Recombinant Helicobacter Pylori Antigens — For Vaccine Research and Development

Helicobacter pylori (H. pylori), a powerful carcinogenic pathogen, is responsible for the induction of 75% of gastric cancers worldwide. In general, the current treatment for patients who are infected with H. pylori consists of daily administration of three antibiotics, proton pump inhibitor, amoxicillin, clarithromycin. But the resistance of H. pylori to antibiotics is increasing day by day. Effective vaccine is a promising alternative to reach the global eradication of H. pylori. However, most vaccines currently under development are at a very early stage.
Creative Diagnostics offers a series of recombinant H. pylori antigens, including catalase, urease, CagA, VacA and other recombinant proteins. These potential H. pylori candidate antigens are designed to support your vaccine development.

Product List

Cat_N	Target	Tag	Expression System
DAG-WT416	Catalase (KatA)	His	E. coli
DAGA-059	Urease (UreA)	Unconjugated	Yeast
DAGA-061	Urease (UreB)	Unconjugated	E. coli
DAGA-056	Cytotoxin-associated gene A (CagA)	His	E. coli
DAGA-057	Vacuolating cytotoxin A (VacA)	Unconjugated	E. coli
DAG-WT419	Heat Shock Proteins (HSP)	Unconjugated	E. coli
DAGA-063	Flagellin A (FlaA)	Unconjugated	E. coli
DAG4324	Outer Membrane Proteins (OMP)	His	E. coli
DAGC470	HP0305	His	E. coli
DAG-WT420	CagA, HSP	Unconjugated	E. coli

Introduction

Helicobacter Pylori (H. pylori) is a gram-negative, flagellated, microaerophilic bacterium that selectively colonizes the gastric mucosa. H. pylori is unique in that the bacterium can persist in the harsh stomach environment, where it damages the gastric mucosa and alters the pattern of gastric hormone release, thereby affecting gastric physiology. Upon infection, H. pylori activates multiple intracellular pathways in epithelial cells, such as MAPK, NF-kB, activator protein AP-1, Wnt/b-catenin, PI3K pathways and signal transducers and activators of transcription STAT3. These affect various cellular functions, leading to increased inflammatory cytokine production, altered apoptosis rate, epithelial cell proliferation and differentiation, and finally resulting in epithelial cell oncogenic transformation.

The role of bacterial adherence in Helicobacter pylori virulence

Fig. 1 The role of bacterial adherence in Helicobacter pylori virulence (Oleastro M, et al. 2013)

Virulence factors

Flagella located at one pole of the bacterial cell. Each flagellum is principally composed of a filament made of the flagellin A and B (FlaA/B), surrounded by a membranous sheath containing many different proteins. H. pylori flagella may influence their colonization in bacteria, inflammation, and immune evasion.
Urease, an important virulence factor involved in a series of processes that allow bacteria to colonize and induce a strong inflammatory response in the gastric epithelium. Urease consisting of a dodecameric organization of two subunits (UreA, 26.5 kDa; UreB, 61.7 kDa).
The outer membrane protein plays a pivotal role in the attachment and colonization of gastric cells. Sialic acid-binding adhesin (SabA), blood-group-antigen-binding adhesin (BabA), adherence-associated lipoprotein A and B (AlpA/B), outer inflammatory protein A (OipA), and Helicobacter outer membrane protein Q (HopQ) were involved in adhesion.
The cytotoxin-associated genes (cag) pathogenicity island and the vacuolating cytotoxin (VacA) are two major cytotoxins associated with more severe disease. CagA affects the adhesion, spreading, and migration of the cell. VacA can help H. pylori colonization. Moreover, CagA and VacA can also affect the host cell in several aspects.

References

Sutton P, Boag JM. (2019). Status of vaccine research and development for Helicobacter pylori. Vaccine. 37(50), 7295-7299.
Viana IDS, Santos MLC, Marques HS, et al. (2021). Vaccine development against Helicobacter pylori: from ideal antigens to the current landscape. Expert Review of Vaccines. 20(8), 989-999.
Matsuo Y, Kido Y, Yamaoka Y. (2017). Helicobacter pylori Outer Membrane Protein-Related Pathogenesis. Toxins. 9(3), 101.
Chang WL, Yeh YC, Sheu BS. (2018). The impacts of H. pylori virulence factors on the development of gastroduodenal diseases. Journal of Biomedical Science. 25(1), 68.
Skene C, Young A, Every A, et al. (2007). Helicobacter pylori flagella: antigenic profile and protective immunity. FEMS Immunology & Medical Microbiology. 50(2), 249–256.
Oleastro M, Ménard A. (2013). "The Role of Helicobacter pylori Outer Membrane Proteins in Adherence and Pathogenesis." Biology. 2(3), 1110-1134.