In Western countries an average of 2 in 100,000 children aged between 10 and 19 years suffer from Inflammatory Bowel Disease (IBD), a broader term (as already explained on this blog) for Crohn’s disease and ulcerative colitis. And experts are warning that the number of cases of this condition is on the rise.
Once diagnosed, children face a lifetime of illness with many potential consequences for their health. In the case of Crohn’s disease, early onset can lead to a range of consequences including delaying both growth and puberty and weakened bones. That is why it is essential to identify quickly whether a treatment is effective. Young patients are currently treated with antibiotics, an anti-inflammatory drug called anti-TNF or a highly restrictive diet. In spite of this, it is not known how these treatments work and this, together with the lack of knowledge about what causes the disease, is hindering the development of new therapeutic options for patients.
Now, the findings of a new study published in Cell Host and Microbe and led by researchers from the Perelman School of Medicine at the University of Pennsylvania could suggest new strategies for diagnosing and treating IBD in young patients.
The researchers, in collaboration with the Children’s Hospital of Philadelphia, Seattle Children’s Hospital and Canada’s IWK Health Centre and Hospital for Sick Children, analysed the gut microbiota of children suffering from Crohn’s disease who were receiving treatment. They observed that both diet-based and anti-inflammatory therapies can alter the gut microbial composition without fully restoring the natural stability of gut bacteria and fungi. As it is also known that Crohn’s disease is characterised by an altered gut microbial composition, these results could be used in future to develop new strategies for diagnosing and treating patients with IBD.
“We showed that microbes in the gut respond to IBD treatment in a much more complex way than has been previously appreciated,” said co-principal investigator Gary Wu of the University of Pennsylvania in a statement. “The results of our study provide information that could be used to track or predict disease, as well as new diet-based therapeutic strategies,” he added.
Wu and his colleagues led an international study of 90 children with Crohn’s disease and 26 healthy control children. They tracked symptoms, inflammation and microbial changes over 8 weeks and carried out a metagenomic sequencing analysis of the subjects’ stool samples in order to observe the effect therapeutic treatments had on their imbalanced gut microbiota. At the end, they collected more than half a trillion bases of DNA sequence information and used them to characterise gut microbes’ behaviour over time.
The first finding was that none of the treatments was able to restore the normal balance of the gut’s microorganisms. For instance, they saw that using antibiotics was linked to highly disturbed bacterial communities and an abundance of fungi in the gut. Meanwhile, formula-based diets were able to reduce inflammation and decrease fungal abundance, but were not able to correct the imbalance of the bacterial population. And although anti-TNF therapy allowed the microbial community to approach what could be understood as healthy state, it did not reduce fungal abundance.
“The formula-based diet helped the children to improve their symptoms and inflammation despite making the microbiota initially more dysbiotic [imbalanced],” explained Wu. “This is an intriguing finding implying that it may not be necessary to completely restore a healthy microbiome in order to provide a beneficial effect.”
According to this study, while dysbiosis is an important part of Crohn’s disease, the reaction of gut microbes to different treatments can vary significantly. Although more research is needed, the discovery could pave the way for new ways to diagnose and choose the right therapy for each patient.
Cell Host & Microbe, Lewis and Chen et al.: “Inflammation, Antibiotics, and Diet as Environmental Stressors of the Gut Microbiome in Pediatric Crohn’s Disease” http://dx.doi.org/10.1016/j.chom.2015.09.008
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