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.
|DAG-WT416||Catalase (KatA)||His||E. coli|
|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|
|DAG-WT420||CagA, HSP||Unconjugated||E. coli|
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.
Fig. 1 The role of bacterial adherence in Helicobacter pylori virulence (Oleastro M, et al. 2013)