Good vs bad bacteria: the bugs responsible for Crohn’s disease

The make up of a person’s gut bacteria changes when they develop Crohn’s disease. Ohmega1982/Shutterstock

New links between the bacteria in your gut and disease are being made almost daily. We know, for instance, that the microbial communities residing in your intestines have a role in your mood and levels of stress. And the wrong types of bacteria are associated with obesity and related disorders such as type 2 diabetes.

The gut microbiome, which is made up of thousands of strains of bacteria, can alter your ability to fight off intestinal infections and may trigger inflammatory bowel diseases, a group of conditions that irritate the the colon and small intestine.

Patients with conditions such as Crohn’s disease or ulcerative colitis are thought to have an abnormal immune response to the presence of gut bacteria. But it was not clear if these bacteria were present at normal levels or if high levels of some “bad” strains triggered the immune response – until now.

A study published today in the journal Cell Host & Microbe reveals that the make up of a person’s gut bacteria changes when they develop Crohn’s disease. A relatively small number of bacterial types increase and a larger number decrease.

Could altering the gut microbiome protect you against Crohn’s disease? Shutterstock

The researchers, led by Dirk Gevers from the Broad Institute of Harvard and MIT, found that it’s not the presence of these bacteria that are likely to cause the problems, but what they do. The bacteria that were increased contributed to pathways involved in inflammation. Bacteria that were decreased participated in pathways important for energy and nutrient metabolism.

The study was one of the largest of its type with samples taken mainly from children and young adults who were newly diagnosed with Crohn’s. The researchers correlated their results in unaffected people, and in children or adults with advanced disease.

This strategy overcomes two shortcomings of previous work. The wide sampling from 28 centres ensured that the findings are relevant to the general public. And by targeting newly diagnosed patients they ensured that the typical treatment regimes for Crohn’s had not themselves irrevocably altered the gut microbiome.

But do these bad bacteria cause Crohn’s disease – or is it perhaps the absence of the good bacteria?

With other bacteria-caused disease, if enough of the bacteria are present, then almost anyone will show symptoms of that disease. This was illustrated by Australian Professor of Microbiology Barry Marshall when he drank a culture of Helicobacter pylori and gave himself stomach ulcers.

He firmly established the role of this bacteria in the formation of ulcers and (with much subsequent work) he and his colleague Robin Warren won the 2005 Nobel Prize in Physiology or Medicine.

2005 Nobel Prize winner Barry Marshall gave himself stomach ulcers to prove his hypothesis. AAP Image/Tony McDonough

But while Helicobacter can be killed with a two-week course of antibiotics, Gevers’ study found that antibiotic use in the Crohn’s patients correlated with a worsening in the already unbalanced bacterial community.

Despite the failure of antibiotic therapy, it’s worth thinking about the balance of bacteria. Would altering the gut microbiome protect you against Crohn’s disease? Equally, would re-balancing the microbial community reduce active disease? Unfortunately the answers to these questions are that we don’t yet know enough.

There has been some success with re-balancing the gut bacteria using fecal transplant. Yet, despite its popularity among patients, this is not yet a proven therapy for inflammatory bowel diseases and it should be considered a blunt tool, at best.

What Gevers’ study shows is that people newly diagnosed with Crohn’s have a common pattern of bacteria, which was seen from easily collected rectal samples. If this pattern is present prior to the overt symptoms of Crohn’s, the findings could lead to the development of an early warning system for Crohn’s disease.

More broadly, the research may provide us with the targets that future therapies would strive towards. If altering these key bacteria can help reduce the severity of Crohn’s, then this study has given us the means to gauge the effectiveness of future therapies on their bacterial targets.

For now, it’s encouraging to see large-scale efforts being made to understand such a debilitating and often overlooked disease. And perhaps we can hope that a new Nobel Prize for inflammatory bowel disease research is waiting just around the corner.