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• W4253165061 abstract "Helicobacter pylori infection is highly prevalent worldwide and is an important cause of gastritis, peptic ulcer disease, gastric mucosa-associated lymphoid tissue lymphoma (MALToma), and gastric adenocarcinoma. Infection is usually acquired during childhood and tends to persist unless treated. Because eradication requires treatment with multidrug regimens, prevention of initial infection by a suitable vaccine is attractive. Although immunization with H pylori protein subunits has been encouraging in animals, similar vaccine trials in humans have shown adjuvant-related adverse effects and only moderate effectiveness. Newer immunization approaches (use of DNA, live vectors, bacterial ghosts, and microspheres) are being developed. Several questions about when and whom to vaccinate will need to be appropriately answered, and a cost-effective vaccine production and delivery strategy will have to be useful for developing countries. For this review, we searched MEDLINE using the Medical Subject Heading (MeSH) terms Helicobacter pylori and vaccines for articles in English from 1990 to 2007. Helicobacter pylori infection is highly prevalent worldwide and is an important cause of gastritis, peptic ulcer disease, gastric mucosa-associated lymphoid tissue lymphoma (MALToma), and gastric adenocarcinoma. Infection is usually acquired during childhood and tends to persist unless treated. Because eradication requires treatment with multidrug regimens, prevention of initial infection by a suitable vaccine is attractive. Although immunization with H pylori protein subunits has been encouraging in animals, similar vaccine trials in humans have shown adjuvant-related adverse effects and only moderate effectiveness. Newer immunization approaches (use of DNA, live vectors, bacterial ghosts, and microspheres) are being developed. Several questions about when and whom to vaccinate will need to be appropriately answered, and a cost-effective vaccine production and delivery strategy will have to be useful for developing countries. For this review, we searched MEDLINE using the Medical Subject Heading (MeSH) terms Helicobacter pylori and vaccines for articles in English from 1990 to 2007. Helicobacter pylori infection is one of the most common infections in human beings worldwide. It causes chronic gastritis, produces duodenal and gastric ulcers, and is an important risk factor for gastric cancer later in life. Also, H pylori is key to development of gastric mucosa-associated lymphoid tissue lymphoma (MALToma).1Wotherspoon AC Doglioni C Diss TC et al.Regression of primary low-grade B-cell gastric lymphoma of mucosa-associated lymphoid tissue type after eradication of Helicobacter pylori.Lancet. 1993; 342: 575-577Abstract PubMed Scopus (1987) Google Scholar Experts link H pylori and several extragastric diseases involving the head and neck and the cardiovascular, hepatobiliary, pulmonary, dermatological, immunologic, and hematologic systems.2Franceschi F Gasbarrini A Helicobacter pylori and extragastric diseases.Best Pract Res Clin Gastroenterol. 2007; 21: 325-334Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar The prevalence of H pylori infection is about 52% in the United States.3Graham DY Malaty HM Evans DG et al.Epidemiology of Helicobacter pylori in an asymptomatic population in the United States: effect of age, race, and socioeconomic status.Gastroenterology. 1991; 100: 1495-1501PubMed Google Scholar In developing countries, up to 80% of children younger than 10 years4Das JC Paul N Epidemiology and pathophysiology of Helicobacter pylori infection in children.Indian J Pediatr. 2007; 74: 287-290Crossref PubMed Scopus (34) Google Scholar and more than 90% of adults are infected.5Sougioultzis S Lee CK Alsahli M et al.Safety and efficacy of E coli enterotoxin adjuvant for urease-based rectal immunization against Helicobacter pylori.Vaccine. 2002; 21: 194-201Crossref PubMed Scopus (52) Google Scholar Infection is almost always acquired in childhood and can be lifelong unless treated. Treatment of H pylori requires multidrug regimens because the organism resides in a layer of mucus that acts as a barrier to antibiotic penetration. Resistance is also an issue with some of the commonly used antibiotics: metronidazole, amoxicillin, erythromycin, and clarithromycin.6Fallahi GH Maleknejad S Helicobacter pylori culture and antimicrobial resistance in Iran.Indian J Pediatr. 2007; 74: 127-130Crossref PubMed Scopus (45) Google Scholar, 7Lopes AI Oleastro M Palha A Fernandes A Monteiro L Antibiotic-resistant Helicobacter pylori strains in Portuguese children.Pediatr Infect Dis J. 2005; 24: 404-409Crossref PubMed Scopus (46) Google Scholar Almost 90% of patients have no symptoms. Diagnosing H pylori infection clinically can be difficult, especially in children, who often have other more common causes of dyspepsia. The cost of offering adequate diagnostic tests and pharmacological eradication would be overwhelming. Vaccination against H pylori, both to prevent and to treat infection, appears to be a better approach to this problem. Immunization against H pylori, once thought to be impossible, is now widely considered the only practical approach to large-scale elimination of the bacterium from susceptible populations. Nonetheless, developing a successful vaccine is proving to be more difficult than earlier thought, perhaps because H pylori colonizes the gastric mucosa without crossing the epithelium, making the bacterium inaccessible to many immune effector mechanisms.8Emancipator D Nedrud JG Czinn SJ Helicobacter pylori vaccines: is DNA the answer [editorial]?.Helicobacter. 2006; 11: 513-516Crossref PubMed Scopus (4) Google Scholar In many studies, immunization not only prevented new H pylori infection but also cured animals of ongoing infection, paving the way for design of both prophylactic and therapeutic vaccines. For this review, we searched the MEDLINE database using the Medical Subject Heading (MeSH) terms Helicobacter pylori and vaccines for original articles that described both human and animal research, reviews, letters to editors, and editorials restricted to the English language from 1990 to 2007. We also used bibliographies of the already retrieved articles to search additional literature and then did an author search on PubMed and MEDLINE to review all relevant publications by the known authorities on this subject, some of which were published in the 1980s. Finally, we scanned several current issues of the journal Helicobacter for any additional information. Several factors are more common with disease-associated H pylori strains, many of which are now considered true virulence factors because of their ability to enhance disease risk through induction of cytokines, especially interleukin 8.9Robinson K Argent RH Atherton JC The inflammatory and immune response to Helicobacter pylori infection.Best Pract Res Clin Gastroenterol. 2007; 21: 237-259Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar, 10Lu H Yamaoka Y Graham DY Helicobacter pylori virulence factors: facts and fantasies.Curr Opin Gastroenterol. 2005; 21: 653-659Crossref PubMed Scopus (101) Google Scholar The cytotoxin-associated gene (Cag) pathogenicity island is the most important virulence factor associated with peptic ulcer or gastric adenocarcinoma in the host. It is a group of approximately 30 genes, many of which encode a type IV secretion system—a sort of “molecular syringe”—through which a protein encoded on the pathogenicity island, Cag type A, is “injected” into the gastric epithelial cell cytosol. The type IV secretion system is an important stimulus of epithelial cell proinflammatory cytokine expression that leads to increased gastric inflammation and neoplastic risk.9Robinson K Argent RH Atherton JC The inflammatory and immune response to Helicobacter pylori infection.Best Pract Res Clin Gastroenterol. 2007; 21: 237-259Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar Outer inflammatory protein A, duodenal ulcer-promoting gene, and blood group antigen-binding adhesin A have also been shown to be associated with duodenal ulcer.11Yamaoka Y Ojo O Fujimoto S et al.Helicobacter pylori outer membrane proteins and gastroduodenal disease.Gut. 2006 Jun; 55 (Epub 2005 Dec 1.): 775-781Crossref PubMed Scopus (195) Google Scholar, 12Lu H Hsu PI Graham DY Yamaoka Y Duodenal ulcer promoting gene of Helicobacter pylori.Gastroenterology. 2005; 128: 833-848Abstract Full Text Full Text PDF PubMed Scopus (244) Google Scholar, 13Gerhard M Lehn N Neumayer N et al.Clinical relevance of the Helicobacter pylori gene for blood-group antigen-binding adhesin.Proc Natl Acad Sci U S A. 1999; 96: 12778-12783Crossref PubMed Scopus (526) Google Scholar Although outer inflammatory protein A and blood group antigen-binding adhesin A have been linked with gastric cancer,11Yamaoka Y Ojo O Fujimoto S et al.Helicobacter pylori outer membrane proteins and gastroduodenal disease.Gut. 2006 Jun; 55 (Epub 2005 Dec 1.): 775-781Crossref PubMed Scopus (195) Google Scholar, 13Gerhard M Lehn N Neumayer N et al.Clinical relevance of the Helicobacter pylori gene for blood-group antigen-binding adhesin.Proc Natl Acad Sci U S A. 1999; 96: 12778-12783Crossref PubMed Scopus (526) Google Scholar duodenal ulcer-promoting gene is a recently identified gene found to protect against gastric cancer in some parts of Asia and South America.12Lu H Hsu PI Graham DY Yamaoka Y Duodenal ulcer promoting gene of Helicobacter pylori.Gastroenterology. 2005; 128: 833-848Abstract Full Text Full Text PDF PubMed Scopus (244) Google Scholar Another factor using the interleukin 8 pathway, RNA polymerase β-subunit, has recently been shown to increase the risk of development of more severe gastroduodenal disease in East Asia.14Lee KH Cho MJ Yamaoka Y et al.Alanine-threonine polymorphism of Helicobacter pylori RpoB is correlated with differential induction of interleukin-8 in MKN45 cells.J Clin Microbiol. 2004; 42: 3518-3524Crossref PubMed Scopus (14) Google Scholar Several other factors have a role in the interaction of the bacterium with cells and cell lines in vitro and could have potential in vaccine development. Cytotoxin-associated gene type A was one of the first such factors identified.15Nedrud JG Blanchard SS Czinn SJ Helicobacter pylori inflammation and immunity.Helicobacter. 2002; 7: 24-29Crossref PubMed Scopus (29) Google Scholar Vacuolating cytotoxin A (VacA), first described by Leunk et al,16Leunk RD Johnson PT David BC Kraft WG Morgan DR Cytotoxic activity in broth-culture filtrates of Campylobacter pylori.J Med Microbiol. 1988; 26: 93-99Crossref PubMed Scopus (535) Google Scholar can cause vacuolar degeneration in epithelial cell lines, such as HeLa cell lines.17Harris PR Cover TL Crowe DR et al.Helicobacter pylori cytotoxin induces vacuolation of primary human mucosal epithelial cells.Infect Immun. 1996; 64: 4867-4871PubMed Google Scholar A role for either Cag type A or VacA in the regulation of T and B lymphocytes and in disease pathogenesis has not yet been established in vivo.10Lu H Yamaoka Y Graham DY Helicobacter pylori virulence factors: facts and fantasies.Curr Opin Gastroenterol. 2005; 21: 653-659Crossref PubMed Scopus (101) Google Scholar Urease B is the strongest antigen among the 4 subunits of urease enzyme and can help promote gastric colonization by hydrolyzing urea to carbon dioxide and ammonia, thereby neutralizing gastric acid.18Ha NC Oh ST Sung JY Cha KA Lee MH Oh BH Supramolecular assembly and acid resistance of Helicobacter pylori urease.Nat Struct Biol. 2001; 8: 505-509Crossref PubMed Scopus (379) Google Scholar H pylori adhesion factor is key to the microbe's ability to adhere to and colonize the gastric epithelium.19Evans DG Karjalainen TK Evans Jr, DJ Graham DV Lee CH Cloning, nucleotide sequence, and expression of a gene encoding an adhesin subunit protein of Helicobacter pylori.J Bacteriol. 1993; 175: 674-683PubMed Google Scholar Neutrophil-activating protein (NAP) causes release of active oxygen radicals from neutrophils, resulting in injury to human gastric mucosal tissue.20Evans Jr, DJ Evans DG Takemura T et al.Characterization of a Helicobacter pylori neutrophil-activating protein.Infect Immun. 1995; 63: 2213-2220PubMed Google Scholar Flagellin is another important pathogenic factor for H pylori colonization, persistent infection, and inflammatory reaction.21Ottemann KM Lowenthal AC Helicobacter pylori uses motility for initial colonization and to attain robust infection.Infect Immun. 2002; 70: 1984-1990Crossref PubMed Scopus (229) Google Scholar H pylori stimulates both innate and acquired immune responses. Colonization of the gastric mucosa by the bacterium triggers innate host defense mechanisms; toll-like receptors discriminate between pathogen-associated molecular patterns, stimulating the expression of proinflammatory and antibacterial factors by gastric epithelial cells.9Robinson K Argent RH Atherton JC The inflammatory and immune response to Helicobacter pylori infection.Best Pract Res Clin Gastroenterol. 2007; 21: 237-259Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar, 22Blaser MJ Atherton JC Helicobacter pylori persistence: biology and disease.J Clin Invest. 2004; 113: 321-333PubMed Google Scholar This innate response might not only result in gastritis but also be an important mediator in gastric carcinogenesis.9Robinson K Argent RH Atherton JC The inflammatory and immune response to Helicobacter pylori infection.Best Pract Res Clin Gastroenterol. 2007; 21: 237-259Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar Although there are also strong local and systemic antibody- and cell-mediated immune responses to infection, these acquired immune responses could be inadequate to clear the bacteria, and the infection could be lifelong without treatment.22Blaser MJ Atherton JC Helicobacter pylori persistence: biology and disease.J Clin Invest. 2004; 113: 321-333PubMed Google Scholar In addition, these responses could actually contribute to the gastrointestinal pathologic processes.23Zevering Y Jacob L Meyer TF Naturally acquired human immune responses against Helicobacter pylori and implications for vaccine development.Gut. 1999; 45: 465-474Crossref PubMed Scopus (49) Google Scholar H pylori persists despite immune activation because it reduces recognition by immune sensors by generating diversity through point mutations and recombinations. It also evades and manipulates immune systems by sequestering itself in the gut lumen beyond the reach of the host immune system, mimicking host antigens, and down-regulating activation of immune cells.22Blaser MJ Atherton JC Helicobacter pylori persistence: biology and disease.J Clin Invest. 2004; 113: 321-333PubMed Google Scholar People with H pylori infections have high titers of IgG-, IgA-, and IgM-specific antibodies against the bacterium.24Crabtree JE Shallcross TM Wyatt JI et al.Mucosal humoral immune response to Helicobacter pylori in patients with duodenitis.Dig Dis Sci. 1991; 36: 1266-1273Crossref PubMed Scopus (51) Google Scholar However, the role of this antibody response in bacterial colonization remains controversial. Earlier studies showed that mucosal IgA antibodies, and to some extent serum IgA antibodies, have a role in immunity. A role for IgG antibodies in protection was also suggested by various studies that showed an increase in IgG antibodies after immunization.25Ferrero RL Thiberge JM Labigne A Local immunoglobulin G antibodies in the stomach may contribute to immunity against Helicobacter infection in mice.Gastroenterology. 1997; 113: 185-194Abstract Full Text PDF PubMed Scopus (72) Google Scholar Immunization with H pylori sonicates or proteins causes elevation of H pylori-specific antibodies and also confers protection in animals. Whether the 2 phenomena are connected or other processes are involved is still unclear. Protection can be achieved even in the absence of antibodies, whereas infection can persist despite increased production of IgA.26Wyatt JI Rathbone BJ Heatley RV Local immune response to gastric Campylobacter in non-ulcer dyspepsia.J Clin Pathol. 1986; 39: 863-870Crossref PubMed Scopus (151) Google Scholar Specific IgG and IgA antibodies have been shown to actually promote bacterial colonization and prevent protective immune mechanisms.27Akhiani AA Schon K Franzen LE Pappo J Lycke N Helicobacter pylori-specific antibodies impair the development of gastritis, facilitate bacterial colonization, and counteract resistance against infection.J Immunol. 2004; 172: 5024-5033Crossref PubMed Scopus (89) Google Scholar Further, the antibody response can cause more damage by cross-reacting with some host antigens in an H pylori-precipitated autoimmune process.28D'Elios MM Appelmelk BJ Amedei A Bergman MP Del Prete G Gastric autoimmunity: the role of Helicobacter pylori and molecular mimicry.Trends Mol Med. 2004; 10: 316-323Abstract Full Text Full Text PDF PubMed Scopus (128) Google Scholar Because H pylori colonizes the epithelial surface and the mucous layer of the stomach, secretory IgA antibodies might be expected to be protective. Instead, surprisingly, several animal studies have suggested T-cell responses are more important.29Chmiela M Michetti P Inflammation, immunity, vaccines for Helicobacter infection.Helicobacter. 2006; 11: 21-26Crossref PubMed Scopus (26) Google Scholar Gastric biopsy samples from infected patients showed an increase in T cells that correlated with the grade of gastritis and density of bacterial colonization.30Oberhuber G Bodingbauer M Mosberger I Stolte M Vogelsang H High proportion of granzyme B-positive (activated) intraepithelial and lamina propria lymphocytes in lymphocytic gastritis.Am J Surg Pathol. 1998; 22: 450-458Crossref PubMed Scopus (53) Google Scholar Helper T cells type 1 (TH1) predominate in gastric mucosa among naturally infected people, but given the persistence of natural infection in the body, this response can be presumed to be largely ineffective.31Sutton P Lee A Review article: Helicobacter pylori vaccines—the current status.Aliment Pharmacol Ther. 2000; 14: 1107-1118Crossref PubMed Scopus (21) Google Scholar Mixed results have been demonstrated; some studies show a TH1 response and others a helper T cell type 2 (TH2) response to be more important in protecting against H pylori infection. Systemic immunization of mice using adjuvants that induce either a TH1 or TH2 response leads to reduced colonization after bacterial challenge.32Gottwein JM Blanchard TG Targoni OS et al.Protective anti-Helicobacter immunity is induced with aluminum hydroxide or complete Freund's adjuvant by systemic immunization.J Infect Dis. 2001 Aug 1; 184 (Epub 2001 Jul 10.): 308-314Crossref PubMed Scopus (87) Google Scholar Whatever the mechanism, at least we can infer that cell-mediated immunity is important in protecting against H pylori infection. Recently, CD4+ T cells and major histocompatibility complex class II expression were established to be essential for vaccine-induced protection.33Pappo J Torrey D Castriotta L Savinainen A Kabok Z Ibragimov A Helicobacter pylori infection in immunized mice lacking major histocompatibility complex class I and class II functions.Infect Immun. 1999; 67: 337-341PubMed Google Scholar A collaboration between CD4+ T cells and mast cells has also been suggested as protective.34Velin D Bachmann D Bouzourene H Michetti P Mast cells are critical mediators of vaccine-induced Helicobacter clearance in the mouse model.Gastroenterology. 2005; 129: 142-155Abstract Full Text Full Text PDF PubMed Scopus (76) Google Scholar Whole bacterial cell sonicates (first-generation vaccines) and the individual H pylori proteins (second-generation vaccines) have been used as antigens to stimulate immunity in the host but require adjuvants to elicit effective protection. They have been studied extensively in animal models but minimally in humans. Colonization of Helicobacter felis (a close relative of H pylori isolated from cats) in germ-free mice fed with pure cultures of this bacterium opened the doors for vaccine development only in the 1990s.35Sutton P Progress in vaccination against Helicobacter pylori.Vaccine. 2001; 19: 2286-2290Crossref PubMed Scopus (16) Google Scholar Repetitive oral immunization with cholera toxin (CT) was shown to induce mucosal immunity in rodents as early as 1984.36Elson CO Ealding W Generalized systemic and mucosal immunity in mice after mucosal stimulation with cholera toxin.J Immunol. 1984; 132: 2736-2741PubMed Google Scholar, 37Lycke N Holmgren J Intestinal mucosal memory and presence of memory cells in lamina propria and Peyer's patches in mice 2 years after oral immunization with cholera toxin.Scand J Immunol. 1986; 23: 611-616Crossref PubMed Scopus (66) Google Scholar, 38Nedrud JG Liang XP Hague N Lamm ME Combined oral/nasal immunization protects mice from Sendai virus infection.J Immunol. 1987; 139: 3484-3492PubMed Google Scholar On the basis of this finding, Czinn and Nedrud39Czinn SJ Nedrud JG Oral immunization against Helicobacter pylori.Infect Immun. 1991; 59: 2359-2363PubMed Google Scholar orally administered killed H pylori to mice, inducing anti-H pylori IgA and IgG antibodies in both gastrointestinal secretions and serum samples among the animals. In 1990, Pallen and Clayton40Pallen MJ Clayton CL Vaccination against Helicobacter pylori urease [letter].Lancet. 1990; 336: 186-187PubMed Google Scholar recognized the protective effect of enzymatically inactive urease enzyme and suggested its use for vaccine preparation. Recombinant urease (rUre) enzyme of H pylori given orally protected 60% to 100% of mice against challenge with virulent H felis.41Lee CK Weltzin R Thomas Jr, WD et al.Oral immunization with recombinant Helicobacter pylori urease induces secretory IgA antibodies and protects mice from challenge with Helicobacter felis.J Infect Dis. 1995; 172: 161-172Crossref PubMed Scopus (203) Google Scholar Inclusion of CT in the immunization protocol as a mucosal adjuvant enhanced the antibody response.39Czinn SJ Nedrud JG Oral immunization against Helicobacter pylori.Infect Immun. 1991; 59: 2359-2363PubMed Google Scholar This finding was confirmed in later studies.42Marchetti M Arico B Burroni D Figura N Rappuoli R Ghiara P Development of a mouse model of Helicobacter pylori infection that mimics human disease.Science. 1995; 267: 1655-1658Crossref PubMed Scopus (531) Google Scholar, 43Czinn SJ Cai A Nedrud JG Protection of germ-free mice from infection by Helicobacter felis after active oral or passive IgA immunization.Vaccine. 1993; 11: 637-642Crossref PubMed Scopus (228) Google Scholar Orogastric immunization of mice with GroES and GroEL, heat-shock proteins of H pylori, also conferred considerable protection against a test dose of the bacterium.44Ferrero RL Thiberge JM Kansau I Wuscher N Huerre M Labigne A The GroES homolog of Helicobacter pylori confers protective immunity against mucosal infection in mice.Proc Natl Acad Sci U S A. 1995; 92: 6499-6503Crossref PubMed Scopus (256) Google Scholar Recently, the H pylori adhesion factor has been used to immunize mice against H pylori infection with promising results.45Nystrom J Svennerholm AM Oral immunization with HpaA affords therapeutic protective immunity against H. pylori that is reflected by specific mucosal immune responses.Vaccine. 2007 Mar 30; 25 (Epub 2006 Dec 26.): 2591-2598Crossref PubMed Scopus (57) Google Scholar Another recent study showed urease B138 to interfere with infection in mice by generating IgA in the serum, although it is not clear how the antibody inhibits urease activity against infection.46Morihara F Fujii R Hifumi E Nishizono A Uda T Effects of vaccination by a recombinant antigen ureB138 (a segment of the beta-subunit of urease) against Helicobacter pylori infection.J Med Microbiol. 2007; 56: 847-853Crossref PubMed Scopus (14) Google Scholar Several other proteins, such as Cag type A and VacA,47Ghiara P Rossi M Marchetti M et al.Therapeutic intragastric vaccination against Helicobacter pylori in mice eradicates an otherwise chronic infection and confers protection against reinfection.Infect Immun. 1997; 65: 4996-5002PubMed Google Scholar NAP,48Satin B Del Giudice G Della Bianca V et al.The neutrophil-activating protein (HP-NAP) of Helicobacter pylori is a protective antigen and a major virulence factor.J Exp Med. 2000; 191: 1467-1476Crossref PubMed Scopus (266) Google Scholar catalase,49Radcliff FJ Hazell SL Kolesnikow T Doidge C Lee A Catalase, a novel antigen for Helicobacter pylori vaccination.Infect Immun. 1997; 65: 4668-4674PubMed Google Scholar and lipoprotein 20,50Keenan J Oliaro J Domigan N et al.Immune response to an 18-kilodalton outer membrane antigen identifies lipoprotein 20 as a Helicobacter pylori vaccine candidate.Infect Immun. 2000; 68: 3337-3343Crossref PubMed Scopus (106) Google Scholar have been shown to be effective in various animal studies and are being proposed as candidate vaccines. The rodent model used in initial36Elson CO Ealding W Generalized systemic and mucosal immunity in mice after mucosal stimulation with cholera toxin.J Immunol. 1984; 132: 2736-2741PubMed Google Scholar, 37Lycke N Holmgren J Intestinal mucosal memory and presence of memory cells in lamina propria and Peyer's patches in mice 2 years after oral immunization with cholera toxin.Scand J Immunol. 1986; 23: 611-616Crossref PubMed Scopus (66) Google Scholar, 38Nedrud JG Liang XP Hague N Lamm ME Combined oral/nasal immunization protects mice from Sendai virus infection.J Immunol. 1987; 139: 3484-3492PubMed Google Scholar studies is not ideal for several reasons. The mouse is not a natural host for either H felis or H pylori; establishment of a chronic infection requires selection of particular strains of H pylori; the duration of observation is limited by the life span of the animal; and finally, there are many differences between rodents and human beings.51Dubois A Lee CK Fiala N Kleanthous H Mehlman PT Monath T Immunization against natural Helicobacter pylori infection in nonhuman primates.Infect Immun. 1998; 66: 4340-4346PubMed Google Scholar However, the simplicity and practicality of this model made it popular and formed the basis of H pylori vaccine development. Research on rhesus monkeys provides a more humanlike model of H pylori infection. This species can be naturally infected with H pylori when socially housed.52Dubois A Fiala N Heman-Ackah LM et al.Natural gastric infection with Helicobacter pylori in monkeys: a model for spiral bacteria infection in humans.Gastroenterology. 1994; 106: 1405-1417PubMed Google Scholar, 53Dubois A Fiala N Weichbrod RH et al.Seroepizootiology of Helicobacter pylori gastric infection in nonhuman primates housed in social environments.J Clin Microbiol. 1995; 33: 1492-1495PubMed Google Scholar They can develop persistent infection after a single intragastric administration of H pylori isolated from humans,54Dubois A Berg DE Incecik ET et al.Transient and persistent experimental infection of nonhuman primates with Helicobacter pylori: implications for human disease.Infect Immun. 1996; 64: 2885-2891PubMed Google Scholar and, as in humans, antibiotic treatment rarely cures the infection.52Dubois A Fiala N Heman-Ackah LM et al.Natural gastric infection with Helicobacter pylori in monkeys: a model for spiral bacteria infection in humans.Gastroenterology. 1994; 106: 1405-1417PubMed Google Scholar In a rhesus monkey model, oral rUre enzyme along with Escherichia coli heat-labile toxin (LT) was able to protect against H pylori infection without causing adverse effects.51Dubois A Lee CK Fiala N Kleanthous H Mehlman PT Monath T Immunization against natural Helicobacter pylori infection in nonhuman primates.Infect Immun. 1998; 66: 4340-4346PubMed Google Scholar To demonstrate safety of H pylori vaccines, Kreiss et al55Kreiss C Buclin T Cosma M Corthesy-Theulaz I Michetti P Safety of oral immunisation with recombinant urease in patients with Helicobacter pylori infection [letter].Lancet. 1996; 347: 1630-1631Abstract PubMed Google Scholar administered rUre orally without adjuvant to 12 healthy volunteers who were already infected. As expected, no immune response was seen, but safety of this vaccine in humans was demonstrated. Michetti et al,56Michetti P Kreiss C Kotloff KL et al.Oral immunization with urease and Escherichia coli heat-labile enterotoxin is safe and immunogenic in Helicobacter pylori-infected adults.Gastroenterology. 1999; 116: 804-812Abstract Full Text Full Text PDF PubMed Scopus (272) Google Scholar using 5 μg of LT (adjuvant) with rUre, showed a dose-dependent serum IgA response of LT and a decrease in bacterial density in gastric biopsy specimens, but H pylori infection was not eradicated. Diarrhea was seen in as many as two-thirds of the volunteers, most likely from the LT adjuvant because it was independent of the dose of rUre.56Michetti P Kreiss C Kotloff KL et al.Oral immunization with urease and Escherichia coli heat-labile enterotoxin is safe and immunogenic in Helicobacter pylori-infected adults.Gastroenterology. 1999; 116: 804-812Abstract Full Text Full Text PDF PubMed Scopus (272) Google Scholar This speculation was confirmed in a later study of uninfected adults, in which rUre vaccines containing lower (2.5 μg) doses of LT reduced adverse effects without compromising adjuvant effects.57Banerjee S Medina-Fatimi A Nichols R et al.Safety and efficacy of low dose Escherichia coli enterotoxin adjuvant for urease based oral immunisation against Helicobacter pylori in healthy volunteers.Gut. 2002; 51: 634-640Crossref PubMed Scopus (79) Google Scholar A rectally administered vaccine containing urease with varying doses of LT caused no adverse effects, but antiurease response was unsatisfactory, despite good anti-LT response.5Sougioultzis" @default.
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• W4253165061 title "Helicobacter pylori Vaccine: From Past to Future" @default.
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