Findings show that a fibre-deprived gut microbiota deteriorates the protective mucus lining in the colon, triggering IBD development in a genetically susceptible host that could form the basis of future treatments.
“These findings open avenues for potential interventions in humans, including optimising exclusive enteral nutrition formulations and manipulating commensal bacteria to enhance beneficial metabolites,” said senior study author Professor Mahesh Desai.
“By unravelling the intricate connections between diet, gut microbiome, and metabolites, we aim to pave the way for more targeted interventions and treatments for IBD patients.”
Effects of fibre on inflammation and role of an enteral nutrition diet
Interestingly, the study found that feeding subjects with a fibre-rich diet prevented inflammation from developing, and that a switch from a low-fibre to a high-fibre diet led to a peak in inflammation, followed by a decline.
The team, from the Luxembourg Institute of Health and the University of Michigan Medical School, concluded that fibre can reverse the deleterious effects of mucus erosion on inflammation.
Ironically, IBD, especially in children, is often treated with a formula-based diet called exclusive enteral nutrition, which lacks fibre.
Despite a lack of fibre, this diet does result in reduced inflammation in people, which the research team could not explain.
“It seems one of the ways these exclusive enteral nutrition diets could possibly work in people is by triggering certain bacteria to make beneficial metabolites,” said Eric C Martens, study team member and professor of microbiology and immunology at the University of Michigan Medical School.
Fibre-free diet may increase reactions to increased numbers of mucin-degrading bacteria
The study, which was published in the journal Cell Host and Microbe, also found that the inflammation triggered by the fibre-free diets appeared to increase in reaction to the increased abundance of mucin-degrading bacteria Akkermansia muciniphila and Bacteroides caccae.
“These bacteria start foraging on the mucus layer for nutrients, reducing its thickness and barrier function, and brings microbes just 10 to 100 microns closer to the host tissue. That was enough in subjects with IBD genetics to make them sick,” said Martens.
Encouraged by these findings, the team now plan to further investigate how diet and bacteria interact to improve on therapies for paediatric IBD, as well as to answer how to potentially reverse or prevent the onset of these diseases by manipulation of these environmental triggers.
“Our findings suggest a potential new path for treating IBD. By tailoring specific dietary interventions to influence gut microbiome function, we may be able to manipulate these bacterial communities to alleviate inflammation,” said first study author Gabriel Pereira.
IBD and its link to ‘Westernised’ low-fibre diets
The findings come as incidences of IBD increase amid increasing industrialisation, and as more immigrant populations move to industrialised countries.
Dietary changes associated with this shift, characterised by decreased fibre and increased processed foods, emulsifiers, and sugars, have been identified as potential triggers for IBD.
It has been well established that microbes inhabiting the gut are continuously influenced by diet, especially fibre polysaccharides that are not digested in the upper gastrointestinal tract and arrive in the colon, providing nutrients for microbes.
Several studies that have fed subjects a low-fibre, high-sugar, or other “Westernised” diet have shown changes in the microbiome that are linked to reduced integrity of the mucus barrier.
This includes increased activity of mucin-degrading bacteria and reduced mucus thickness and increased mucus penetrability.
“As IBDs persist as global challenges, our research offers valuable insights to advance the understanding and treatment of these complex diseases,” added Desai, who is group leader of the eco-immunology and microbiome team at the Luxembourg Institute of Health.
