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.
- Anon said Isn’t anti- A,B an expected antibody, just as anti-A and anti-B are, due to plant lectins (bas...
- Dr.Govind said excellent explanation thank you very much.
- Dr.Govind said nice
- nouf said 🙂
- Dr Govind said very simple explanation thank u very much..
- Dr Govind said nicely explained.
- Ana said Dope!! I love your summary….keep it up
- Kristine said Hi Michelle – thank you so much for your kind words! I’m SO glad you find useful stuff o...
- Michelle Stoffel said From a second year pathology resident who has been a fan of your site since discovering it as a 3rd...
- abhiram said crisp nd clear….thnk u…..
- Nelmary said I Had the same confusion with myelosupression and aplastic anemia thanks for clarifying my doubt.
- Sameera said Thank u, simple and clear