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H. pylori electron micrograph showing one bacterium with 4 polar flagella

Meet Helicobacter pylori, the stomach bacteria that’s also considered a carcinogen

Posted on September 8, 2026September 8, 2026 by Jennifer Tsang

I’m so excited to introduce you to my favorite bacteria – and the subject from my PhD research – Helicobacter pylori. After spending the early 2010s growing this somewhat finicky bacterium and studying how it builds the flagellum (a tail-like structure it uses to move around). In fact, the picture above is a transmission electron micrograph image I took. I’ve since moved away from the bench, but I’m still in awe with how enigmatic and intriguing H. pylori is.

Helicobacter pylori quick facts

Name: Helicobacter pylori

Type of microbe: Bacteria

Habitat: Stomach (primarily human)

Harmful or helpful (to humans): A bit of both

Claim to fame: Considered a class 1 carcinogen

Helicobacter pylori‘s superpower: Living in the stomach

Scientists once thought that the stomach was a sterile organ because its low pH presumably made it inhospitable to bacteria. However, in the 1980s, scientists began reporting a number of bacteria detectable in the stomach, which includes H. pylori.

There is a catch though: while H. pylori lives in the stomach, it doesn’t prefer acidic conditions. You could say that it’s acid tolerance rather than an acidophile. The bacterium produces copious amounts of urease, an enzyme that buffers the pH around its cell, generating a “shield” of pH to counteract the stomach’s acidic conditions.

However, this urease shield is not a long term solution for survival. The bacterium must swim to the stomach mucosa lining where the pH is closer to neutral. To do so, H. pylori uses flagella to propel the organism forward while urease activity liquidfies the thick mucus. Once reaching the mucosal lining H. pylori can then cause ulcers and other disease symptoms.

Must keep swimming! Source: Zina Deretsky, National Science Foundation

How was Helicobacter pylori discovered?

Stomach ulcers were historically thought to be caused by stress. However, in 1982 Barry Marshall and Robin Warren discovered that H. pylori is actually the cause of these ulcers. These scientists found that almost all stomach biopsies from patients with gastric ulcers contained this helical shaped bacteria (hence the name Helicobacter). Barry and Marshall’s discovery was met with much skepticism at the time. Desperate to prove that H. pylori caused gastric ulcers, Marshall tested this on himself – Koch’s postulate style. He drank a culture of H. pylori, developed gastritis, and found the bacteria in his gastric biopsies. He then cured himself of the infection by taking antibiotics. For this discovery Marshall and Warren were awarded the Nobel Prize in Physiology or Medicine in 2005. 

Friend, foe, or both?

As I mentioned in the quick facts box, H. pylori can be thought of as a harmful bacterium since it causes gastritis, ulcers, and gastric cancer. This only happens in a small proportion of people that carry the bacterium. Over half of the world’s population are infected with H. pylori but out of those, just 10-15% get ulcers and about 1% get stomach cancer. Most people with H. pylori infections get it early on in childhood and the infection can persist for a lifetime without any symptoms or needed treatment. You might even have H. pylori without knowing it.

Why are infection outcomes different?

H. pylori infection outcomes depend on the interaction between the bacterium, the environment, and host genetics. Not all H. pylori strains are the same. Some strains make proteins that make the bacterium more likely to cause damage These proteins are CagA, which are toxins injected into cells lining the stomach, and VacA, which is a pore-forming toxin secreted by the bacterium (more details about CagA and VacA here). Where H. pylori infects the stomach also matters and researchers have proposed using a combination of location + atrophy to identify those at high risk of developing gastric cancer.

The fact that H. pylori is found in so much of the human population and only causes disease in a small fraction has some scientists viewing H. pylori as part of the microbiome as a commensal symbiont. One of these scientists is Martin Blaser who found an inverse relationship between childhood H. pylori infection and asthma and allergies. Scientists have also found that H. pylori infections are linked to lower risks of obesity, inflammatory bowel disease, gastroesophageal reflux disease, and esophageal cancer.

This topic is one of the reasons why I’m so fascinated by H. pylori. It’s the perfect illustration of how bacteria can’t be categorized as “black and white.” The bacterium is considered a pathogen and even a carcinogen, but still, the bacterium has evolved with us for ~100,000 years and seems to play protective roles in other diseases. 

If you love this post, check out the other microbes in the Meet a Microbe series!

What microbe should we feature next? Let us know in the comments below!

Further reading

  • A Tale of Two Toxins: Helicobacter Pylori CagA and VacA Modulate Host Pathways that Impact Disease. Frontiers in Microbiology. 2010.
  • Age of the Association between Helicobacter pylori and Man. PLOS Pathogens. 2012.
  • Attempt to fulfil Koch’s postulates for pyloric Campylobacter. Medical Journal of Australia. 1985.
  • Evaluation of gastric cancer risk using topography of histological gastritis: a large-scaled cross-sectional study. Digestive Diseases and Sciences. 2008.
  • Gastrointestinal microbiome and Helicobacter pylori: Eradicate, leave it as it is, or take a personalized benefit–risk approach? World Journal of Gastroenterology. 2022.
  • Inverse Associations of Helicobacter pylori With Asthma and Allergy. JAMA Internal Medicine. 2007.
  • Helicobacter pylori: Have potential benefits been overlooked? JGH Open. 2022.
  • Reservoir bugs: Study shows why stomach pathogen is so tough to eradicate. Stanford Medicine. 2019.
  • The human gastric microbiota: Is it time to rethink the pathogenesis of stomach diseases? UEG Journal. 2015.

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