Viral Antigens
Product List
CagA Pylori
Helicobacter Pylori Cytotoxin-Associated Gene A Recombinant
CagA Pylori recombinant antigen is a laboratory-produced version of the CagA protein from H. pylori. It is generated using E. coli bacteria as a production factory. The protein has a molecular weight of 34 kDa. For purification and research purposes, a His-tag is attached to the C-terminus of the protein. The purification process involves specialized chromatographic techniques to isolate the CagA protein.
Escherichia Coli.
HP-NAP
Neutrophil-activating protein A Helicobacter Pylori Recombinant
Omp Pylori
Helicobacter Pylori Outer Membrane Protein Recombinant
Introduction
Helicobacter pylori (H. pylori) is a gram-negative, flagellated, helical bacterium that colonizes the gastric mucosa. It was previously known as Campylobacter pylori . This bacterium is classified under the domain Bacteria, phylum Campylobacterota, class “Campylobacteria,” order Campylobacterales, family Helicobacteraceae, and genus Helicobacter .
Key Biological Properties: H. pylori is microaerophilic, requiring oxygen but at lower concentrations than in the atmosphere . It contains urease, an enzyme that converts urea to ammonia and carbon dioxide, raising the local pH and promoting its survival in the acidic stomach environment .
Expression Patterns and Tissue Distribution: H. pylori primarily infects the stomach lining, particularly the antrum . It is highly adapted to the gastric environment and can persist for decades if untreated .
Primary Biological Functions: H. pylori plays a significant role in the development of gastric disorders, including gastritis, peptic ulcers, and gastric cancer . It triggers both innate and adaptive immune responses, although these are often insufficient to clear the infection .
Role in Immune Responses and Pathogen Recognition: H. pylori can modulate the host’s immune response, leading to chronic inflammation and contributing to its pathogenicity .
Mechanisms with Other Molecules and Cells: H. pylori employs several mechanisms to establish infection, including the production of urease to neutralize stomach acid and the use of flagella for motility . It also produces adhesins that facilitate attachment to gastric epithelial cells .
Binding Partners and Downstream Signaling Cascades: Key adhesins include BabA, SabA, and CagA, which interact with host cell receptors to promote colonization and induce signaling pathways that alter cell behavior .
Regulatory Mechanisms Controlling Expression and Activity: The expression of H. pylori’s virulence factors is tightly regulated by transcriptional regulators such as Fur and NikR, which respond to metal ion availability . These regulators form complex networks that ensure the bacterium’s adaptation to the gastric environment .
Transcriptional Regulation and Post-Translational Modifications: H. pylori’s ability to survive and persist is also influenced by post-translational modifications of its proteins, which can affect their function and stability .
Biomedical Research: H. pylori has been instrumental in understanding the pathogenesis of gastric diseases and the development of diagnostic tools and therapeutic strategies . Research into its immune escape mechanisms has provided insights into potential biomarkers for early cancer detection .
Diagnostic Tools and Therapeutic Strategies: Diagnostic methods for H. pylori include invasive techniques like endoscopy and non-invasive methods such as breath tests and serology . Therapeutic strategies often involve antibiotics and proton pump inhibitors .
Role Throughout the Life Cycle: H. pylori’s life cycle involves colonization of the gastric mucosa, replication, and persistence . It can survive in the acidic stomach environment by producing urease and forming biofilms . The bacterium’s ability to adapt to various conditions throughout its life cycle contributes to its chronic colonization and pathogenicity .
