The molecular mechanism permitting the bacterium Helicobacter pylori (H. pylori) to survive in nearly 50% of humans' stomachs has been identified, according to research published in Science Advances
The molecular mechanism permitting the bacterium Helicobacter pylori (H. pylori) to survive in nearly 50% of humans’ stomachs has been identified, according to research published in Science Advances.
One of the most common worldwide bacterial infections, H. pylori is able to avoid the antiseptic effects of the stomach’s acid and latch onto the mucus layer that coats stomach walls.
Researchers from the University of Nottingham School of Pharmacy in the United Kingdom studied the bacterium using powerful x-rays to observe the atomic level interactions between the H. pylori adhesion proteins called BabA and Lewisb sugars of the gastric mucus. BabA has a specific latch which enables it to attach to Lewisb using hydrogen bonds.
However, the researchers found that if some of the hydrogen bonds were interrupted, the latch malfunctions and the binding to the mucus wall does not hold the H. pylori cell in place. The scientists believed this knowledge was the first step in heading toward developing strategies to combat the treatment of H. pylori infections.
“Because BabA is unique to H. pylori, we can specifically target, and hopefully eradicate, this bacterium without affecting the other good bacteria in our normal flora,” explained Naim Hage, a postgraduate researcher who worked on the project as part of his doctoral thesis. “If successful, this therapeutic strategy will also be extremely useful for treating H. pylori infections that are already resistant to antibiotics.”
The research was partially funded by AstraZeneca R&D, who will next be looking into developing anti adhesion strategies to clear H. pylori from stomachs. The researchers said that by dislodging the BabA to Lewisb inhibitors, infections would be able to be treated. The H. pylori infections are gaining resistance worldwide to conventional antibiotic therapies.
“While this study answers long standing questions about how H. pylori colonizes the stomach, it represents the very first step in the development of novel therapies,” concluded principal investigator Franco Falcone. “The next few years of laboratory based research will be crucial to determine if an anti BabA adhesion approach is viable and can progress to clinical development. A similar approach is already showing promising results for the treatment of urinary tract infections in preclinical models. Looking forward, we are excited to continue working closely with AstraZeneca R&D who have provided a tremendous amount of support to achieve this discovery.”