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.
Tagsacute leukemia acute lymphoblastic leukemia acute myeloid leukemia acute promyelocytic leukemia Add new tag anemia b cells blood smear bone marrow brain tumors carcinoma cases chronic myelofibrosis chronic myeloid leukemia chronic myeloproliferative disorders coagulation cortisol cytochemistry cytogenetics essential thrombocythemia heart hemophilia immunology infection inflammation kaplan kidney laboratory tests lymphocyte lymphocytes lymphoma macrophages neoplasia neutrophil normal photoblog polycythemia vera red blood cells red cells sickle cell anemia skin squamous cell carcinoma stains student questions t cells
- rachel said Ahh. Thank you very much!!!
- Abu Jar said Nice explanation….
- M said Thank you! You don’t know how much it helps me!! 🙂
- sai teja said Nice explanation
- Prashant waichal said Excellent and simple to the point review
- Julia said Thanks again for the clarification Dr Krafts!
- Kyaw said Thanks a million. This helps me a lot.
- Kristine said Good question – I believe so! I can’t think of an example of a type II hypersensitivity...
- gbadebo said Nice! But this brings up another question- are all examples of type II hypersensitivity reactions au...
- Dr.sunil Kumar.c. said very useful and nice explanation thank you so much…
- Luis said You are GREAT.
- dr sunil kumar laad said excellent