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| 1 | H pylori and host interactions that influence pathogenesis显示文摘H pylori is probably the most prevalent human patho- gen worldwide. Since it was initially suggested in 1983 by Marshall and Warren to be implicated in gastritis and peptic ulcer disease, H pylori has also been implicated in gastric carcinoma and was classified as a class I car- cinogen. In the last two decades, a noteworthy body of research has revealed the multiple processes that this gram negative bacterium activates to cause gastroduo- denal disease in humans. Most infections are acquired early in life and may persist for the life of the individual. While infected individuals mount an inflammatory re- sponse that becomes chronic, along with a detectable adaptive immune response, these responses are ineffec- tive in clearing the infection. H pylori has unique features that allow it to reside within the harsh conditions of the gastric environment, and also to evade the host immune response. In this review, we discuss the various virulence factors expressed by this bacterium and how they inter- act with the host epithelium to influence pathogenesis. | Ellen J Beswick Giovanni Suarez Victor E Reyes | 2006 | World Journal of Gastroenterology2006，12，35： | 20 |
| 2 | Effect of Helicobacter pylori on gastric epithelial cells显示文摘The gastrointestinal epithelium has cells with features that make them a powerful line of defense in innate mucosal immunity. Features that allow gastrointestinal epithelial cells to contribute in innate defense include cell barrier integrity, cell turnover, autophagy, and innate immune responses. Helicobacter pylori(H. pylori) is a spiral shape gram negative bacterium that selectively colonizes the gastric epithelium of more than half of the world's population. The infection invariably becomes persistent due to highly specialized mechanisms that facilitate H. pylori 's avoidance of this initial line of host defense as well as adaptive immune mechanisms. The host response is thus unsuccessful in clearing the infection and as a result becomes established as a persistent infection promoting chronic inflammation. In some individuals the associated inflammation contributes to ulcerogenesis or neoplasia. H. pylori has an array of different strategies to interact intimately with epithelial cells and manipulate their cellular processes and functions. Among the multiple aspects that H. pylori affects in gastric epithelial cells are their distribution of epithelial junctions, DNA damage, apoptosis, proliferation, stimulation of cytokine production, and cell transformation. Some of these processes are initiated as a result of the activation of signaling mechanisms activated on binding of H. pylori to cell surface receptors or via soluble virulence factors that gain access to the epithelium. The multiple responses by the epithelium to the infection contribute to pathogenesis associated with H. pylori. | Shatha Alzahrani Taslima T Lina Jazmin Gonzalez Irina V Pinchuk Ellen J Beswick Victor E Reyes | 2014 | World Journal of Gastroenterology2014，20，36： | 15 |
| 3 | CD74 in antigen presentation,inflammation,and cancers of the gastrointestinal tract显示文摘CD74 is a protein whose initial role in antigen presentation was recognized two decades ago. Recent studies have revealed that it has additional functions as a receptor for macrophage migration inhibitory factor and as a receptor for an important human pathogen, Helicobacter pylori (H pylori). The role of CD74 as a receptor is important because after binding of migration inhibitory factor or H pylori, NF-κB and Erk1/2 activation occurs, along with the induction of proinflammatory cytokine secretion. This review provides an up-to-date account of the functions of CD74 and how it might be involved in inflammation and cancer within the gastrointestinal tract. | Ellen J Beswick Victor E Reyes | 2009 | World Journal of Gastroenterology2009，15，23： | 10 |
| 4 | Immune evasion strategies used by Helicobacter pylori显示文摘Helicobacter pylori(H. pylori) is perhaps the most ubiquitous and successful human pathogen, since it colonizes the stomach of more than half of humankind. Infection with this bacterium is commonly acquired during childhood. Once infected, people carry the bacteria for decades or even for life, if not treated. Persistent infection with this pathogen causes gastritis, peptic ulcer disease and is also strongly associated with the development of gastric cancer. Despite induction of innate and adaptive immune responses in the infected individual, the host is unable to clear the bacteria. One widely accepted hallmark of H. pylori is that it successfully and stealthily evades host defense mechanisms. Though the gastric mucosa is well protected against infection, H. pylori is able to reside under the mucus, attach to gastric epithelial cells and cause persistent infection by evading immune responses mediated by host. In this review, we discuss how H. pylori avoids innate and acquired immune response elements, uses gastric epithelial cells as mediators to manipulate host T cell responses and uses virulence factors to avoid adaptive immune responses by T cells to establish a persistent infection. We also discuss in this review how the genetic diversity of this pathogen helps for its survival. | Taslima T Lina Shatha Alzahrani Jazmin Gonzalez Irina V Pinchuk Ellen J Beswick Victor E Reyes | 2014 | World Journal of Gastroenterology2014，20，36： | 7 |
| 5 | H pylori receptor MHC classⅡcontributes to the dynamic gastric epithelial apoptotic response显示文摘AIM: To investigate the role of MHC classⅡin the modulation of gastric epithelial cell apoptosis induced by H pylon infection. METHODS: After stimulating a human gastric epithelial cell line with bacteria or agonist antibodies specific for MHC classⅡand CD95, the quantitation of apoptotic and anti-apoptotic events, including caspase activation, BCL-2 activation, and FADD recruitment, was performed with a fluorometric assay, a cytometric bead array, and confocal microscopy, respectively. RESULTS: Pretreatment of N87 cells with the anti-MHC classⅡIgM antibody RFD1 resulted in a reduction in global caspase activation at 24 h of H pylori infection. When caspase 3 activation was specifically measured, crosslinking of MHC class n resulted in markedly reduced caspase activation, while simple ligation of MHC classⅡdid not. Crosslinking of MHC class n also resulted in an increased activation of the anti-apoptosis molecule BCL-2 compared to simple ligation. Confocal microscope analysis demonstrated that the pretreatment of gastric epithelial cells with a crosslinking anti-MHC classⅡIgM blocked the recruitment of FADD to the cell surface. CONCLUSION: The ability of MHC class n to modulate gastric epithelial apoptosis is at least partially dependent on its crosslinking. The crosslinking of this molecule has anti-apoptotic effects during the earlier time points of H pylori infection. This effect is possibly mediated by the ability of MHC classⅡto modulate the activation of the pro-apoptotic receptor Fas by blocking the recruitment of the accessory molecule FADD, and this delay in apoptosis induction could allow for prolonged cytokine secretion by H pylori-infected gastric epithelial cells. | David A Bland Giovanni Suarez Ellen J Beswick Johanna C Sierra Victor E Reyes | 2006 | World Journal of Gastroenterology2006，12，29： | 3 |
| 6 | H pylori receptor MHC class Ⅱ contributes to the dynamic gastric epithelial apoptotic response显示文摘AIM: To investigate the role of MHC class Ⅱ in the modulation of gastric epithelial cell apoptosis induced by H pylori infection.METHODS: After stimulating a human gastric epithelial cell line with bacteria or agonist antibodies specifi c for MHC class Ⅱ and CD95, the quantitation of apoptotic and anti-apoptotic events, including caspase activation, BCL-2 activation, and FADD recruitment, was performed with a ? uorometric assay, a cytometric bead array, and confocal microscopy, respectively.RESULTS: Pretreatment of N87 cells with the anti-MHC class Ⅱ IgM antibody RFD1 resulted in a reduction in global caspase activation at 24 h of H pylori infection. When caspase 3 activation was specifically measured, crosslinking of MHC class Ⅱ resulted in a marked re-duced caspase activation, while simple ligation of MHC class Ⅱ did not. Crosslinking of MHC class Ⅱ also re-sulted in an increased activation of the anti-apoptosis molecule BCL-2 compared to simple ligation. Confocal microscope analysis demonstrated that the pretreatment of gastric epithelial cells with a crosslinking anti-MHC class Ⅱ IgM blocked the recruitment of FADD to the cell surface.CONCLUSION: The results presented here demonstrate that the ability of MHC class Ⅱ to modulate gastric epi-thelial apoptosis is at least partially dependent on its crosslinking. Furthermore, while previous research has demonstrated that MHC class Ⅱ signaling can be pro-apoptotic during extended ligation, we have shown that the crosslinking of this molecule has anti-apoptotic ef-fects during the earlier time points of H pylori infection. This effect is possibly mediated by the ability of MHC class Ⅱ to modulate the activation of the pro-apoptotic receptor Fas by blocking the recruitment of the accessory molecule FADD, and this delay in apoptosis induction could allow for prolonged cytokine secretion by H pylori-infected gastric epithelial cells. | David A Bland Giovanni Suarez Ellen J Beswick Johanna C Sierra Victor E Reyes | 2006 | World Journal of Gastroenterology2006，12，33： | 2 |
| 7 | Optimal performance of an irreversible solar-assisted heat pump显示文摘 | Torres Reyes E Cervantes de Gortari J | 2001 | Exergy Int J2001，1，2： | 1 |
| 8 | Surgical management of cerebral metastases显示文摘 | Emery E Redondo A Rey A | 1999 | Neurochirurgie1999，45，： | 1 |
| 9 | Speech/music classification based on distributed evolutionary fuzzy logic for intelligent audio coding显示文摘 | Munoz J E Reyes N R Galan S G | 2007 | Pattern Recognition and Image2007，4478，： | 1 |
| 10 | Spanish muhicenter taflu- prost tolerability study 显示文摘 | M1LLA E STIRBU O REY A | 2012 | Br J Ophthalmol2012，96，6： | 1 |
| 11 | Vasoactive intestinal peptide induces regulatory T ceils during experimental autoimnmne encephalomyelitis 显示文摘 | FERNANDEZ MARTIN A GONZALEZ REY E CHORNY A et al | 2006 | Eur J Immunol2006，36，2： | 1 |
| 12 | gammadelta T cells are required for maximal expression of allergic conjunctivitis显示文摘 | Reyes N J Mayhew E Chen PW | 2011 | Invest Ophthalmol Vis Sci2011，52，5： | 1 |
| 13 | Metabolomic a-nalysis in food science:A review显示文摘 | CEVALLOS J M REYES J I ETXEBERRIA E | 2009 | Trends Food Science and Technology2009，20，1112： | 1 |
| 14 | Procalcitonin and C-reactive protein as markers of systemic inflammatory response syndrome severity in critically ill children 显示文摘 | Corsino Rey Marta Los Arcos Andr e s Concha | 2007 | Intensive Care Med2007，33，3： | 1 |
| 15 | Human inflammatory synovial fibmblasts induce enhanced myeloid cell recruitment and angiogenesis through a hypoxia-inducible transcription factor 1 alpha/vascular endothelial growth factor-mediated pathway in immunodeficient mice显示文摘 | del Rey MJ Izquierdo E Caja S | 2009 | Arthritis Rheum2009，60，10： | 1 |
| 16 | Pilot clinical study of an endoscopic, removable duodenal-jejunal bypass liner for the treat- ment of type 2 diabetes 显示文摘 | Rodriguez L Reyes E Fagalde P | 2009 | Diabetes Technol Ther2009，11，11： | 1 |
| 17 | Direct asymmetric intermolecular aldol reactions catalyzed by amino acids and small peptides显示文摘 | Cordova A Zou W Dziedzic P Ibrahem I Reyes E Xu Y | 2006 | Chem Eur J2006，12，： | 1 |
| 18 | Abnormal gamma- IFN and alpha-TNF secretion in purified CD2^+ cells from autoimmune thrombocytopenic purpua (ATP) patient : their implication in the clinical course of the disease显示文摘 | GARCIA-SUAREZ J PRIETO A REYES E | 1995 | Am H Hematol1995，49，4： | 1 |
| 19 | Kullback Leibler divergence measure for multivariate skewnormal distributions显示文摘 | Contreras Reyes J E Arellano Valle R B | 2012 | Entropy2012，14，： | 1 |
| 20 | Dalteparin for the prevention of recurrence of placental-mediated complications of pregnancy in women without thrombophilia:a pilot randomized controlled trial显示文摘 | Rey E Garneau P David M Gauthier R Leduc L Michon N | 2009 | J Thromb Haemost2009，7，1： | 1 |
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