Helicobacter pylori: the pathway in the body · Biomarker & Stool Analysis

Helicobacter pylori is part of the pathway “Helicobacter pylori”. This page shows the whole pathway; the station of Helicobacter pylori is highlighted.

Where this laboratory value sits: Helicobacter pylori — spiral-shaped bacterium. Helicobacter pylori is a corkscrew-shaped bacterium that can colonise the human stomach. It prefers to live in the mucus directly above the stomach wall. There it splits urea with its urease. Source 1

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 stomach lining responds with an inflammatory reaction.

The pathway step by step

Each station states what the compound does there. Three signs: ↑ supplies — builds up or makes available · ↓ depletes — inhibits, consumes or withholds · ↕ both, depending on amount. Behind it stands what the statement rests on: established physiology, observed in studies, or contested. The signs do not grade; they name the direction.

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. Its corkscrew shape helps with this. Source 1↑ supplies The flagella drive the bacterium through the thick mucus; its corkscrew shape helps with this. It swims away from the acidic gastric juice towards the stomach wall, where the pH is close to neutral. established physiology Source 1
   ⚖ When the balance tips

   too much — If the gastric juice is very acidic, the bacterium survives it only briefly, as long as its urease buffers; it then moves all the more towards the stomach wall.

   too little — If the bacterium lacks motile flagella, it cannot cross the mucus and is washed away with the stomach contents; in animal models such strains do not colonise the stomach.

   observed in studies · Source 1, 2

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. The lining responds with an inflammatory reaction. Source 3↑ supplies BabA binds Lewis b sugars, SabA sialylated sugars of the lining. The firm binding holds the bacterium close to the cells; from there bacterial substances enter the cells and trigger an inflammatory reaction. observed in studies Source 3
   ⚖ When the balance tips

   too much — If the cells form more sialylated sugars, as described during an inflammatory reaction of the lining, SabA finds more binding sites, and more bacteria adhere.

   too little — If BabA and SabA find few matching sugars, fewer bacteria adhere; more of them remain in the mucus or are washed away with the stomach contents.

   observed in studies · Source 3

3. At the stomach wall → Bacterial protein Dead bacteria and detached protein fragments move on through the gut with the stomach contents. As long as the bacterium lives in the stomach, more keeps coming. Source 5↑ supplies The detached protein fragments carry components of the bacterium through the gut. Part of them survives the passage well enough for antibodies to still recognise it in the stool. established physiology Source 5
   ⚖ When the balance tips

   too much — If many bacteria live in the stomach, more bacterial protein reaches the gut and more antigen reaches the stool.

   too little — If few bacteria live in the stomach, or the bacterium is no longer present, little or no bacterial protein reaches the gut.

   established physiology · Source 5, 4

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. It is present only while the bacterium lives in the stomach. Source 5, 4↑ supplies The antigen no longer has a task of its own in the gut; it is a remnant of the bacterium. Because it arises only while the bacterium lives in the stomach, it indicates a current colonisation, unlike antibodies in the blood. established physiology Source 5, 4
   ⚖ When the balance tips

   too much — If there is a lot of antigen in the stool, more test antibodies bind, and the test signal becomes stronger.

   too little — If there is little antigen in the stool, for instance with low colonisation or shortly after acid-suppressing drugs or antibiotics, it may remain below the detection limit of the test.

   established physiology · 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. Both substances buffer acid. Source 2↕ both, depending on amount Ammonia and CO₂ are the bacterium's buffers: ammonia captures protons, CO₂ is turned into bicarbonate by carbonic anhydrase. In larger amounts ammonia burdens the bacterium itself; the amount decides. observed in studies Source 2, 7
   ⚖ When the balance tips

   too much — If ammonia builds up, the bacterium becomes too alkaline inside; it then incorporates ammonia into amino acids and throttles urea inflow via UreI.

   too little — If little ammonia forms, for instance when nickel for urease is missing, the bacterium hardly buffers acid; it then survives only briefly in the acidic gastric juice.

   observed in studies · 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. If it becomes too alkaline, the bacterium throttles urea inflow. Source 2↑ supplies Ammonia binds protons to form ammonium. The bacterium thus keeps its interior and its immediate surroundings close to neutral, while the gastric juice around it stays strongly acidic. established physiology Source 2
   ⚖ When the balance tips

   too much — If the bacterium buffers too strongly, its surroundings become alkaline; in the laboratory it then grows less well. This is why urease is fully active only at acidic pH.

   too little — If it buffers too little, acid enters the bacterium; its proteins and its metabolism then come to a standstill.

   observed in studies · 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. The CO₂ thus leaves the body. Source 4↓ depletes The CO₂ from urease leaves the body via blood and lungs. If the swallowed urea carries a labelled carbon, it appears in the breath only when urease has split it off. established physiology Source 4
   ⚖ When the balance tips

   too much — If a lot of urease is active in the stomach, more labelled urea is split, and more labelled CO₂ appears in the breath.

   too little — If little urease is active, for instance with low colonisation or under acid-suppressing drugs, little labelled urea is split, and hardly any label appears in the breath.

   established physiology · 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. They do not show whether the bacterium is still present. Source 4↑ supplies The IgG antibodies bind components of the bacterium but usually do not eliminate it. They show that the immune system has encountered the bacterium; they do not tell whether it still lives in the stomach. established physiology Source 4
   ⚖ When the balance tips

   too much — If the bacterium stays in the stomach for a long time, B cells keep forming IgG, and the antibodies remain in the blood.

   too little — Once the bacterium has disappeared, IgG falls only slowly over months; shortly after colonisation begins it is often not yet measurable.

   established physiology · Source 4

Further stations

• Helicobacter pylori — spiral-shaped bacterium Helicobacter pylori is a corkscrew-shaped bacterium that can colonise the human stomach. It prefers to live in the mucus directly above the stomach wall. There it splits urea with its urease. Source 1↓ depletes The bacterium uses the stomach as its habitat: it consumes human urea, occupies the mucus above the wall and triggers a persistent inflammatory reaction of the lining there. established physiology Source 1, 4
  ⚖ When the balance tips

  too much — If many bacteria live in the stomach, more urea is split and more bacterial protein is released into the stool; breath and stool tests then respond more clearly.

  too little — If few bacteria live in the stomach, for instance under acid-suppressing drugs, little urease activity and little antigen arise; breath and stool tests may then miss them.

  established physiology · Source 4, 5

• Urea — present in gastric juice Urea arises from protein breakdown in humans and passes from the blood into gastric juice. The bacterium absorbs it through a channel of its own. The channel opens only at acidic pH. Source 2↑ supplies Urea is the raw material of urease. The UreI channel opens only at acidic pH; urea thus enters the bacterium mainly when it needs ammonia for buffering. established physiology Source 2
  ⚖ When the balance tips

  too much — If plenty of urea is available and UreI is open, more ammonia forms; when the surroundings become neutral, the channel closes and the inflow stops.

  too little — If there is little urea in the gastric juice, urease can form less ammonia, and the bacterium buffers less acid.

  established physiology · Source 2

• Antigens — parts of the bacterium At the stomach wall, the immune system encounters components of the bacterium – surface proteins, flagella and urease. Immune cells then migrate into the lining. Source 4↑ supplies Immune cells of the lining recognise the bacterial components. This sets off an inflammatory reaction: immune cells migrate into the stomach lining, and B cells are stimulated to form antibodies. established physiology Source 4
  ⚖ When the balance tips

  too much — If many antigens meet the lining, more immune cells migrate in, and the inflammatory reaction of the lining becomes stronger.

  too little — If few antigens meet the immune system, the response stays weak, and fewer antibodies are formed.

  established physiology · Source 4

Cofactors in this pathway

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

Whole pathway: Helicobacter pylori

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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