Gut inflammation may alter how bacteria process food.
A new study published in Gastroenterology finds that gut inflammation can change how gut bacteria break down food, possibly triggering immune reactions to foods that were previously tolerated. The findings may help explain why many people with IBD react adversely to foods such as dairy or gluten, even in remission.
About two-thirds of patients with IBD report food intolerances. Dairy, wheat and fibre are the most frequently blamed triggers, but the mechanisms have remained unclear.
The gut microbiota may hold the answer. Prior research has shown that patients with IBD often have an altered microbiota. This study identifies a novel mechanism by which that alteration drives food reactions.
“The microbiome acts as a metabolic organ, helping us digest food components, including those that can trigger gut reactions,” said Dr Alberto Caminero. “Our study shows that inflammation impairs this microbial digestive capacity, potentially contributing to adverse food reactions and opening new possibilities for microbiome-based therapies to restore this function in patients with IBD.”
Other key authors from McMaster University Medical Centre included Dr Bruna Barbosa and senior clinical collaborators Dr Neeraj Narula and Dr Premysl Bercik.
Using two mouse models of colitis, researchers found that inflammation made animals more prone to developing food sensitivities. After inflammation, exposure to dairy or gluten triggered an allergic-type immune response in the colon; reintroducing those foods later caused heightened gut sensitivity and worse colitis symptoms.
The cause traced back to the microbiota: inflammation depleted the specific bacteria that normally break down these food triggers. That shift alone was enough to increase sensitisation risk – transferring gut bacteria from inflamed mice into germ-free mice made those mice more prone to sensitisation to the same foods, while restoring the missing bacteria reduced these effects.
The pattern held in humans, too. Among patients with IBD, those who self-reported food intolerances were more likely to have both a reduced ability to break down common trigger foods and lower levels of the bacteria responsible for that job.
The researchers note that microbiota disruption is likely just one piece of a larger picture that also includes genetics, infections and stress – all of which need further research.
Together, the findings point to a possible mechanism behind food sensitivities in IBD: inflammation disrupts the gut bacteria that normally process certain foods, and this disruption – not the foods themselves – helps trigger the immune reactions patients experience.
