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Helicobacter pylori (or H pylori) is a common bacterium which lives in the human stomach. In parts of the UK, infection rates are as low as 15%. However, globally around 50% of the world’s population are infected, with rates being higher in less economically developed countries (LEDCs). In most cases, we don’t realise we are infected with H pylori and it does not cause any problems in the stomach. However, there is a strong association between infection with H pylori and increased risks of developing peptic ulcer disease and gastric cancer.
To quote the paper Wroblewski and colleagues (2010):
“Approximately half of the world’s population is infected with H pylori” and “long-term carriage of H pylori significantly increases the risk of site-specific diseases. Among infected individuals, approximately 10% develop peptic ulcer disease, 1-3% develop gastric adenocarcinoma …”
This gives some indication of the importance of managing H Pylori infection worldwide. In fact, it is of utmost importance to target populations where H pylori rates are higher to try and decrease gastric cancer rates.
The stomach is a harsh environment for any organism to live in, due to the acidic environment. One of H pylori’s survival mechanisms is having an extracellular urease enzyme creating a blanket of alkaline ammonia to buffer the stomach acid. This coupled with hiding away in the folds of the stomach allows H pylori to survive.
Interestingly, H pylori makes urease intracellularly (inside the cell) but it does not have a mechanism to transport the urease onto the outside of the bacterial cell wall. Instead, something quite remarkable happens! Whenever an H pylori dies, it bursts open and releases all of its intracellular urease molecules which then attach to neighbouring H pylori and help them survive. This has been termed “autocratic autolysis” – H pylori die for one another! Ok…. So how can urease inhibition help?
Urease is a strong virulence factor for H pylori helping it survive in the stomach, and it is widely believed that inhibiting urease would drastically weaken H pylori’s defences.
Our current research focuses on testing our Watercress Tonic against H pylori to see if we can achieve any one of a few outcomes:
1) Direct destruction of H pylori – in which case we have made a new antibiotic!
2) Improving susceptibility to antibiotics.
a. This may mean shorter courses or lower doses are effective, which could reduce side effects.
b. It may be that we increase the range of antibiotics that are effective. This is important given the rise in antimicrobial resistance seen in H pylori.
3) Reduction in virulence – we may make the H pylori more “quiescent”, i.e. it may not be entirely destroyed but we may reduce the incidence of disease associated with it.
Hopefully we will find out soon whether our Watercress Tonic can be effective in combatting any of these outcomes!