Inflammatory bowel disease (IBD) is a common term for two conditions, namely Crohn’s disease and ulcerative colitis, that are marked by chronic inflammation of the digestive tract. With symptoms such as pain, fatigue and reduced appetite, IBD can significantly impact the patient’s quality of life and working efficiency.
The onset and development of IBD is generally considered to be influenced by two factors: infection and the patient’s immune response. Recent studies, however, have shown that not all infections or pathogen exposures affect the development of IBD in the same way.
For instance, Helicobacter pylori (H. pylori), a bacterium responsible for gastritis, peptic ulcers, and gastric cancer, has recently been shown to exhibit a negative correlation with IBD. While several explanations have been put forward for this surprising find, the exact role of H. pylori in IBD and its effect on the immune system has remained elusive.
In a recent review article, researchers from the Chinese Academy of Medical Sciences and Peking Union Medical College led by Dr. Hong Yang have now shed light on this front, taking stock of the research on the potential effects of H. pylori on intestinal microbiota and IBD. This paper was made available online on February 27, 2022 and was published offline in Volume 135 Issue 6 of the Chinese Medical Journal on March 20, 2022.
Some studies have suggested that a disordered gut microbiome and the imbalance between beneficial and harmful bacteria is the underlying cause of IBD. There are two ways by which IBD alters the microbiota. One, patients with IBD usually have lower overall diversity and abundance of gut microbiota compared to their healthy counterparts. IBD patients also show a decreased abundance of Firmicutes and Bacteroidetes, two of the most important fecal microbiota found in humans.
Patients with IBD also exhibit lesser concentrations of short-chain fatty acids (SCFAs). This sheds light on the influence of Ruminococcaceae, a butyrate producer and an enabler of IBD.
“This is where the role of H. pylori comes in,” explains Dr. Yang. “The positive role played by H. pylori in asthma, rheumatoid arthritis, and IBD has changed its image from a harmful, disease-causing microorganism to a beneficial one”
While the incidence and prevalence of IBD vary across geographical areas, it follows an interesting trend. For instance, in the Asian continent, an area with a high abundance of H. pylori, the prevalence of IBD is surprisingly low. This suggests a negative correlation between the prevalence of H. pylori and IBD. Furthermore, some studies have observed this inverse correlation between H. pylori infection and IBD in mice models.
Moreover, certain phenomena induced by H. pylori are known to alter the gut microbiota. A study analysing the gut microbiota following a chronic H. pylori infection revealed an abundance of Akkermansia, a short-chain fatty acid-producing bacterium and an important member of healthy microbiota in the intestinal mucosa. Another study observed a significant decrease in the abundance of Bacteroidetes in patients with H. pylori infection and an increase in Firmicutes.
On the other hand, eradication treatments for H. pylori significantly was shown to lead to a loss of gut microbiota diversity. The results showed improvement when the therapy was supplemented with probiotics.
With these findings, the researchers indicate that H. pylori might, in fact, make the host less vulnerable to IBD. “Along with inducing changes in the gastric microenvironment, H. pylori interacts with microbiota in the large intestine, thereby creating a new physiological balance in the gastrointestinal tract which might protect against IBD,” says Dr. Yang.
Additionally, she puts forward a suggestion for clinicians managing IBD. “Rather than an indiscriminate eradication advised in some guidelines, selective eradication and surveillance of patient subgroups with a high risk of H. pylori infection is the most suitable course of action,” she recommends.
There is certainly more to H. pylori than meets the eye!
This article is based on a press release from Cactus Communications.