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Updated: May 12, 2026

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
Published on: June 18, 2016
The complement regulator CD46 is bactericidal to Helicobacter pylori and blocks urease activity
Rahma Basmarke-Wehelie1, Hong Sjölinder, Wiktor Jurkowski
1Department of Genetics, Microbiology and Toxicology, Stockholm University, Stockholm, Sweden.
Insights
The complement regulator CD46 acts as an antimicrobial agent against Helicobacter pylori. CD46 peptides show potential for eradicating H. pylori infections, offering a new therapeutic approach.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- CD46 is a complement regulator and pathogen receptor.
- Helicobacter pylori causes gastric diseases.
- The interaction between CD46 and H. pylori was investigated.
Purpose of the Study:
- To examine the interaction between CD46 and H. pylori.
- To determine if CD46 can inhibit H. pylori growth and pathogenicity.
Main Methods:
- Gastric epithelial cells and H. pylori strains were used.
- Flow cytometry, microscopy, and ELISAs evaluated bacterial interaction with CD46.
- Bacterial survival assays and in vivo studies were performed.
Main Results:
- H. pylori infection led to CD46 shedding.
- Soluble CD46 inhibited H. pylori growth by targeting urease and alkyl hydroperoxide reductase.
- CD46 peptides blocked bacterial urease activity and acid survival.
- Oral CD46 peptide treatment eradicated H. pylori in mice.
Conclusions:
- CD46 demonstrates antimicrobial properties against H. pylori.
- CD46 peptides represent a potential therapeutic strategy for H. pylori infections.
Background & Aims:
CD46 is a C3b/C4b binding complement regulator and a receptor for several human pathogens. We examined the interaction between CD46 and Helicobacter pylori (a bacterium that colonizes the human gastric mucosa and causes gastritis), peptic ulcers, and cancer.
Methods:
Using gastric epithelial cells, we analyzed a set of H pylori strains and mutants for their ability to interact with CD46 and/or influence CD46 expression. Bacterial interaction with full-length CD46 and small CD46 peptides was evaluated by flow cytometry, fluorescence microscopy, enzyme-linked immunosorbent assay, and bacterial survival analyses.
Results:
H pylori infection caused shedding of CD46 into the extracellular environment. A soluble form of CD46 bound to H pylori and inhibited growth, in a dose- and time-dependent manner, by interacting with urease and alkyl hydroperoxide reductase, which are essential bacterial pathogenicity-associated factors. Binding of CD46 or CD46-derived synthetic peptides blocked the urease activity and ability of bacteria to survive in acidic environments. Oral administration of one CD46 peptide eradicated H pylori from infected mice.
Conclusions:
CD46 is an antimicrobial agent that can eradicate H pylori. CD46 peptides might be developed to treat H pylori infection.
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