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27 results on '"Bergman, Mathijs P."'

1. Gastric Autoimmunity

Author

Bergman, Mathijs P., primary, Faller, Gerhard, additional, D'Elios, Mario M., additional, Del Prete, Gianfranco, additional, Vandenbroucke-Grauls, Christina M. J. E., additional, and Appelmelk, Ben J., additional

Published
2014
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3. List of Contributors

Author

Abu-Shakra, Mahmoud, primary, Achiron, Anat, additional, Adelman, Miranda K., additional, Afanasyeva, Marina, additional, Akaogi, Jun, additional, Alcocer-Varela, Jorge, additional, Amedei, Amedeo, additional, Appelmelk, Ben J., additional, Aron-Maor, Anabel, additional, Asherson, Ronald A., additional, van den Berg, Leonard H., additional, Bergman, Mathijs P., additional, Blank, M., additional, Bombardieri, Stefano, additional, Buc, Milan, additional, Bussel, James, additional, Cainelli, Francesco, additional, Cervera, Ricard, additional, Chou, Alexander J., additional, Cohen, Irun R., additional, Cohen, Pascal, additional, Acuña, J.C. Crispin, additional, Cunha-Neto, Edecio, additional, Cutolo, Maurizio, additional, David, Michael, additional, D'Elios, Mario M., additional, Del Prete, Gianfranco, additional, Denman, A.M., additional, Detrick, Barbara, additional, Doria, Andrea, additional, Dugué, C., additional, Durai, Malarvizhi, additional, Ebringer, Alan, additional, Eisenstein, Miriam, additional, Ferri, Clodoveo, additional, Frostegård, Johan, additional, Gambari, Pier Franca, additional, Garvey, Marjorie A., additional, Gershwin, M. Eric, additional, Ghirardello, Anna, additional, Giacomelli, Roberto, additional, Guiducci, Serena, additional, Fonseca, Simone Gonçalves, additional, Guilherme, Luiza, additional, Guillevin, Loïc, additional, Hafler, David A., additional, Hatemi, Gülen, additional, He, Xiao-Song, additional, Hooks, John J., additional, Iaccarino, Luca, additional, Jacobson, Steven, additional, Jansen, M.D., additional, Jara, Luis J., additional, Jun, Hee-Sook, additional, Kalil, Jorge, additional, Kapsogeorgou, Efstathia K., additional, Iwai, Leo Kei, additional, Kelly, Kindra M., additional, Krause, Ilan, additional, Krebs, Philippe, additional, Kuroda, Yoshiki, additional, Lerner, Aaron, additional, Liakos, Dimitrios A., additional, Lim, Dong-Gyun, additional, Ludewig, Burkhard, additional, Marchalonis, John J., additional, Cerinic, Marco Matucci, additional, Medina, Gabriela, additional, Miller, Stephen D., additional, Milo, Gui, additional, Mimouni, Daniel, additional, Miranda, Juan M., additional, Bilate, Angelina Morand B., additional, Moudgil, Kamal D., additional, Moutsopoulos, Haralampos M., additional, Nacionales, Dina C., additional, Navarro, Carmen, additional, Nussenblatt, Robert, additional, Pagnoux, Christian, additional, Pender, Michael P., additional, Pers, Jaques-Olivier, additional, van der Pol, W-Ludo, additional, Prummel, Mark F., additional, Quintana, Francisco J., additional, Rager-Zisman, B., additional, Rashid, Taha, additional, Reeves, Westley H., additional, Reif, Shimon, additional, Renaudineau, Yves, additional, Rose, Noel R., additional, Rovenský, Jozef, additional, Satoh, Minoru, additional, Schmidt, Reinhold E., additional, Seriolo, Bruno, additional, Severin, Marianne C., additional, Shoenfeld, Yehuda, additional, Sibilia, Jean, additional, Snider, Lisa A., additional, Soldan, Samantha S., additional, Sorge, N.M. van, additional, Steere, Allen C., additional, Stoll, Matthias, additional, Sulli, Alberto, additional, Swedo, Susan E., additional, Tishler, Moshe, additional, Tomer, Yaron, additional, Tyndall, Alan, additional, Vandenbroucke-Grauls, Christina M., additional, VanderLugt-Castaneda, Carol L., additional, Vassilopoulos, Dimitrios, additional, Vento, Sandro, additional, Vera-Lastra, Olga, additional, Villanueva, Ronald, additional, Wachsmann, Dominique, additional, Weinstock, Joel V., additional, Wick, Georg, additional, Wiersinga, Wilmar M., additional, Wilson, Clyde, additional, van de Winkel, Jan G.J., additional, Wucherpfennig, Kai W., additional, Xu, Qingbo, additional, Yazici, Hasan, additional, Yocum, David E., additional, Yoon, Ji-Won, additional, Youinou, Pierre, additional, Zampieri, Sandra, additional, and Zandman-Goddard, Gisele, additional

Published
2004
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7. Identification of DNA sequence variation in Campylobacter jejuni strains associated with the Guillain-Barré syndrome by high-throughput AFLP analysis

Author

Endtz Hubert P, Lastovica Albert J, van den Braak Nicole, Simons Guus, Gorkink Raymond FJ, Bergman Mathijs P, Godschalk Peggy CR, Verbrugh Henri A, and van Belkum Alex

Subjects
Microbiology, QR1-502
Abstract

Abstract Background Campylobacter jejuni is the predominant cause of antecedent infection in post-infectious neuropathies such as the Guillain-Barré (GBS) and Miller Fisher syndromes (MFS). GBS and MFS are probably induced by molecular mimicry between human gangliosides and bacterial lipo-oligosaccharides (LOS). This study describes a new C. jejuni-specific high-throughput AFLP (htAFLP) approach for detection and identification of DNA polymorphism, in general, and of putative GBS/MFS-markers, in particular. Results We compared 6 different isolates of the "genome strain" NCTC 11168 obtained from different laboratories. HtAFLP analysis generated approximately 3000 markers per stain, 19 of which were polymorphic. The DNA polymorphisms could not be confirmed by PCR-RFLP analysis, suggesting a baseline level of 0.6% AFLP artefacts. Comparison of NCTC 11168 with 4 GBS-associated strains revealed 23 potentially GBS-specific markers, 17 of which were identified by DNA sequencing. A collection of 27 GBS/MFS-associated and 17 enteritis control strains was analyzed with PCR-RFLP tests based on 11 of these markers. We identified 3 markers, located in the LOS biosynthesis genes cj1136, cj1138 and cj1139c, that were significantly associated with GBS (P = 0.024, P = 0.047 and P < 0.001, respectively). HtAFLP analysis of 13 highly clonal South African GBS/MFS-associated and enteritis control strains did not reveal GBS-specific markers. Conclusion This study shows that bacterial GBS markers are limited in number and located in the LOS biosynthesis genes, which corroborates the current consensus that LOS mimicry may be the prime etiologic determinant of GBS. Furthermore, our results demonstrate that htAFLP, with its high reproducibility and resolution, is an effective technique for the detection and subsequent identification of putative bacterial disease markers.

Published
2006
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8. Cytotoxic T Cells in H. pylori-Related Gastric Autoimmunity and Gastric Lymphoma

Author

Bergman, Mathijs P. and D'Elios, Mario M.

Subjects
Article Subject, digestive system diseases
Abstract

Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop gastric B-cell lymphoma, gastric autoimmunity, or other life threatening diseases, as gastric cancer or peptic ulcer. The type of host immune response against H. pylori, particularly the cytolytic effector functions of T cells, is crucial for the outcome of the infection. T cells are potentially able to kill a target via different mechanisms, such as perforins or Fas-Fas ligand interaction. In H. pylori-infected patients with gastric autoimmunity cytolytic T cells, that cross-recognize different epitopes of H. pylori proteins and H + K + -ATPase autoantigen, infiltrate the gastric mucosa and lead to gastric atrophy via long-lasting activation of Fas ligand-mediated appotosis and perforin-induced cytotoxicity. On the other hand, gastric T cells from MALT lymphoma exhibit defective perforin- and Fas-Fas ligand-mediated killing of B cells, with consequent abnormal help for B-cell proliferation, suggesting that deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support both the onset and the promotion of low-grade B-cell lymphoma.

Published
2010
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14. The Story So Far:Helicobacter Pyloriand Gastric Autoimmunity

Author

Bergman, Mathijs P., primary, Vandenbroucke-Grauls, Christina M. J. E., additional, Appelmelk, Ben J., additional, D'Elios, Mario M., additional, Amedei, Amedeo, additional, Azzurri, Annalisa, additional, Benagiano, Marisa, additional, and Del Prete, Gianfranco, additional

Published
2005
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16. Helicobacter pylori Modulates the T Helper Cell 1/T Helper Cell 2 Balance through Phase-variable Interaction between Lipopolysaccharide and DC-SIGN

Author

Bergman, Mathijs P., primary, Engering, Anneke, additional, Smits, Hermelijn H., additional, van Vliet, Sandra J., additional, van Bodegraven, Ad A., additional, Wirth, Hans-Peter, additional, Kapsenberg, Martien L., additional, Vandenbroucke-Grauls, Christina M.J.E., additional, van Kooyk, Yvette, additional, and Appelmelk, Ben J., additional

Published
2004
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17. Molecular Mimicry between Helicobacter pylori Antigens and H+,K+–Adenosine Triphosphatase in Human Gastric Autoimmunity

Author

Amedei, Amedeo, primary, Bergman, Mathijs P., additional, Appelmelk, Ben J., additional, Azzurri, Annalisa, additional, Benagiano, Marisa, additional, Tamburini, Carlo, additional, van der Zee, Ruurd, additional, Telford, John L., additional, Vandenbroucke-Grauls, Christina M.J.E., additional, D'Elios, Mario M., additional, and Del Prete, Gianfranco, additional

Published
2003
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22. The Story So Far: Helicobacter Pylori and Gastric Autoimmunity.

Author

Bergman, Mathijs P., Vandenbroucke-Grauls, Christina M. J. E., Appelmelk, Ben J., D'Elios, Mario M., Amedei, Amedeo, Azzurri, Annalisa, Benagiano, Marisa, and Del Prete, Gianfranco

Subjects
*HELICOBACTER pylori, *PATHOGENIC microorganisms, *GASTRIC mucosa, *AUTOIMMUNITY, *IMMUNOGLOBULINS
Abstract

The gastric mucosal pathogen Helicobacter pylori induces autoantibodies directed against the gastric proton pump H + ,K + -ATPase in 20–30% of infected patients. The presence of these autoantibodies is associated with severity of gastritis, increased atrophy, and apoptosis in the corpus mucosa, and patients with these autoantibodies infected with H. pylori display histopathological and clinical features that are similar to those of autoimmune gastritis (AIG). This review will focus on the T helper cell responses, cytokines, and adhesion molecules involved in corpus mucosal atrophy in chronic H. pylori gastritis and in AIG, and the role of H. pylori in the onset of AIG. [ABSTRACT FROM AUTHOR]

Published
2005
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23. Characterization of H.

Author

Bergman, Mathijs P., Amedei, Amedeo, D'Elios, Mario M., Azzurri, Annalisa, Benagiano, Marisa, Tamburini, Carlo, van der Zee, Ruurd, Vandenbroucke-Grauls, Christina M., Appelmelk, Ben J., and Prete, Gianfranco Del

Published
2003
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24. The Sialylated Lipooligosaccharide Outer Core in Campylobacter jejuniIs an Important Determinant for Epithelial Cell Invasion

Author

Louwen, Rogier, Heikema, Astrid, van Belkum, Alex, Ott, Alewijn, Gilbert, Michel, Ang, Wim, Endtz, Hubert P., Bergman, Mathijs P., and Nieuwenhuis, Edward E.

Abstract

ABSTRACTCampylobacter jejuniis a frequent cause of bacterial gastroenteritis worldwide. Lipooligosaccharide (LOS) has been identified as an important virulence factor that may play a role in microbial adhesion and invasion. Here we specifically address the question of whether LOS sialylation affects the interaction of C. jejuniwith human epithelial cells. For this purpose, 14 strains associated with Guillain-Barré syndrome (GBS), 34 enteritis-associated strains, the 81-176 reference strain, and 6 Penner serotype strains were tested for invasion of two epithelial cell lines. C. jejunistrains expressing sialylated LOS (classes A, B, and C) invaded cells significantly more frequently than strains expressing nonsialylated LOS (classes D and E) (P< 0.0001). To further explore this observation, we inactivated the LOS sialyltransferase (Cst-II) via knockout mutagenesis in three GBS-associated C. jejunistrains expressing sialylated LOS (GB2, GB11, and GB19). All knockout strains displayed significantly lower levels of invasion than the respective wild types. Complementation of a Δcst-IImutant strain restored LOS sialylation and reset the invasiveness to wild-type levels. Finally, formalin-fixed wild-type strains GB2, GB11 and GB19, but not the isogenic Δcst-IImutants that lack sialic acid, were able to inhibit epithelial invasion by viable GB2, GB11, and GB19 strains. We conclude that sialylation of the LOS outer core contributes significantly to epithelial invasion by C. jejuniand may thus play a role in subsequent postinfectious pathologies.

Published
2008
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25. Characterization of H+,K+-ATPase T 3;cell epitopes in human autoimmune gastritis

Author

Bergman, Mathijs 3;P., Amedei, Amedeo, D'Elios, Mario 3;M., Azzurri, Annalisa, Benagiano, Marisa, Tamburini, Carlo, van der Zee, Ruurd, Vandenbroucke-Grauls, Christina 3;M., Appelmelk, Ben 3;J., and Prete, Gianfranco 3;Del

Abstract

Human autoimmune gastritis (AIG) is an organ-specific inflammatory disorder leading to gastric atrophy and pernicious anemia. Gastric H+,K+-ATPase was identified as the autoantigen in both human disease and experimental murine AIG (EAIG). Studies of EAIG significantly contributed to current knowledge of human AIG, but to what extent EAIG mimics AIG is still debated, andthe autoantigenic epitopes in AIG are yet unknown. This study aimed to identify the H+,K+-ATPase epitopes recognized by gastric T 3;cell clones from AIG patients, to define their TCR 3;Vβ usage and epitope-induced cytokine response. Sixteen H+,K+-ATPase-reactive CD4+ gastric T 3;cell clones of four AIG patients were tested for proliferation to overlapping 15-mer peptides spanning the α 3;and β 3;chains of H+,K+-ATPase. We identified 6 epitopes in the α 3;chain and 5 in the β 3;chain; TCR 3;Vβ usage was not restricted. Four (36%) of the 11 H+,K+-ATPase epitopes recognized in AIG were found to overlap with epitopes that are relevant in EAIG, including a previously described gastritogenic epitope. Gastric T 3;cell recognition of the peptide epitopes resulted in secretion of Th1 cytokines. Our data suggest a striking similarity between human AIG and EAIG, at the epitope level, with regard to cytokinesecretion and likely also with regard to pathogenic mechanisms.

Published
2003
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27. Molecular mimicry between Helicobacter pylori antigens and H+, K+ --adenosine triphosphatase in human gastric autoimmunity.

Author

Amedei A, Bergman MP, Appelmelk BJ, Azzurri A, Benagiano M, Tamburini C, van der Zee R, Telford JL, Vandenbroucke-Grauls CM, D'Elios MM, and Del Prete G

Subjects
Adult, Autoantigens immunology, Cross Reactions, Epitopes, T-Lymphocyte immunology, Female, Gastric Mucosa immunology, Gastritis, Atrophic microbiology, HLA-DQ Antigens immunology, HLA-DR Antigens immunology, Helicobacter Infections immunology, Humans, Lymphocyte Activation, Middle Aged, Stomach immunology, T-Lymphocytes immunology, Antigens, Bacterial immunology, Autoimmune Diseases microbiology, Gastritis, Atrophic immunology, H(+)-K(+)-Exchanging ATPase immunology, Helicobacter pylori immunology, Molecular Mimicry
Abstract

Autoimmune gastritis and Helicobacter pylori-associated gastric atrophy develop through similar mechanisms involving the proton pump H+,K+-adenosine triphosphatase as autoantigen. Here, we report that H. pylori-infected patients with gastric autoimmunity harbor in vivo-activated gastric CD4+ T cells that recognize both H+, K+-adenosine triphosphatase and H. pylori antigens. We characterized the submolecular specificity of such gastric T cells and identified cross-reactive epitopes from nine H. pylori proteins. Cross-reactive H. pylori peptides induced T cell proliferation and expression of T helper type 1 functions. We suggest that in genetically susceptible individuals, H. pylori infection can activate cross-reactive gastric T cells leading to gastric autoimmunity via molecular mimicry.

Published
2003
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