Mucosal Immunization with a Urease B DNA Vaccine Induces Innate and Cellular Immune Responses Against <i>Helicobacter pylori</i>

Hatzifoti, Caterina; Roussel, Yvonne; Harris, Andrew G.; Wren, Brendan W.; Morrow, John W.; Bajaj-Elliott, Mona

doi:10.1111/j.1523-5378.2006.00385.x

Cited by 28 publications

(37 citation statements)

References 60 publications

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“…186 Mucosal administration of a ureB DNA vaccine was recently shown to induce innate and cellular immunity in the gastric mucosa of mice and to significantly reduce H. pylori colonisation densities after a challenge infection. 187 The intranasal delivery of H. pylori lysate antigen with a novel non-toxic mucosal adjuvant showed promise, yielding a 20-fold reduction in colonisation density after challenge infection. 188 Since people usually acquire H. pylori infections in early childhood, 189 possibly whilst the immune system is still developing, 190 it may be difficult to ensure that prophylactic vaccines are administered early enough and are able to stimulate good levels of protective immunity.…”

Section: Prospects For Future Vaccinesmentioning

confidence: 99%

The inflammatory and immune response to Helicobacter pylori infection

Robinson

Argent

Atherton

2007

Best Practice & Research Clinical Gastroenterology

157

149

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Section: Prospects For Future Vaccinesmentioning

confidence: 99%

The inflammatory and immune response to Helicobacter pylori infection

Robinson

Argent

Atherton

2007

Best Practice & Research Clinical Gastroenterology

157

149

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“…Upon immunization, the IL-10 − / − and IgA − / − double-mutant mice showed an increased postimmunization gastritis and eliminated faster the infection than IL-10 − / − IgA+/+ simple mutants or wild type animals, suggesting that it may not be ideal for a vaccine candidate to elicit exaggerated IgA response. Gastric IFN-γ also increase following immunization and seems essential protection [48,49]. While the role of antibodies in protection remains controversial, in deficient mice models, Fas ligand was found crucial for protection, further indicating that cellular responses are involved [47].…”

Section: Vaccine Development and Probioticsmentioning

confidence: 99%

Inflammation, Immunity, Vaccines for Helicobacter Infection

Chmiela

Michetti

2006

Helicobacter

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The reason why some individuals remain Helicobacter pylori infected for life but without any symptoms while others develop severe diseases is only partially clarified. Presumably, it depends on multifactorial interactions among host immunologic and physiologic factors, bacterial virulence determinants, and environmental influences modulating the host response. Much effort has been made to identify host genetic factors that may explain an individual susceptibility of the host to H. pylori infection. The identification of H. pylori determinants and the elucidation of their role in modifying the host immune responses were further delineated. The ability of H. pylori to overcome the defense mechanisms on mucosal surfaces as well as to modulate the immune response by interfering with host recognition and transduction systems has been shown. Also new bacterial anti-inflammatory defense systems have been described. Findings in experimental animal models and humans with natural H. pylori infection suggested a double role of regulatory T cells in the course of H. pylori infection: protecting the infected host against excessive gastric inflammation and, in contrast, promoting bacterial colonization.

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“…Ammonia generated by the hydrolysis of urea neutralizes gastric acidity and forms a neutral microenvironment surrounding the bacterium within the gastric lumen. Mice immunized with whole-cell lysate or purified urease B protein were protected against experimental H. pylori SS1 infection (Hatzifoti et al, 2006;Li et al, 2010;Zhao et al, 2007). Despite these encouraging findings, an effective H. pylori vaccine remains elusive because immunization of mice reduces but rarely eliminates Helicobacter organisms in the stomach (Czinn & Blanchard, 2011).…”

Section: Introductionmentioning

confidence: 98%

Expression of Helicobacter pylori urease B on the surface of Bacillus subtilis spores

Zhou

Gong

et al. 2015

Journal of Medical Microbiology

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Helicobacter pylori infection is a major risk factor for chronic gastritis, digestive ulcers, gastric adenocarcinoma and lymphoma. Due to the decreasing efficacy of anti-H. pylori antibiotic therapy in clinical practice, there is renewed interest in the development of anti-H. pylori vaccines. Bacillus subtilis is non-pathogenic and can produce endospores, which can survive under extreme conditions. These features make the B. subtilis spore an ideal vehicle for delivery of heterologous antigens to extreme environments such as the gastrointestinal tract. In this study, we displayed H. pylori urease B protein on the B. subtilis spore coat using the spore coat protein CotC as a fusion partner. Western blot analyses were used to verify urease B surface expression on spores. Recombinant spores displaying the urease B antigen were used for oral immunization and were shown to generate humoral response in mice. Urease B-specific secretory IgA in faeces and IgG in serum reached significant levels 2 weeks after oral dosing. In addition, oral immunization of recombinant urease B spores induced a significant reduction (84 %) in the stomach bacterial load (0.25±0.13¾10 6 c.f.u.) compared to that in the non-recombinant spores treated group (1.56±0.3¾10 6 c.f.u.; P,0.01). This report shows that urease B expressed on B. subtilis spores was immunogenic, and oral administration of urease B spores can provide protection against H. pylori infection. INTRODUCTIONHelicobacter pylori is a Gram-negative bacterium that colonizes the stomach in approximately half the world's population. Infection may progress to pathological states, such as peptic ulcer disease and gastric adenocarcinoma, resulting in significant morbidity and mortality worldwide (de Martel et al., 2012;Nakamura et al., 2012;Toller et al., 2011; Uemura et al., 2001; You et al., 2012). Current regimens for treatment of H. pylori infection consist of a proton pump inhibitor (PPI) and antibiotics including amoxicillin, clarithromycin and metronidazole. Despite an eradication rate greater than 80 %, there are some limitations to the PPI-based triple therapy, such as poor patient compliance, emerging antibiotic resistance, frequent reinfection and high cost (Lee et al., 2013;Su et al., 2013). Vaccination would therefore be a suitable alternative or complement to antibiotic treatment to eradicate the bacterium and prevent reinfection (Czinn & Blanchard, 2011).Identification of antigens that can induce effective immune responses is a crucial step in vaccine development. Many protein molecules expressed by H. pylori have been shown to possess immunogenicity, including urease, cytotoxinassociated antigen, neutrophil-activating protein A, H. pylori adhesin A, vacuolating toxin A, catalase and outermembrane protein (Czinn & Blanchard, 2011;Liu et al., 2011).Among these antigens the B subunit of the urease protein (urease B), a 61 kDa protein encoded by a 1.7 kbp gene, is the most promising one. H. pylori produces a large amount of urease, which is essential for the survival and path...

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Mucosal Immunization with a Urease B DNA Vaccine Induces Innate and Cellular Immune Responses Against Helicobacter pylori

Cited by 28 publications

References 60 publications

The inflammatory and immune response to Helicobacter pylori infection

The inflammatory and immune response to Helicobacter pylori infection

Inflammation, Immunity, Vaccines for Helicobacter Infection

Expression of Helicobacter pylori urease B on the surface of Bacillus subtilis spores

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