H. pylori is one crazy bug.

It lives in one of the most hostile environments in the body: the highly acidic stomach. In fact, it not only lives there, it seems to thrive! It has managed to colonize over half of the world’s population. It’s a nasty bug too, at least in some ways: it causes gastritis, gastric ulcer, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. How does it manage to do all these things and still look pretty?

H. pylori has a ton of cool features that allow it to survive in the stomach and cause disease there. Here’s a short list:

1. Urease. This is one of the most important features of H. pylori; without it, the bug could not survive in the stomach. Urease is an enzyme that breaks urea (an abundant substance in the body) into carbon dioxide and ammonia. The carbon dioxide gets blown off, but the ammonia stays and surrounds the bug, raising the pH and allowing the bug to sit comfortably in this otherwise deadly environment.

2. Mucinase. Here’s another cool enzyme in H. pylori‘s arsenal. Mucinase does just what the name suggests: it busts apart the thick mucin layer that normally overlies the gastric epithelium, allowing H. pylori to walk on through this layer of protection and get right onto the surface of the epithelial cells.

3. Corkscrew motility. H. pylori is curved, and it has a few nice flagellae at one end. So it sort of corkscrews itself down through the mucin to reach the epithelial layer. Much more effective than a regular old straight rod trying to push its way through.

4. CagA. This is a virulence factor that does a ton of stuff, including disrupting cell junctions, affecting cell proliferation and differentiation, and inducing inflammation. Patients who have cagA positive strains generally have more severe gastritis, and a significantly increased risk of developing ulcers and carcinoma.

5. VacA. This is another virulence factor that does a ton of stuff, including making vacuoles, inducing apoptosis, disrupting cell pathways, inducing inflammation, and modulating the immune system (it allows H. pylori bugs to live in macrophages, and also inhibits T-cell production by decreasing IL-2 production). Nasty. Patients with vacA positive strains also have an increased risk of severe gastritis, ulcers and carcinoma.


Tagged with:

8 Responses to H. pylori: How does it do it all?

  1. Joseph Ferrara says:

    I have patients from the deep South, some of African American heritage. One of my older patients tells me that when he was a young man his doctor would treat him with antibiotics for peptic ulcer disease and it worked.

  2. Kristine says:

    Interesting how sometimes those older, useful remedies turn out to have a scientific explanation!

  3. Srivatsav says:

    The explanation is amazing, its so simple and effective to remember, simply like spoon feeding, thanks a lot please explain some more topics like this.

  4. Kristine says:

    Thanks so much! Glad it was helpful. 🙂

  5. Ahmed Yusuf says:

    This is very easy way to remember about H.Pylori. thanks

  6. Sviatoslav Redko says:

    Kristine thank you so much. I have never thought that path can be tought in such an exciting way!

    Here in Belarus Metranidazole in combo with Ampicillin had been used early before the discovery of the possible causative agent. Ironically, the monographs written in seventies in order to lay down a theoretical basis to that empiric discovery propose side effects of this drugs (literally increase in mucus production) as a possible mechanism of action. That’s because the causes of PUD were thought to be well established at that time and any attempts to change something in this field might not be taken with owing seriousness.

  7. Jacklyn Joseph says:

    Thanks for that H. Pylori info in a nutshell

  8. Kristine says:

    Very interesting! It’s odd how an unproven theory (ulcers are caused by stress and excess acid), if repeated long enough, can become accepted as fact. And then it takes a long time to change it, even in the face of scientific proof (Helicobacter causes ulcers)! Also interesting how they proposed side effects as the reason the antibiotics worked! Nobody talks about it much, but the first person to describe what would eventually be called Helicobacter was a Polish researcher, Jaworski, in Krakow, Poland (at Jagiellonian) in the late 1800s…

Leave a Reply

Your email address will not be published. Required fields are marked *