Helicobacter pylori: the pathway in the body

This page shows the biochemical pathway behind the laboratory value Helicobacter pylori, Helicobacter pylori antigen (stool): which stations follow one another, which enzymes carry out each step and which cofactors they use. Every statement has a source. The page describes general textbook knowledge and says nothing about any individual person.

In brief

Helicobacter pylori is a spiral-shaped bacterium living in the mucus above the stomach wall. With the enzyme urease it splits urea into ammonia and carbon dioxide, keeping its surroundings less acidic.

The pathway step by step

1. Helicobacter pylori → In the gastric mucus · Flagella Using several flagella, the bacterium bores through the thick mucus. It follows the acid gradient towards the less acidic stomach wall. Source 1
2. In the gastric mucus → At the stomach wall · BabA, SabA The surface proteins BabA and SabA bind to sugar structures of the stomach lining. The bacterium thus stays in place instead of being washed onward. Source 3
3. At the stomach wall → Bacterial protein Dead bacteria and detached protein fragments move on through the gut with the stomach contents. Source 5
4. Bacterial protein → Antigen in the stool These protein fragments can be detected in stool: the test uses antibodies that bind specifically to components of Helicobacter pylori. Source 5, 4
5. Urea → Ammonia and CO₂ Urease · Nickel The enzyme urease splits urea into ammonia and carbon dioxide. It needs nickel at its centre and is one of the most abundant proteins of this bacterium. Source 2
6. Ammonia and CO₂ → Neutral surroundings · Ammonia Ammonia binds acid. The area around the bacterium therefore stays less acidic than the rest of the stomach, and the bacterium can persist there. Source 2
7. Ammonia and CO₂ → CO₂ in exhaled air The CO₂ from the splitting enters the blood and is breathed out. In the breath test, labelled urea is swallowed; if the label appears in exhaled air, urease is at work. Source 4
8. Antigens → IgG antibodies · B cells B cells form antibodies of the IgG class against them. These remain measurable in the blood even after the bacterium has left the stomach. Source 4

Cofactors in this pathway

• Nickel — Sits at the centre of urease; without nickel built in, the enzyme splits no urea Source 2
• GTP — Used by the accessory protein UreG when nickel is inserted into urease Source 6
• Zinc — Cofactor of the periplasmic carbonic anhydrase that converts CO₂ into bicarbonate Source 7
• Protons (gastric acid) — Open the UreI channel at acidic pH, through which urea enters the bacterium Source 2

Sources

1. Yoshiyama H, Nakazawa T. Unique mechanism of Helicobacter pylori for colonizing the gastric mucus. Microbes Infect 2000 · PubMed 10717541
2. Stingl K, De Reuse H. Staying alive overdosed: how does Helicobacter pylori control urease activity? Int J Med Microbiol 2005 · PubMed 16173497
3. Doohan D, Rezkitha YAA, Waskito LA et al. Helicobacter pylori BabA-SabA Key Roles in the Adherence Phase: The Synergic Mechanism for Successful Colonization and Disease Development. Toxins (Basel) 2021 · PubMed 34357957
4. Ansari S, Yamaoka Y. Helicobacter pylori Infection, Its Laboratory Diagnosis, and Antimicrobial Resistance: a Perspective of Clinical Relevance. Clin Microbiol Rev 2022 · PubMed 35404105
5. Gisbert JP, Pajares JM. Stool antigen test for the diagnosis of Helicobacter pylori infection: a systematic review. Helicobacter 2004 · PubMed 15270750
6. Yuen MH, Fong YH, Nim YS et al. Structural insights into how GTP-dependent conformational changes in a metallochaperone UreG facilitate urease maturation. Proc Natl Acad Sci U S A 2017 · PubMed 29203664
7. Modak JK, Liu YC, Machuca MA et al. Structural Basis for the Inhibition of Helicobacter pylori alpha-Carbonic Anhydrase by Sulfonamides. PLoS One 2015 · PubMed 26010545

Related pathways

• Alanine — urea
• Borrelia — igg antibodies

As of 2026-09-16. Draft, written by Claude to schema v2; sources checked in PubMed; expert approval pending
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