epithelial cells for binding to the extracellular matrix.
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(1997)
Infect Immun
, vol.65
, pp. 916-923
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Valkonen, K.H.1
Wadstrom, T.2
Moran, A.P.3
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12
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0029901525
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The urease enzyme of Helicobacter pylori does not function as an adhesin
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Clyne M, Drumm B: The urease enzyme of Helicobacter pylori does not function as an adhesin. Infect Immun 1996, 64:2817-2820. An H. pylori strain and its corresponding isogenic urease-negative mutant were shown to have similar binding characteristics to isolated human gastric cells, indicating that the role of urease during colonization is not related to adhesion.
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(1996)
Infect Immun
, vol.64
, pp. 2817-2820
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Clyne, M.1
Drumm, B.2
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13
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0030927162
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Absence of effect of Lewis A and Lewis B expression on adherence of Helicobacter pylori to human gastric cells
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Clyne M, Drumm B: Absence of effect of Lewis A and Lewis B expression on adherence of Helicobacter pylori to human gastric cells. Gastroenterology 1997, 113:72-80. The ABO and Lewis blood types of 13 individuals were determined, and the expression of Lewis antigens by the gastric cells of these subjects analyzed. These cells were then used in binding experiments to determine the role of Lewis antigen expression in the binding of H. pylori. This detailed study indicates that H. pylori adheres to gastric cells in a manner that is independent of Lewis expression by the host gastric cells, and that expression of Lewis antigen on the gastric mucosa is not related to Lewis expression on erythrocytes.
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(1997)
Gastroenterology
, vol.113
, pp. 72-80
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Clyne, M.1
Drumm, B.2
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14
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0031025291
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Helicobacter pylori lipopolysaccharide can activate 70Z/3 cells via CD14
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Kirkland T, Viriyakosol S, Perez-Perez GI, Blaser MJ: Helicobacter pylori lipopolysaccharide can activate 70Z/3 cells via CD14. Infect Immun 1997, 65:604-608.
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(1997)
Infect Immun
, vol.65
, pp. 604-608
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Kirkland, T.1
Viriyakosol, S.2
Perez-Perez, G.I.3
Blaser, M.J.4
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15
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0029758163
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Helicobacter pylori and Porphyromonas gingivalis lipopolysaccharides
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Cunningham MD, Seachord C, Ratcliffe K, Bainbridge B, Aruffo A, Darveau RP: Helicobacter pylori and Porphyromonas gingivalis lipopolysaccharides. Infect Immun 1996, 64:3601-3608. LPS binding to CD14 is strongly enhanced by previous association of LPS to LPS-binding protein and secondary transfer to CD14. The transfer of H. pylori LPS is shown in this study to be 60 times slower than other bacterial LPS, the limiting step being the association of H. pylori LPS with LPS-binding protein. This is consistent with the poor stimulatory effect of H. pylori LPS on endothelial cells and monocytes.
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(1996)
Infect Immun
, vol.64
, pp. 3601-3608
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Cunningham, M.D.1
Seachord, C.2
Ratcliffe, K.3
Bainbridge, B.4
Aruffo, A.5
Darveau, R.P.6
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16
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0029811230
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Effect of Helicobacter pylori lipopolysaccharide (LPS) and LPS derivatives on the production of tissue factor and plasminogen activator inhibitor type 2 by human blood mononuclear cells
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Semeraro N, Montemurro P, Piccoli C, Muolc V, Colucci M, Giuliani G, Fumarola D, Pece S, Moran AP: Effect of Helicobacter pylori lipopolysaccharide (LPS) and LPS derivatives on the production of tissue factor and plasminogen activator inhibitor type 2 by human blood mononuclear cells. J Infect Dis 1996, 174:1255-1260.
-
(1996)
J Infect Dis
, vol.174
, pp. 1255-1260
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Semeraro, N.1
Montemurro, P.2
Piccoli, C.3
Muolc, V.4
Colucci, M.5
Giuliani, G.6
Fumarola, D.7
Pece, S.8
Moran, A.P.9
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17
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0030885426
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Lipopolysaccharides of Helicobacter pylori serogroups O-3 and O-6: Structures of a class of lipopolysaccharides with reference to the location of oligomeric units of d-glycero-alpha-d-manno-heptose residues
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Aspinall GO, Monteiro MA, Shaver RT, Kurjanczyk LA, Penner JL: Lipopolysaccharides of Helicobacter pylori serogroups O-3 and O-6: structures of a class of lipopolysaccharides with reference to the location of oligomeric units of d-glycero-alpha-d-manno-heptose residues. Eur J Biochem 1997, 248:592-601. A detailed chemical and spectrometric study of the LPS of different H. pylori strains that demonstrates both the structural heterogeneity of LPS produced by different H. pylori strains and the variation of LPS structure within a given strain. This study highlights that LPS assembly in H. pylori may be more related to eukaryotic glycosylation than to the typical repetitive assembly of subunits usually seen in bacteria. This phenomenon may underlie the molecular mimicry between H. pylori LPS and the glycosylation patterns of its host.
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(1997)
Eur J Biochem
, vol.248
, pp. 592-601
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Aspinall, G.O.1
Monteiro, M.A.2
Shaver, R.T.3
Kurjanczyk, L.A.4
Penner, J.L.5
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18
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0030025952
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Lipopolysaccharide of the Helicobacter pylori type strain NCTC 11637 (ATCC 43504): Structure of the O antigen chain and core oligosaccharide regions
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Aspinall GO, Monteiro MA, Pang H, Walsh EJ, Moran AP: Lipopolysaccharide of the Helicobacter pylori type strain NCTC 11637 (ATCC 43504): structure of the O antigen chain and core oligosaccharide regions. Biochemistry 1996, 35:2489-2497. The complete structure of H. pylori LPS is analyzed in this study and the homologies observed by immunological methods between H. pylori LPS and human glycoconjugates are confirmed by biochemical methods.
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(1996)
Biochemistry
, vol.35
, pp. 2489-2497
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Aspinall, G.O.1
Monteiro, M.A.2
Pang, H.3
Walsh, E.J.4
Moran, A.P.5
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19
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9444239829
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Typing of Helicobacter pylori with monoclonal antibodies against Lewis antigens in lipopolysaccharide
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Simoons-Smit IM, Appelmelk BJ, Verboom T, Negrini R, Penner JL, Aspinall GO, Moran AP, She FF, Shi BS, Rudnica W, Savio A, Degraaff J: Typing of Helicobacter pylori with monoclonal antibodies against Lewis antigens in lipopolysaccharide. J Clin Microb 1996, 34:2196-2200.
-
(1996)
J Clin Microb
, vol.34
, pp. 2196-2200
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Simoons-Smit, I.M.1
Appelmelk, B.J.2
Verboom, T.3
Negrini, R.4
Penner, J.L.5
Aspinall, G.O.6
Moran, A.P.7
She, F.F.8
Shi, B.S.9
Rudnica, W.10
Savio, A.11
Degraaff, J.12
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20
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0029961317
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Expression of the human cell surface glycoconjugates Lewis X and Y by Helicobacter pylori isolates is related to cagA status
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Wirth HP, Yang M, Karita M, Blaser MJ: Expression of the human cell surface glycoconjugates Lewis X and Y by Helicobacter pylori isolates is related to cagA status. Infect Immun 1996, 64:4598-4605.
-
(1996)
Infect Immun
, vol.64
, pp. 4598-4605
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Wirth, H.P.1
Yang, M.2
Karita, M.3
Blaser, M.J.4
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21
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0030760661
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Helicobacter pylori Lewis expression is related to the host Lewis phenotype
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y by a given strain corresponds to the Lewis antigen expression of the host. This observation exemplifies the adaptative selection pressure maintained on the pathogen by its host.
-
(1997)
Gastroenterology
, vol.113
, pp. 1091-1098
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Wirth, H.P.1
Yang, M.2
Peek, R.M.3
Tham, K.T.4
Blaser, M.J.5
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22
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0029811855
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Antigenic mimicry between Helicobacter pylori and gastric mucosa in the pathogenesis of body atrophic gastritis
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Negrini R, Savio A, Poiesi C, Appelmelk BJ, Buffoli F, Paterlini A, Cesari P, Graffeo M, Vaira D, Franzin G: Antigenic mimicry between Helicobacter pylori and gastric mucosa in the pathogenesis of body atrophic gastritis. Gastroenterology 1996, 111:655-665.
-
(1996)
Gastroenterology
, vol.111
, pp. 655-665
-
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Negrini, R.1
Savio, A.2
Poiesi, C.3
Appelmelk, B.J.4
Buffoli, F.5
Paterlini, A.6
Cesari, P.7
Graffeo, M.8
Vaira, D.9
Franzin, G.10
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23
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0029548939
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Antigastric antibodies in Helicobacter pylori gastritis: Prevalence, in situ binding, and clues for clinical relevance
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Faller G, Steininger H, Eck M, Hensen J, Hahn EG, Kirchner T: Antigastric antibodies in Helicobacter pylori gastritis: prevalence, in situ binding, and clues for clinical relevance. Virchows Arch 1996, 427:483-486.
-
(1996)
Virchows Arch
, vol.427
, pp. 483-486
-
-
Faller, G.1
Steininger, H.2
Eck, M.3
Hensen, J.4
Hahn, E.G.5
Kirchner, T.6
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24
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9344248024
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Potential role of molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood group antigens in autoimmunity
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Appelmelk BJ, Simoons-Smit I, Negrini R, Moran AP, Aspinall GO, Forte JG, De Vries T, Quan H, Verboom T, Maaskant JJ, Ghiara P, Kuipers EJ, Bloemena E, Tadema TM, Townsend RR, Tyagarajan K, Crothers JM, Jr., Monteiro MA, Savio A, de Graaff J: Potential role of molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood group antigens in autoimmunity. Infect Immun 1996, 64:2031-2040.
-
(1996)
Infect Immun
, vol.64
, pp. 2031-2040
-
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Appelmelk, B.J.1
Simoons-Smit, I.2
Negrini, R.3
Moran, A.P.4
Aspinall, G.O.5
Forte, J.G.6
De Vries, T.7
Quan, H.8
Verboom, T.9
Maaskant, J.J.10
Ghiara, P.11
Kuipers, E.J.12
Bloemena, E.13
Tadema, T.M.14
Townsend, R.R.15
Tyagarajan, K.16
Crothers Jr., J.M.17
Monteiro, M.A.18
Savio, A.19
De Graaff, J.20
more..
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25
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0030859330
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The endotoxin of Helicobacter pylori is a modulator of host-dependent gastritis
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Sakagami T, Vella J, Dixon MF, O'Rourke J, Radcliff F, Sutton P, Shimoyama T, Beagley K, Lee A: The endotoxin of Helicobacter pylori is a modulator of host-dependent gastritis. Infect Immun 1997, 65:3310-3316. This study, performed in natural mutant mice which are nonresponsive to LPS/endotoxin, shows that, despite normal susceptibility to H. felis infection, these mice do not develop gastric atrophy following long-term infection. Antibody responses were identical in both wild-type and mutant mice, but macrophage infiltration was reduced in the mutant animals. These findings indirectly suggest that an anti-LPS response is required for atrophy to occur.
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(1997)
Infect Immun
, vol.65
, pp. 3310-3316
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Sakagami, T.1
Vella, J.2
Dixon, M.F.3
O'Rourke, J.4
Radcliff, F.5
Sutton, P.6
Shimoyama, T.7
Beagley, K.8
Lee, A.9
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26
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0009078106
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Preliminary studies of lipopolysaccharides from Helicobacter mustelae and H. felis
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Monteiro MA, Perry MB, Moran AP, Lee A: Preliminary studies of lipopolysaccharides from Helicobacter mustelae and H. felis. Irish J Med Sci 1997, 166(Suppl 5):32.
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(1997)
Irish J Med Sci
, vol.166
, Issue.5 SUPPL.
, pp. 32
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Monteiro, M.A.1
Perry, M.B.2
Moran, A.P.3
Lee, A.4
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27
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0030796155
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Helicobacter pylori and gastric autoimmunity
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Appelmelk BJ, Negrini R: Helicobacter pylori and gastric autoimmunity. Curr Opin Gastroenterol 1997, 13:31-34. Recent and detailed review focusing on the links between H. pylori infection, humoral and cellular autoimmune responses to Lewis antigens, and the development of gastric atrophy.
-
(1997)
Curr Opin Gastroenterol
, vol.13
, pp. 31-34
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Appelmelk, B.J.1
Negrini, R.2
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0031567981
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T helper 1 effector cells specific for Helicobacter pylori in the gastric antrum of patients with peptic ulcer disease
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D'Elios MM, Manghetti M, De Carli M, Costa F, Baldari CT, Burroni D, Telford JL, Romagnani S, Del Prete G: T helper 1 effector cells specific for Helicobacter pylori in the gastric antrum of patients with peptic ulcer disease. J Immunol 1997, 158:962-967. H. pylori-specific T-cell clones were obtained from antral biopsies of H. pylori-infected individuals. These clones mainly expressed T-helper type 1 cytokines and most reacted to cagA and VacA antigens.
-
(1997)
J Immunol
, vol.158
, pp. 962-967
-
-
D'Elios, M.M.1
Manghetti, M.2
De Carli, M.3
Costa, F.4
Baldari, C.T.5
Burroni, D.6
Telford, J.L.7
Romagnani, S.8
Del Prete, G.9
-
29
-
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0029998975
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Characterization of lymphocytic infiltrates in Helicobacter pylori-associated gastritis
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Hatz RA, Meimarakis G, Bayerdorffer E, Stolte M, Kirchner T, Enders G: Characterization of lymphocytic infiltrates in Helicobacter pylori-associated gastritis. Scand J Gastroenterol 1996, 31:222-228.
-
(1996)
Scand J Gastroenterol
, vol.31
, pp. 222-228
-
-
Hatz, R.A.1
Meimarakis, G.2
Bayerdorffer, E.3
Stolte, M.4
Kirchner, T.5
Enders, G.6
-
30
-
-
0030891986
-
+ T-cell activation during Helicobacter pylori infection
-
+ T-cell activation during Helicobacter pylori infection. J Clin Invest 1997, 99:1628-1636.
-
(1997)
J Clin Invest
, vol.99
, pp. 1628-1636
-
-
Ye, G.1
Barrera, C.2
Fan, X.3
Gourley, W.K.4
Crowe, S.E.5
Ernst, P.B.6
Reyes, V.E.7
-
31
-
-
0030958673
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Did the inheritance of a pathogenicity Island modify the virulence of Helicobacter pylori?
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Covacci A, Falkow S, Berg DE, Rappuoli R: Did the inheritance of a pathogenicity Island modify the virulence of Helicobacter pylori? Trends Microbiol 1997, 5:205-208.
-
(1997)
Trends Microbiol
, vol.5
, pp. 205-208
-
-
Covacci, A.1
Falkow, S.2
Berg, D.E.3
Rappuoli, R.4
-
32
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0029963677
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cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors
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Censini S, Lange C, Xiang Z, Crabtree JE, Ghiara P, Borodovsky M, Rappuoli R, Covacci A: cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc Natl Acad Sci USA 1996, 93:14648-14653. Sequencing of the cag region suggests that it was acquired en bloc, at some point in evolution, from another bacterium and thus is a pathogenicity island. The cag region often includes sequences encoding for transposases that result in frequent insertions and homologous recombinations. This genetic heterogeneity can result in H. pylori strains which carry the cagA marker gene but lack other cag virulence genes associated with risk for gastroduodenal diseases. Many putative cag region proteins show homology with proteins of the type IV secretion systems of other bacteria. Thus cag gene products may function to export factors involved in H. pylori host-cell interaction, including those required to activate interleukin-8 production by gastric epithelial cells.
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(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 14648-14653
-
-
Censini, S.1
Lange, C.2
Xiang, Z.3
Crabtree, J.E.4
Ghiara, P.5
Borodovsky, M.6
Rappuoli, R.7
Covacci, A.8
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33
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Analysis of expression of CagA and VacA virulence factors in 43 strains of Helicobacter pylori reveals that clinical isolates can be divided into two major types and that CagA is not necessary for expression of the vacuolating cytotoxin
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Xiang Z, Censini S, Bayeli PF, Telford JL, Figura N, Rappuoli R, Covacci A: Analysis of expression of CagA and VacA virulence factors in 43 strains of Helicobacter pylori reveals that clinical isolates can be divided into two major types and that CagA is not necessary for expression of the vacuolating cytotoxin. Infect Immun 1995, 63:94-98.
-
(1995)
Infect Immun
, vol.63
, pp. 94-98
-
-
Xiang, Z.1
Censini, S.2
Bayeli, P.F.3
Telford, J.L.4
Figura, N.5
Rappuoli, R.6
Covacci, A.7
-
34
-
-
0031032033
-
Clinical and pathological importance of heterogeneity in vacA, the vacuolating cytotoxin gene of Helicobacter pylori
-
Atherton JC, Peek RM, Jr., Tham KT, Cover TL, Blaser MJ: Clinical and pathological importance of heterogeneity in vacA, the vacuolating cytotoxin gene of Helicobacter pylori. Gastroenterology 1997, 112:92-99.
-
(1997)
Gastroenterology
, vol.112
, pp. 92-99
-
-
Atherton, J.C.1
Peek Jr., R.M.2
Tham, K.T.3
Cover, T.L.4
Blaser, M.J.5
-
35
-
-
0029953751
-
The interrelationship between cytotoxin-associated gene A, vacuolating cytotoxin, and Helicobacter pylori-related diseases
-
Weel JF, van der Hulst RW, Gerrits Y, Roorda P, Feller M, Dankert J, Tytgat GN, van der Ende A: The interrelationship between cytotoxin-associated gene A, vacuolating cytotoxin, and Helicobacter pylori-related diseases. J Infect Dis 1996, 173:1171-1175.
-
(1996)
J Infect Dis
, vol.173
, pp. 1171-1175
-
-
Weel, J.F.1
Van Der Hulst, R.W.2
Gerrits, Y.3
Roorda, P.4
Feller, M.5
Dankert, J.6
Tytgat, G.N.7
Van Der Ende, A.8
-
36
-
-
0029756653
-
Density of Helicobacter pylori infection in vivo as assessed by quantitative culture and histology
-
Atherton JC, Tham KT, Peek RM, Jr., Cover TL, Blaser MJ: Density of Helicobacter pylori infection in vivo as assessed by quantitative culture and histology. J Inf Dis 1996, 174:552-556. The density of bacterial infection was measured by quantitative culture of gastric biopsy specimens taken from 29 H. pylori-infected patients and results correlated with bacterial cagA and vacA genotypes. Strains carrying cagA and vacA s1 showed a fourfold higher mean density of infection in the antrum compared to cagAlvacA negative s2 strains. More dense infection was also associated with a more pronounced inflammatory cell infiltrate, more severe epithelial injury, and duodenal ulceration.
-
(1996)
J Inf Dis
, vol.174
, pp. 552-556
-
-
Atherton, J.C.1
Tham, K.T.2
Peek Jr., R.M.3
Cover, T.L.4
Blaser, M.J.5
-
37
-
-
0030950402
-
Effect of Helicobacter pylori eradication on gastritis in relation to cagA: A prospective 1-year follow-up study
-
van der Hulst RW, van der Ende A, Dekker FW, Ten Kate FJ, Weel JF, Keller JJ, Kruizinga SP, Dankert J, Tytgat GN: Effect of Helicobacter pylori eradication on gastritis in relation to cagA: a prospective 1-year follow-up study. Gastroenterology 1997, 113:25-30.
-
(1997)
Gastroenterology
, vol.113
, pp. 25-30
-
-
Van Der Hulst, R.W.1
Van Der Ende, A.2
Dekker, F.W.3
Ten Kate, F.J.4
Weel, J.F.5
Keller, J.J.6
Kruizinga, S.P.7
Dankert, J.8
Tytgat, G.N.9
-
38
-
-
0029891126
-
Helicobacter pylori cagA gene and expression of cytokine messenger RNA in gastric mucosa
-
Yamaoka Y, Kita M, Kodama T, Sawai N, Imanishi J: Helicobacter pylori cagA gene and expression of cytokine messenger RNA in gastric mucosa. Gastroenterology 1996, 110:1 744-1 752. Infection with cagA-positive or cagA-negative strains of H. pylori was correlated with cytokine mRNA levels in gastric biopsy samples from 160 patients. Specimens infected with cagA-positive bacteria showed more severe gastritis and higher levels of interleukin-8 mRNA when compared to cagA-negative infection. These findings support the relevance of in vitro studies showing that cag region genes are required to activate interleukin-8 gene transcription in human gastric epithelial cell lines.
-
(1996)
Gastroenterology
, vol.110
, pp. 1744-1752
-
-
Yamaoka, Y.1
Kita, M.2
Kodama, T.3
Sawai, N.4
Imanishi, J.5
-
39
-
-
0030951122
-
Seroprevalence of CagA-positive strains among Helicobacter pylori-infected, healthy young adults
-
Parsonnet J, Replogle M, Yang S, Hiatt R: Seroprevalence of CagA-positive strains among Helicobacter pylori-infected, healthy young adults. J Inf Dis 1997, 175:1240-1242. Sera from H. pylori-infected healthy adults in California were tested for anti-CagA IgG by ELISA. The prevalence of serum CagA antibodies differed substantially between different racial and ethnic groups: 79.4% in blacks, 63.8% in Hispanics, and 50% in whites. Individuals born in developing nations also showed a higher prevalence of infection with CagA-positive strains than those born in industrialized countries. These findings indicate strain-specific transmission of H. pylori infection within genetically, ethnically, or geographically segregated population groups.
-
(1997)
J Inf Dis
, vol.175
, pp. 1240-1242
-
-
Parsonnet, J.1
Replogle, M.2
Yang, S.3
Hiatt, R.4
-
40
-
-
0030892896
-
MALT-type lymphoma of the stomach is associated with Helicobacter pylori strains expressing the CagA protein
-
Eck M, Schmausser B, Haas R, Greiner A, Czub S, Muller-Hermelink HK: MALT-type lymphoma of the stomach is associated with Helicobacter pylori strains expressing the CagA protein. Gastroenterology 1997, 112:1482-1486.
-
(1997)
Gastroenterology
, vol.112
, pp. 1482-1486
-
-
Eck, M.1
Schmausser, B.2
Haas, R.3
Greiner, A.4
Czub, S.5
Muller-Hermelink, H.K.6
-
41
-
-
0030975595
-
Risk for gastric cancer in people with CagA positive or CagA negative
-
Parsonnet J, Friedman GD, Orentreich N, Vogelman H: Risk for gastric cancer in people with CagA positive or CagA negative. Gut 1997, 40:297-301. Serum samples from a nested, case-control study of gastnc cancer were examined for antibodies against CagA protein. Subjects who had serologic evidence of infection with CagA-positive H. pylori strains showed a substantially increased risk for gastric cancer (odds ratio 5.8; 95% Cl, 2.6-13.0). H. pylori-infected individuals who lacked antibodies against CagA showed a much lower risk for gastric cancer (odds ratio 2.2; 0.9-5.4). Low serum levels of pepsinogen I were also associated with an increased cancer risk.
-
(1997)
Gut
, vol.40
, pp. 297-301
-
-
Parsonnet, J.1
Friedman, G.D.2
Orentreich, N.3
Vogelman, H.4
-
42
-
-
0030891113
-
Not all Helicobacter pylori strains are created equal: Should all be eliminated?
-
Blaser MJ: Not all Helicobacter pylori strains are created equal: should all be eliminated? Lancet 1997, 349:1020-1022.
-
(1997)
Lancet
, vol.349
, pp. 1020-1022
-
-
Blaser, M.J.1
-
43
-
-
0030281235
-
CagA and the outcome of Helicobacter pylori infection
-
Blaser MJ, Crabtree JE: CagA and the outcome of Helicobacter pylori infection. Am J Clin Path 1996, 106:565-567.
-
(1996)
Am J Clin Path
, vol.106
, pp. 565-567
-
-
Blaser, M.J.1
Crabtree, J.E.2
-
44
-
-
0029899369
-
Antibodies to CagA protein are associated with gastric atrophy in Helicobacter pylori infection
-
Beales IL, Crabtree JE, Scunes D, Covacci A, Calam J: Antibodies to CagA protein are associated with gastric atrophy in Helicobacter pylori infection. Eur J Gastroenterol Hepatol 1996, 8:645-649.
-
(1996)
Eur J Gastroenterol Hepatol
, vol.8
, pp. 645-649
-
-
Beales, I.L.1
Crabtree, J.E.2
Scunes, D.3
Covacci, A.4
Calam, J.5
-
45
-
-
0030997873
-
High prevalence of the cagA-positive Helicobacter pylori strains in Japanese asymptomatic patients and in gastric cancer patients
-
Shimoyama T, Fukuda S, Taneka M, Mikami T, Saito Y, Munakata A: High prevalence of the cagA-positive Helicobacter pylori strains in Japanese asymptomatic patients and in gastric cancer patients. Scand J Gastroenterol 1997, 32:465-468.
-
(1997)
Scand J Gastroenterol
, vol.32
, pp. 465-468
-
-
Shimoyama, T.1
Fukuda, S.2
Taneka, M.3
Mikami, T.4
Saito, Y.5
Munakata, A.6
-
46
-
-
0029797430
-
Serum CagA antibodies in asymptomatic subjects and patients with peptic ulcer: Lack of correlation of IgG antibody in patients with peptic ulcer or asymptomatic Helicobacter pylori gastritis
-
Graham DY, Genta RM, Graham DP, Crabtree JE: Serum CagA antibodies in asymptomatic subjects and patients with peptic ulcer: lack of correlation of IgG antibody in patients with peptic ulcer or asymptomatic Helicobacter pylori gastritis. J Clin Path 1996, 49:829-832.
-
(1996)
J Clin Path
, vol.49
, pp. 829-832
-
-
Graham, D.Y.1
Genta, R.M.2
Graham, D.P.3
Crabtree, J.E.4
-
47
-
-
0029848785
-
Gastric non-Hodgkin lymphomas of mucosa-assoclated lymphoid tissue are not associated with more aggressive Helicobacter pylori strains as identified by CagA
-
de Jong D, van der Hulst RW, Pals G, van Dijk WC, van der Ende A, Tytgat GN, Taal BG, Boot H: Gastric non-Hodgkin lymphomas of mucosa-assoclated lymphoid tissue are not associated with more aggressive Helicobacter pylori strains as identified by CagA. Am J Clin Path 1996, 106:670-675.
-
(1996)
Am J Clin Path
, vol.106
, pp. 670-675
-
-
De Jong, D.1
Van Der Hulst, R.W.2
Pals, G.3
Van Dijk, W.C.4
Van Der Ende, A.5
Tytgat, G.N.6
Taal, B.G.7
Boot, H.8
-
48
-
-
8044223422
-
Profile of Helicobacter pylori cytotoxin derived from two areas of Japan with different prevalence of atrophic gastritis
-
Ito S, Azuma T, Murakita H, Hirai M, Miyaji H, Ito Y, Ohtaki Y, Yamazaki Y, Kuriyama M, Keida Y, Kohli Y: Profile of Helicobacter pylori cytotoxin derived from two areas of Japan with different prevalence of atrophic gastritis. Gut 1996, 39:800-806.
-
(1996)
Gut
, vol.39
, pp. 800-806
-
-
Ito, S.1
Azuma, T.2
Murakita, H.3
Hirai, M.4
Miyaji, H.5
Ito, Y.6
Ohtaki, Y.7
Yamazaki, Y.8
Kuriyama, M.9
Keida, Y.10
Kohli, Y.11
-
49
-
-
0029835002
-
Heterogeneous Helicobacter pylon isolates from members of a family with a history of peptic ulcer disease
-
van der Ende A, Rauws EA, Feller M, Mulder CJ, Tytgat GN, Dankert J: Heterogeneous Helicobacter pylon isolates from members of a family with a history of peptic ulcer disease. Gastroenterology 1996, 111:638-647.
-
(1996)
Gastroenterology
, vol.111
, pp. 638-647
-
-
Van Der Ende, A.1
Rauws, E.A.2
Feller, M.3
Mulder, C.J.4
Tytgat, G.N.5
Dankert, J.6
-
50
-
-
0030034805
-
Helicobacter pylori attachment to gastric cells Induces cytoskeletal rearrangements and tyrosine phosphorylation of the host cell proteins
-
Segal ED, Falkow S, Tompkins LS: Helicobacter pylori attachment to gastric cells Induces cytoskeletal rearrangements and tyrosine phosphorylation of the host cell proteins. Proc Natl Acad Sci USA 1996, 93:1259-1264. H. pylori attachment to human gastric epithelial cells resulted in effacement of microvilli, cytoskeletal rearrangement, and formation of an epithelial cell adhesion pedestal at the site of bacterial contact. H. pylori binding also induced tyrosine phosphorylation of host cell proteins.
-
(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 1259-1264
-
-
Segal, E.D.1
Falkow, S.2
Tompkins, L.S.3
-
51
-
-
0030878456
-
Mechanisms Involved in Helicobacter pylori-induced interleukin-8
-
Aihara M, Tsuchimoto D, Takizawa H, Azuma A, Wakebe H, Ohmoto Y, Imagawa K, Kikuchi M, Mukaida N, Matsushima K: Mechanisms Involved in Helicobacter pylori-induced interleukin-8. Infect Immun 1997, 65:3218-3224. Infection of the MKN45 human gastric cell line by H. pylori increased epithelial cell interleukin-8 production. This effect required contact with live bacteria and activation of tyrosine kinase(s). Reporter gene transfection experiments indicated that binding of activated NF-κB to the interleukin-8 promotor was required to upregulate interleukin-8 transcription. The transcription factor AP-1 played a less prominent role in regulating interleukin-8 gene expression.
-
(1997)
Infect Immun
, vol.65
, pp. 3218-3224
-
-
Aihara, M.1
Tsuchimoto, D.2
Takizawa, H.3
Azuma, A.4
Wakebe, H.5
Ohmoto, Y.6
Imagawa, K.7
Kikuchi, M.8
Mukaida, N.9
Matsushima, K.10
-
52
-
-
0030772159
-
Helicobacter pylori activates NF-kappa B in gastric epitheial cells
-
Keates S, Hitti YS, Upton M, Kelly CP: Helicobacter pylori activates NF-kappa B in gastric epitheial cells. Gastroenterology 1997, 113:1099-1109. Infection of either AGS or Kato III human gastric epithelial cell lines by H. pylori resulted in the rapid activation and nuclear translocation of transcription factor NF-κB. This was followed by increased interleukin-8 mRNA and protein production consistent with NF-κB upregulation of interleukin-8 gene transcription. Immunohistochemical studies confirmed activated NF-κB in gastric epithelial cells of patients with H. pylori antral gastritis. Activation of NF-κB by bacterial infection may be an important epithelial cell defense response since this nuclear factor regulates the expression of a wide variety of inflammatory response genes.
-
(1997)
Gastroenterology
, vol.113
, pp. 1099-1109
-
-
Keates, S.1
Hitti, Y.S.2
Upton, M.3
Kelly, C.P.4
-
53
-
-
0030885124
-
Role of adherence in lnterleukln-8 induction in Helicobacter pylori-associated gastritis
-
Rieder G, Hatz RA, Moran AP, Walz A, Stolte M, Enders G: Role of adherence in lnterleukln-8 induction In Helicobacter pylori-associated gastritis. Infect Immun 1997, 65:3622-3630.
-
(1997)
Infect Immun
, vol.65
, pp. 3622-3630
-
-
Rieder, G.1
Hatz, R.A.2
Moran, A.P.3
Walz, A.4
Stolte, M.5
Enders, G.6
-
54
-
-
19244362384
-
Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum
-
Savarino V, Mela GS, Zentilin P, Mele MR, Lapertosa L, Patetta R, Dallorto E, Vassallo A, Mansi C, Vigneri S, Celle G: Circadian gastric acidity In Helicobacter pylori positive ulcer patients with and without gastric metaplasia In the duodenum. Gut 1996, 39:508-512.
-
(1996)
Gut
, vol.39
, pp. 508-512
-
-
Savarino, V.1
Mela, G.S.2
Zentilin, P.3
Mele, M.R.4
Lapertosa, L.5
Patetta, R.6
Dallorto, E.7
Vassallo, A.8
Mansi, C.9
Vigneri, S.10
Celle, G.11
-
55
-
-
0029880057
-
Gastric metaplasia and duodenal ulcer disease in children infected by Helicobacter pylori
-
Gormally SM, Kierce BM, Daly LE, Bourke B, Carroll R, Durnin MT, Drumm B: Gastric metaplasia and duodenal ulcer disease in children infected by Helicobacter pylori. Gut 1996, 38:513-517. Gastric H. pylori infection and duodenal gastric metaplasia were studied in 148 children undergoing upper endoscopy. Twenty-five children had H. pylori gastritis and 34 had duodenal gastric metaplasia. Gastric metaplasia was more common in children aged 12 years or older. Gastric metaplasia was frequently found in children with duodenal ulceration (86%) and was less common in those without ulcers (20%). In fact, duodenal ulceration was evident at endoscopy in over 50% of children who had both gastric metaplasia and H. pylori infection, whereas no duodenal ulcers were detected in children who lacked both risk factors.
-
(1996)
Gut
, vol.38
, pp. 513-517
-
-
Gormally, S.M.1
Kierce, B.M.2
Daly, L.E.3
Bourke, B.4
Carroll, R.5
Durnin, M.T.6
Drumm, B.7
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