Human immune response towards recombinant Helicobacter pylori urease and cellular fractions

Voland, Petra; Zeitner, Marco; Hafsi, Nadia; Prinz, Christian

doi:10.1016/j.vaccine.2005.07.021

Cited by 8 publications

(8 citation statements)

References 39 publications

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“…Thus, even in the absence of complete eradication, therapeutic vaccination may already be beneficial, as it reduces the numbers of bacteria exposed to antibiotics and thus decreases the possibility of inducing antibiotic-resistant H. pylori organisms. Although one should be aware of the limitations of animal models with regard to therapeutics, preliminary human vaccine trials have already been performed and further results are awaited (294,310,327,425,668).…”

Section: Vaccinationmentioning

confidence: 99%

Pathogenesis ofHelicobacter pyloriInfection

2006

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SUMMARY Helicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world's population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Disease outcome is the result of the complex interplay between the host and the bacterium. Host immune gene polymorphisms and gastric acid secretion largely determine the bacterium's ability to colonize a specific gastric niche. Bacterial virulence factors such as the cytotoxin-associated gene pathogenicity island-encoded protein CagA and the vacuolating cytotoxin VacA aid in this colonization of the gastric mucosa and subsequently seem to modulate the host's immune system. This review focuses on the microbiological, clinical, immunological, and biochemical aspects of the pathogenesis of H. pylori.

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Section: Vaccinationmentioning

confidence: 99%

Pathogenesis ofHelicobacter pyloriInfection

2006

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“…25,27 We first nonintegrin (DC-SIGN) is the DC surface receptor that binds H. pylori glycans 11,12 and that H. pylori stimulates DCs predominantly through a Toll-like receptor (TLR)-dependent signaling cascade. 13 H. pylori-pulsed DCs (HP-DC) promote a type 1 helper T cell (Th1) response [14][15][16][17][18][19][20] and, as shown more recently, an interleukin (IL)-17-producing helper T cell (Th17) response. 21 Several studies have suggested the immunoregulatory effects of H. pylori on DCs.…”

Section: Helicobacter Pylori Directs Tolerogenic Programming Of Dendrmentioning

confidence: 99%

Helicobacter pyloridirects tolerogenic programming of dendritic cells

et al. 2010

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3 Gastric CD103 + dendritic cells, which are known to induce mucosal regulatory T cells, were also increased in number, raising the question whether H. pylori infection induces a regulatory T cell-skewed response by way of a bacteria-dendritic cell interaction. In fact, bone marrow-derived dendritic cells underwent tolerogenic programming, skewing the balance between effector and regulatory T cell responses towards regulatory T cell differentiation in a transforming growth factor-β-and interleukin-10-dependent manner. Depletion of regulatory T cell numbers augmented H. pylorispecific effector helper T cell responses, which correlated with a lower degree of H. pylori colonization. These results suggest H. pylori is capable of inducing a regulatory T cell-skewed response that limits the host's ability to eradicate the bacteria, allowing the H. pylori infection to persist. To better understand the mechanism of H. pylori tolerogenic programming we compared the differential expressions of 34 genes critical for dendritic cell function in bone marrowderived dendritic cells pulsed with live H. pylori or other Gram-negative bacteria (e.g., Escherichia coli, Acinetobacter lwoffii). Our data imply that H. pylori targets the Toll-like receptor 2 pathway to induce a regulatory T cell-skewed response. In addition, we show that H.

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“…The major Th1 promoting factor of H. pylori is HP-NAP that stimulates IL-12 production via TLR2 (Amedei et al 2006 ) . However, other Th1 driving factors also exist, such as products of cag, as well as VacA, hsp90, outer membrane protein 18, cysteine-rich protein A, and lipopolysaccharide ( D'Elios et al 1997a ;Guiney et al 2003 ;Deml et al 2005 ;Voland et al 2006 ;Taylor et al 2006 ;Takeshima et al 2011 ) . Hou et al ( 2007 ) studied the association between gastric cancer and several variants in genes responsible for Th1 cell-mediated response, that is typical in H. pylori infection, (D'Elios et al 1997a ;Amedei et al 2006 ) , and in particular the results suggest that a polarized Th1 response may play a role in the genesis of severe clinical forms of disease (D'Elios et al 1997a, b ) , Hou et al ( 2007 ) subsequently reported that carrying the C allele of the interferon gamma receptor 2 ( IFNGR2 ) (Ex7-128) rs4986958 polymorphism was associated with an increased risk of gastric cancer compared with the TT genotype.…”

Section: Immune Response Genesmentioning

confidence: 99%

Gastric Cancer and Helicobacter pylori

Amedei

D’Elios

2011

Bacteria and Cancer

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Helicobacter pylori ( H. pylori ) is a gram-negative bacterium that chronically infects the stomach of more than 50% of the human population and represents a major cause of gastric cancer, gastric lymphoma, gastric autoimmunity and peptic ulcer diseases. The International Agency for Research on Cancer classifi es H. pylori as a human carcinogen for gastric cancer. Eradicating the bacterium in high-risk populations reduces the incidence of gastric cancer. Likewise, antibiotic treatment leads to regression of gastric mucosa-associated lymphoid tissue lymphoma. Gastric infl ammation induced by H. pylori is the main singular risk factor for gastric malignancies. This chapter outlines the bacterial and host factors involved in the genesis of gastric cancer and gastric lymphoma. Treatment options for patients with an advanced gastric malignancy are still limited, but the introduction of an effective vaccine will be the best tool for preventing both H. pylori infection, gastric cancer and gastric lymphoma.

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Human immune response towards recombinant Helicobacter pylori urease and cellular fractions

Cited by 8 publications

References 39 publications

Pathogenesis ofHelicobacter pyloriInfection

Pathogenesis ofHelicobacter pyloriInfection

Helicobacter pyloridirects tolerogenic programming of dendritic cells

Gastric Cancer and Helicobacter pylori

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